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Sample records for neurological deficits caused

  1. Ischemia may be the primary cause of the neurologic deficits in classic migraine

    DEFF Research Database (Denmark)

    Skyhøj Olsen, T; Friberg, L; Lassen, N A

    1987-01-01

    This study investigates whether the cerebral blood flow reduction occurring in attacks of classic migraine is sufficient to cause neurologic deficits. Regional cerebral blood flow measured with the xenon 133 intracarotid injection technique was analyzed in 11 patients in whom a low-flow area...... ischemia and neurologic deficits. Hence, this study suggests a vascular origin of the prodromal neurologic deficits that may accompany attacks of classic migraine....

  2. Focal neurological deficits

    Science.gov (United States)

    ... or head Electromyogram (EMG), nerve conduction velocities (NCV) MRI of the back, neck, or head Spinal tap Alternative Names Neurological deficits - focal Images Brain References Daroff RB, Jankovic ...

  3. Multidetector Row CT Detection of a Patent Foramen Ovale Causing Neurologic Deficits in an Adolescent: A Case Report

    Energy Technology Data Exchange (ETDEWEB)

    Lee, Jung Bin [Dept. of Radiology, Soonchunhyang University College of Medicine, Bucheon (Korea, Republic of); Kim, Dong Hun; Oh, Jae Hee [Dept. of Radiology, Chosun University College of Medicine, Gwangju (Korea, Republic of); Seo, Hye Sun [Dept. of Internal Medicine, Soonchunhyang University College of Medicine, Bucheon (Korea, Republic of); Suk, Eun Ha [Dept. of Anesthesiology and Pain Medicine, Asan Medical Center, Seoul (Korea, Republic of)

    2012-02-15

    A patent foramen ovale (PFO) is a persisting fetal circulation structural abnormality that can cause neurologic deficits such as migraine and cryptogenic stroke. Here we report a case of PFO diagnosed by cardiac multidetector row CT in an adolescent male with chronic migraine and stroke.

  4. Rehabilitative potential of Ayurveda for neurological deficits caused by traumatic spinal cord injury

    Science.gov (United States)

    Rastogi, Sanjeev

    2014-01-01

    Spinal cord injury (SCI) is associated with worst outcomes and requires a prolonged rehabilitation. Ayurvedic indigenous methods of rehabilitation are often utilized to treat such conditions. A case of SCI was followed up for 3 months upon an Ayurvedic composite intervention and subsequently reported. The composite treatment plan involved Ayurvedic oral medications as well as a few selected external and internal pancha karma procedures. A substantial clinical and patient centered outcome improvement in existing neurological deficits and quality of life was observed after 3 months of the Ayurvedic treatment given to this case. PMID:24812477

  5. Rehabilitative potential of Ayurveda for neurological deficits caused by traumatic spinal cord injury

    Directory of Open Access Journals (Sweden)

    Sanjeev Rastogi

    2014-01-01

    Full Text Available Spinal cord injury (SCI is associated with worst outcomes and requires a prolonged rehabilitation. Ayurvedic indigenous methods of rehabilitation are often utilized to treat such conditions. A case of SCI was followed up for 3 months upon an Ayurvedic composite intervention and subsequently reported. The composite treatment plan involved Ayurvedic oral medications as well as a few selected external and internal pancha karma procedures. A substantial clinical and patient centered outcome improvement in existing neurological deficits and quality of life was observed after 3 months of the Ayurvedic treatment given to this case.

  6. Successfully treated transoral crossbow injury to the axial spine causing mild neurologic deficit: case presentation.

    Science.gov (United States)

    Kovari, Viktor Zsolt

    2017-05-01

    To detail the management, complications and results of a crossbow arrow injury, where the broadhead went through the mouth, tongue, soft palate, C2 vertebra, spinal canal, dural sack, exiting the neck posteriorly and the arrow shaft lodged in the spine causing mild spinal cord injury. Case presentation. A penetrating axial cervical spine crossbow injury was treated successfully in spite of the following interdisciplinary complications: meningitis, cerebrospinal fluid leakage, re-bleeding, and cardiac arrest. The shaft was removed from the neck, and C1-3 dorsal stabilization was performed. Controlled Computed Tomography (CT) showed adequate implant position. After 4 months the patient's fine motor skills improved, and he became able to button his shirt on his own, and to eat and drink without any help. Additionally, he was able to walk without any support. At the time of control at the outpatient clinic his behavior was adequate: he cooperated with the examining doctor and answered with short sentences although his psychomotor skills were slightly slower. Although bow and crossbow spine injuries are rare nowadays they still occur. The removal of a penetrating missile resulting in such a spinal injury required a unique solution. General considerations, such as securing the airway, leaving the penetrating arrow in the neck and immobilizing both the arrow and neck for transport, thorough diagnostic imaging, preventing cerebrospinal fluid leakage, administering prophylactic antibiotics with broad coverage and stabilizing the spine if required, are advised.

  7. Intervertebral Disc Characteristic on Progressive Neurological Deficit

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    Farid Yudoyono

    2017-09-01

    Full Text Available Objective: To examine the intervertebral disc characteristic on magnetic resonance imaging (MRI in lumbar herniated disc (LHD patients with progressive neurological deficit. Methods: Patients were collected retrospectively from Dr. Hasan Sadikin General Hospital Database from 2011–2013 with LHD, had neurological deficit such as radiculopathy and cauda equine syndrome for less than four weeks with a positive sign confirmed by neurological examination and confirmatory with MRI examination. Results: A total of 14 patients with lumbar herniated disc disease (10 males, 4 females suffered from progressive neurological deficit with an average age of (52.07±10.9 years old. Early disc height was 9.38±0.5 mm and progressive neurological deficit state disc height was 4.03±0.53 mm, which were significantly different statisticaly (p<0.01. Symptoms of radiculopathy were seen in 11 patients and cauda equine syndrome in three patients. Modic changes grade 1 was found in five patients, grade 2 in eight patients,grade 3 in one patient, Pfirmman grade 2 in eleven patients and grade 3 in three patients. Thecal sac compression 1/3 compression was seen in four patients and 2/3 compression in ten patients. Conclusions: Neurosurgeon should raise concerns on the characteristic changes of intervertebral disc in magnetic resonance imaging examination to avoid further neural injury in lumbar herniated disc patients.

  8. Neurologic deficits and arachnoiditis following neuroaxial anesthesia.

    Science.gov (United States)

    Aldrete, J A

    2003-01-01

    Of late, regional anesthesia has enjoyed unprecedented popularity; this increase in cases has brought a higher frequency of instances of neurological deficit and arachnoiditis that may appear as transient nerve root irritation, cauda equina, and conus medullaris syndromes, and later as radiculitis, clumped nerve roots, fibrosis, scarring dural sac deformities, pachymeningitis, pseudomeningocele, and syringomyelia, etc., all associated with arachnoiditis. Arachnoiditis may be caused by infections, myelograms (mostly from oil-based dyes), blood in the intrathecal space, neuroirritant, neurotoxic and/or neurolytic substances, surgical interventions in the spine, intrathecal corticosteroids, and trauma. Regarding regional anesthesia in the neuroaxis, arachnoiditis has resulted from epidural abscesses, traumatic punctures (blood), local anesthetics, detergents, antiseptics or other substances unintentionally injected into the spinal canal. Direct trauma to nerve roots or the spinal cord may be manifested as paraesthesia that has not been considered an injurious event; however, it usually implies dural penetration, as there are no nerve roots in the epidural space posteriorly. Sudden severe headache while or shortly after an epidural block using the loss of resistance to air approach usually suggests pneumocephalus from an intradural injection of air. Burning severe pain in the lower back and lower extremities, dysesthesia and numbness not following the usual dermatome distribution, along with bladder, bowel and/or sexual dysfunction, are the most common symptoms of direct trauma to the spinal cord. Such patients should be subjected to a neurological examination followed by an MRI of the effected area. Further spinal procedures are best avoided and the prompt administration of IV corticosteroids and NSAIDs need to be considered in the hope of preventing the inflammatory response from evolving into the proliferative phase of arachnoiditis.

  9. CT findings predictive of neurological deficits in throracolumbar burst fractures

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    Moon, Tae Yong; Jeong, Hee Seok; Jeong, Yeo Jin [Pusan National University and Research Institute for Convergence of Biomedical Science and Technology, Dept. of Radiology, Pusan National University Yangsan Hospital, Yangsan (Korea, Republic of); Lee, In Sook [Dept. of Radiology, Pusan National University Hospital, Busan (Korea, Republic of)

    2016-09-15

    To determine the computed tomography (CT) findings predictive of neurological deficits in thoracolumbar spine injuries. One hundred two patients with thoracolumbar spinal burst fractures, after excluding the patients with brain and cervical cord injuries and unconsciousness, who underwent consecutive spine 128-multidetector CT scan formed the study group. The neurological findings were clinically classified as no deficit (n = 58), complete deficit with paraplegia (n = 22), and incomplete deficit with either motor or sensory impairment (n = 22). The following four CT imaging parameters were analyzed: the level of the main burst fracture as the cord (n = 44) and the cauda equina (n = 58) levels; the extent of canal encroachment as central canal ratios (CCRs) below 0.5 (n = 43) and above 0.5 (n = 59); the degree of laminar fracture as no fracture (n = 33), linear fracture (n = 7), separated fracture (n = 27), and displaced fracture (n = 35); fractured vertebra counted as single (n = 53) and multiple (n = 49). Complete neurological deficit was associated with injuries at the cord level (p = 0.000) and displaced laminar fractures (p = 0.000); incomplete neurological deficit was associated with CCRs below 0.5 (p = 0.000) and multiple vertebral injuries (p = 0.002). CT scan can provide additional findings predictive of neurological deficits in thoracolumbar spinal burst fractures.

  10. Iatrogenic neurologic deficit after lumbar spine surgery: A review.

    Science.gov (United States)

    Ghobrial, George M; Williams, Kim A; Arnold, Paul; Fehlings, Michael; Harrop, James S

    2015-12-01

    Iatrogenic neurologic deficits after lumbar spine surgery are rare complications, but important to recognize and manage. Complications such as radiculopathy, spinal cord compression, motor deficits (i.e. foot drop with L5 radiculopathy), and new onset radiculitis, while uncommon do occur. Attempts at mitigating these complications with the use of neuromonitoring have been successful. Guidance in the literature as to the true rate of iatrogenic neurologic deficit is limited to several case studies and retrospective designed studies describing the management, prevention and treatment of these deficits. The authors review the lumbar spinal surgery literature to examine the incidence of iatrogenic neurologic deficit in the lumbar spinal surgery literature. An advanced MEDLINE search conducted on May 14th, 2015 from January 1, 2004 through May 14, 2015, using the following MeSH search terms "postoperative complications," then subterms "lumbar vertebrae," treatment outcome," "spinal fusion," and "radiculopathy" were included together with "postoperative complications" in a single search. Postoperative complications including radiculopathy, weakness, and spinal cord compression were included. The definition of iatrogenic neurologic complication was limited to post-operative radiculopathy, motor weakness or new onset pain/radiculitis. An advanced MEDLINE search conducted on May 14th, 2015 using all of the above terms together yielded 21 results. After careful evaluation, 11 manuscripts were excluded and 10 were carefully reviewed. The most common indications for surgery were degenerative spondylolisthesis, spondylosis, scoliosis, and lumbar stenosis. In 2783 patients in 12 total studies, there were 56 patients who had reported a postoperative neurologic deficit for a rate of 5.7. The rates of deficits ranged from 0.46% to 17% in the studies used. The average rate of reported neurologic complications within these papers was 9% (range 0.46-24%). Thirty patients of a total of

  11. Frida Kahlo's neurological deficits and her art.

    Science.gov (United States)

    Budrys, Valmantas

    2013-01-01

    World-famous Mexican painter Frida Kahlo is an impressive example of a professional artist whose artistic subject matter was extremely influenced by her chronic, severe illness. Many of her best-known works depict her physical and mental suffering. She was one of those very uncommon artists who dared to show their nude, sick body. This chapter describes and explains the biographical events and works of Frida Kahlo that are closely related to neurology: congenital anomaly (spina bifida), poliomyelitis, spine injury, and neuropathic pain. © 2013 Elsevier B.V. All rights reserved.

  12. [Voice disorders caused by neurological diseases].

    Science.gov (United States)

    Gamboa, J; Jiménez-Jiménez, F J; Mate, M A; Cobeta, I

    To review voice disorders in neurological diseases, with special emphasis to acoustic analysis. In the first part of this article we describe data regarding neural control of voice, physiology of phonation, and examination of the patient with voice disturbances, including the use of voice laboratory, acoustic analysis fundamentals, phonetometric measures and aerodynamic measures. In the second part, we review the voice disturbances associated to neurological diseases, emphasizing into movement disorders (specially Parkinson s disease, essential tremor, and spasmodic dysphonia). A number of neurological diseases causing alterations of corticospinal pathway, cerebellum, basal ganglia and upper and/or lower motoneurons can induce voice disturbances. Voice examination using ear, nose & throat examination, endoscopy and videorecording of laryngeal movements, acoustic analysis, elecroglottography, laryngeal electromyography, and aerodynamic measures, could be useful in the clinical examination of some neurological diseases.

  13. Neurological deficit following stereotactic radiosurgery for trigeminal neuralgia

    NARCIS (Netherlands)

    Kemp, S.; Allan, R. S.; Patanjali, N.; Barnett, M. H.; Jonker, B. P.

    2016-01-01

    We report a unique case of neurological deficit from late onset multiple sclerosis (MS), in a 65-year-old woman, after stereotactic radiosurgery (SRS) for trigeminal neuralgia (TN). At 3.5months post-SRS for TN, the patient developed ataxia and left leg paraesthesiae and brain MRI showed altered

  14. An early marker for neurological deficits after perinatal brain lesions

    NARCIS (Netherlands)

    Prechtl, HFR; Einspieler, C; Cioni, G; Bos, AF; Ferrari, F; Sontheimer, D

    1997-01-01

    Background In normal awake infants, fidgety movements are seen from the age of 6 weeks to 20 weeks. The aim of the study was to test the predictive value of absent or abnormal spontaneous movements in young infants for the later development of neurological deficits. Methods In a collaborative study

  15. Findings on low-field cranial MR images in epileptic dogs that lack interictal neurological deficits.

    Science.gov (United States)

    Smith, P M; Talbot, C E; Jeffery, N D

    2008-06-01

    Recurrent seizuring is a common neurological problem in dogs and can present diagnostic difficulties for the attending clinician. Associated interictal neurological deficits strongly suggest brain disease but the frequency of structural abnormalities in patients without such deficits is unknown. In this study the prevalence of clinically significant magnetic resonance imaging (MRI) abnormalities was determined in two groups of interictally normal dogs, those younger than 6 years and those older than 6 years of age. In the former group, only 1/46 dogs (2.2%) had significant MRI abnormalities, whereas in the latter group, 8/30 (26.7%) were abnormal. None of the dogs had an identifiable metabolic cause for the seizures. These findings suggest that the diagnostic yield of advanced neuroimaging techniques in young seizuring dogs without interictal neurological deficits is low, but reaffirms their value in similar older individuals.

  16. Postural control deficits identify lingering post-concussion neurological deficits

    Directory of Open Access Journals (Sweden)

    Thomas A. Buckley

    2016-03-01

    Full Text Available Concussion, or mild traumatic brain injury, incidence rates have reached epidemic levels and impaired postural control is a cardinal symptom. The purpose of this review is to provide an overview of the linear and non-linear assessments of post-concussion postural control. The current acute evaluation for concussion utilizes the subjective balance error scoring system (BESS to assess postural control. While the sensitivity of the overall test battery is high, the sensitivity of the BESS is unacceptably low and, with repeat administration, is unable to accurately identify recovery. Sophisticated measures of postural control, utilizing traditional linear assessments, have identified impairments in postural control well beyond BESS recovery. Both assessments of quiet stance and gait have identified lingering impairments for at least 1 month post-concussion. Recently, the application of non-linear metrics to concussion recovery have begun to receive limited attention with the most commonly utilized metric being approximate entropy (ApEn. ApEn, most commonly in the medial-lateral plane, has successfully identified impaired postural control in the acute post-concussion timeframe even when linear assessments of instrumented measures are equivalent to healthy pre-injury values; unfortunately these studies have not gone beyond the acute phase of recovery. One study has identified lingering deficits in postural control, utilizing Shannon and Renyi entropy metrics, which persist at least through clinical recovery and return to participation. Finally, limited evidence from two studies suggest that individuals with a previous history of a single concussion, even months or years prior, may display altered ApEn metrics. Overall, non-linear metrics provide a fertile area for future study to further the understanding of postural control impairments acutely post-concussion and address the current challenge of sensitive identification of recovery.

  17. Stroke caused auditory attention deficits in children

    Directory of Open Access Journals (Sweden)

    Karla Maria Ibraim da Freiria Elias

    2013-01-01

    Full Text Available OBJECTIVE: To verify the auditory selective attention in children with stroke. METHODS: Dichotic tests of binaural separation (non-verbal and consonant-vowel and binaural integration - digits and Staggered Spondaic Words Test (SSW - were applied in 13 children (7 boys, from 7 to 16 years, with unilateral stroke confirmed by neurological examination and neuroimaging. RESULTS: The attention performance showed significant differences in comparison to the control group in both kinds of tests. In the non-verbal test, identifications the ear opposite the lesion in the free recall stage was diminished and, in the following stages, a difficulty in directing attention was detected. In the consonant- vowel test, a modification in perceptual asymmetry and difficulty in focusing in the attended stages was found. In the digits and SSW tests, ipsilateral, contralateral and bilateral deficits were detected, depending on the characteristics of the lesions and demand of the task. CONCLUSION: Stroke caused auditory attention deficits when dealing with simultaneous sources of auditory information.

  18. Management of Recurrent Delayed Neurologic Deficit After Thoracoabdominal Aortic Operation.

    Science.gov (United States)

    Boutrous, Mina L; Afifi, Rana O; Safi, Hazim J; Estrera, Anthony L

    2016-01-01

    Delayed neurologic deficit (DND) is a devastating adverse event after thoracoabdominal aortic aneurysm repair. Multiple adjuncts have been devised to counteract the development of DND, most notably cerebrospinal fluid (CSF) drainage. We report a case of a 63-year-old woman in whom DND developed four times during the first 10 days after her thoracoabdominal aortic operation. This necessitated lumbar drain "weaning" to allow for a slowly rising CSF pressure and preservation of lower extremity motor function. Copyright © 2016 The Society of Thoracic Surgeons. Published by Elsevier Inc. All rights reserved.

  19. Correlation between neurological leg deficits and reaction time of upper limbs among low-back pain patients.

    Science.gov (United States)

    Venna, S; Hurri, H; Alaranta, H

    1994-06-01

    The purpose of the study was to examine how neurological deficits of the leg, i.e. sensory deficit, deficient reflexes and muscular weakness, correlate with reaction times of upper limbs in a group with chronic low-back pain. Thirty-two patients were studied. Three sets of measurements of simple reaction time and choice reaction time of upper limbs were conducted at one-week intervals. Neurological deficits of the leg were recorded by a physician and the subjects answered a questionnaire about the severity of their low-back symptoms (Oswestry's index). We also defined a neurological index which reflected the total sum of the three types of leg deficits experienced by each of the subjects. Sensory deficit of the leg and the neurological index correlated strongly with slower reaction times of upper limbs, while the other two neurological deficits did not reach a level of significance. Sensory deficits of the leg seem to be an indicator of much greater motor disability than has been thought so far. The motor disability not only appears distally from the lumbar radicular damage caused for example by an intervertebral herniation, it also seems to relate to psychomotor reaction more generally, even on upper limbs.

  20. Comparative Sensitivity of Intraoperative Motor Evoked Potential Monitoring in Predicting Postoperative Neurologic Deficits: Nondegenerative versus Degenerative Myelopathy

    OpenAIRE

    Clark, Aaron J.; Safaee, Michael; Chou, Dean; Weinstein, Philip R.; Molinaro, Annette M.; Clark, John P.; Mummaneni, Praveen V.

    2015-01-01

    Study Design ?Retrospective review. Objective ?Intraoperative motor evoked potential (MEP) monitoring in spine surgery may assist surgeons in taking corrective measures to prevent neurologic deficits. The efficacy of monitoring MEPs intraoperatively in patients with myelopathy from nondegenerative causes has not been quantified. We compared the sensitivity and specificity of intraoperative MEP monitoring in patients with myelopathy caused by nondegenerative processes to patients with degenera...

  1. Retrospective analysis underestimates neurological deficits in complex spinal deformity surgery: a Scoli-RISK-1 Study.

    Science.gov (United States)

    Kelly, Michael P; Lenke, Lawrence G; Godzik, Jakub; Pellise, Ferran; Shaffrey, Christopher I; Smith, Justin S; Lewis, Stephen J; Ames, Christopher P; Carreon, Leah Y; Fehlings, Michael G; Schwab, Frank; Shimer, Adam L

    2017-07-01

    OBJECTIVE The authors conducted a study to compare neurological deficit rates associated with complex adult spinal deformity (ASD) surgery when recorded in retrospective and prospective studies. Retrospective studies may underreport neurological deficits due to selection, detection, and recall biases. Prospective studies are expensive and more difficult to perform, but they likely provide more accurate estimates of new neurological deficit rates. METHODS New neurological deficits were recorded in a prospective study of complex ASD surgeries (pSR1) with a defined outcomes measure (decrement in American Spinal Injury Association lower-extremity motor score) for neurological deficits. Using identical inclusion criteria and a subset of participating surgeons, a retrospective study was created (rSR1) and neurological deficit rates were collected. Continuous variables were compared with the Student t-test, with correction for multiple comparisons. Neurological deficit rates were compared using the Mantel-Haenszel method for standardized risks. Statistical significance for the primary outcome measure was p spinal deformities, and exclusion criteria were identical. Sagittal Cobb measurements were higher in pSR1, although sagittal alignment was similar. Preoperative neurological deficit rates were similar in the groups. Three-column osteotomies were more common in pSR1, particularly vertebral column resection. New neurological deficits were more common in pSR1 (pSR1 17.3% [95% CI 12.6-22.2] and rSR1 9.0% [95% CI 5.0-13.0]; p = 0.01). The majority of deficits in both studies were at the nerve root level, and the distribution of level of injury was similar. CONCLUSIONS New neurological deficit rates were nearly twice as high in the prospective study than the retrospective study with identical inclusion criteria. These findings validate concerns regarding retrospective cohort studies and confirm the need for and value of carefully designed prospective, observational cohort

  2. Catheter-related epidural abscesses -- don't wait for neurological deficits.

    NARCIS (Netherlands)

    Royakkers, A.A.; Willigers, H.; Ven, A.J.A.M. van der; Wilmink, J.T.; Durieux, M.; Kleef, M. van

    2002-01-01

    Epidural abscess is a rare but serious complication of epidural anesthesia for peri- and postoperative analgesia. It is feared because of possible persistent neurological deficits. Epidural abscess presents mostly with a classic triad of symptoms: back pain, fever and variable neurological signs and

  3. Neurological deficits in the life and works of Frida Kahlo.

    Science.gov (United States)

    Budrys, Valmantas

    2006-01-01

    World-famous Mexican painter Frida Kahlo is an impressive example of an artist whose entire life and creativity were extremely influenced by chronic, severe illness. Many of her best-known works depict her physical and mental suffering. She was one of those very uncommon artists who dared to show their nude, sick body. This article describes biographical events and works of Frida Kahlo that are closely related to neurology: congenital anomaly (spina bifida), poliomyelitis, spine injury, neuropathic pain.

  4. The saccadic and neurological deficits in type 3 Gaucher disease.

    Directory of Open Access Journals (Sweden)

    William Benko

    Full Text Available Our objective was to characterize the saccadic eye movements in patients with type 3 Gaucher disease (chronic neuronopathic in relationship to neurological and neurophysiological abnormalities. For approximately 4 years, we prospectively followed a cohort of 15 patients with Gaucher type 3, ages 8-28 years, by measuring saccadic eye movements using the scleral search coil method. We found that patients with type 3 Gaucher disease had a significantly higher regression slope of duration vs amplitude and peak duration vs amplitude compared to healthy controls for both horizontal and vertical saccades. Saccadic latency was significantly increased for horizontal saccades only. Downward saccades were more affected than upward saccades. Saccade abnormalities increased over time in some patients reflecting the slowly progressive nature of the disease. Phase plane plots showed individually characteristic patterns of abnormal saccade trajectories. Oculo-manual dexterity scores on the Purdue Pegboard test were low in virtually all patients, even in those with normal cognitive function. Vertical saccade peak duration vs amplitude slope significantly correlated with IQ and with the performance on the Purdue Pegboard but not with the brainstem and somatosensory evoked potentials. We conclude that, in patients with Gaucher disease type 3, saccadic eye movements and oculo-manual dexterity are representative neurological functions for longitudinal studies and can probably be used as endpoints for therapeutic clinical trials.ClinicalTrials.gov NCT00001289.

  5. Neurological, nutritional and alcohol consumption factors underlie cognitive and motor deficits in chronic alcoholism.

    Science.gov (United States)

    Fama, Rosemary; Le Berre, Anne-Pascale; Hardcastle, Cheshire; Sassoon, Stephanie A; Pfefferbaum, Adolf; Sullivan, Edith V; Zahr, Natalie M

    2017-12-15

    Variations in pattern and extent of cognitive and motor impairment occur in alcoholism (ALC). Causes of such heterogeneity are elusive and inconsistently accounted for by demographic or alcohol consumption differences. We examined neurological and nutritional factors as possible contributors to heterogeneity in impairment. Participants with ALC (n = 96) and a normal comparison group (n = 41) were examined on six cognitive and motor domains. Signs of historically determined subclinical Wernicke's encephalopathy were detected using the Caine et al. criteria, which were based on postmortem examination and chart review of antemortem data of alcoholic cases with postmortem evidence for Wernicke's encephalopathy. Herein, four Caine criteria provided quantification of dietary deficiency, cerebellar dysfunction, low general cognitive functioning and oculomotor abnormalities in 86 of the 96 ALC participants. Subgroups based on Caine criteria yielded a graded effect, where those meeting more criteria exhibited greater impairment than those meeting no to fewer criteria. These results could not be accounted for by history of drug dependence. Multiple regression indicated that compromised performance on ataxia, indicative of cerebellar dysfunction, predicted non-mnemonic and upper motor deficits, whereas low whole blood thiamine level, consistent with limbic circuit dysfunction, predicted mnemonic deficits. This double dissociation indicates biological markers that contribute to heterogeneity in expression of functional impairment in ALC. That non-mnemonic and mnemonic deficits are subserved by the dissociable neural systems of frontocerebellar and limbic circuitry, both commonly disrupted in ALC, suggests neural mechanisms that can differentially affect selective functions, thereby contributing to heterogeneity in pattern and extent of dysfunction in ALC. © 2017 Society for the Study of Addiction.

  6. Persistent neurological deficit from iodinated contrast encephalopathy following intracranial aneurysm coiling. A case report and review of the literature.

    LENUS (Irish Health Repository)

    Leong, S

    2012-03-01

    Neurotoxicity from iodinated contrast agents is a known but rare complication of angiography and neurovascular intervention. Neurotoxicity results from contrast penetrating the blood-brain barrier with resultant cerebral oedema and altered neuronal excitability. Clinical effects include encephalopathy, seizures, cortical blindness and focal neurological deficits. Contrast induced encephalopathy is extensively reported as a transient and reversible phenomenon. We describe a patient with a persistent motor deficit due to an encephalopathy from iodinated contrast media administered during cerebral aneurysm coiling. This observation and a review of the literature highlights that contrast-induced encephalopathy may not always have a benign outcome and can cause permanent deficits. This potential harmful effect should be recognised by the angiographer and the interventionalist.

  7. [Neurological deficits in patients with primary and secondary anticardiolipin syndrome].

    Science.gov (United States)

    Honczarenko, K; Ostanek, L; Grzelec, H; Fabian, A; Fiedorowicz-Fabrycy, I; Fryze, C

    2001-01-01

    27 patients (22 women, 5 men); age 17 to 56 yr. (mean age 37 yr.) were included in this study, 4 had primary antiphospholipid syndrome and 18 secondary antiphospholipid syndrome in the course of systemic connective tissue disease and in 5 cases increased levels of anticardiolipid antibodies were found which did not meet the criteria necessary for diagnosis of secondary antiphospholipid syndrome. The mean duration of the disease was 8 yrs. Among primary antiphospholipid syndrome patients two had ischaemic stroke, one migraine-like headache and seizures. 18 patients had lupus erythematosus, two mixed connective tissue disease, one rheumatoid arthritis, one Sjögren syndrome, one Behçet disease. In 55% of patients migraine-like headache, polyneuropathies, encephalophaties, stroke, seizures and vision disturbances were present. In 18.5% of patients EEG exam revealed focal lesions with tendency for generalisation. On brain stem auditory evoked potentials examination, in 11.1% of patients conductivity lesions in mesencephalon and pons were found, visual evoked potentials, in 11.1% of patients in visual tracts. In 37% of patients, neuropathy was found on EMG exam. Neurological symptoms are one of the most frequent disorders in systemic connective tissue disease associated with the presence of anicardiolipin antibodies.

  8. Identification of risk factors for neurological deficits in patients with pelvic fractures

    DEFF Research Database (Denmark)

    Schmal, Hagen; Hauschild, Oliver; Culemann, Ulf

    2010-01-01

    This multicenter register study was performed to define injury and fracture constellations that are at risk to develop pelvic associated neural lesions. Data of 3607 patients treated from 2004 to 2009 for pelvic fractures were evaluated for neurological deficits depending on Tile classification, ...

  9. Interferon-gamma in progression to chronic demyelination and neurological deficit following acute EAE

    DEFF Research Database (Denmark)

    Renno, T; Taupin, V; Bourbonnière, L

    1998-01-01

    The cytokine interferon-gamma (IFNgamma) is implicated in the induction of acute CNS inflammation, but it is less clear what role if any IFNgamma plays in progression to chronic demyelination and neurological deficit. To address this issue, we have expressed IFNgamma in myelinating oligodendrocyt...

  10. Chagas disease in a Texan horse with neurologic deficits.

    Science.gov (United States)

    Bryan, Laura K; Hamer, Sarah A; Shaw, Sarah; Curtis-Robles, Rachel; Auckland, Lisa D; Hodo, Carolyn L; Chaffin, Keith; Rech, Raquel R

    2016-01-30

    A 10-year-old Quarter Horse gelding presented to the Texas A&M University Veterinary Teaching Hospital with a six month-history of ataxia and lameness in the hind limbs. The horse was treated presumptively for equine protozoal myeloencephalitis (EPM) based on clinical signs but was ultimately euthanized after its condition worsened. Gross lesions were limited to a small area of reddening in the gray matter of the thoracic spinal cord. Histologically, trypanosome amastigotes morphologically similar to Trypanosoma cruzi, the agent of Chagas disease in humans and dogs, were sporadically detected within segments of the thoracic spinal cord surrounded by mild lymphoplasmacytic inflammation. Ancillary testing for Sarcocystis neurona, Neospora spp., Toxoplasma gondii and Leishmania spp. was negative. Conventional and real time polymerase chain reaction (PCR) of affected paraffin embedded spinal cord were positive for T. cruzi, and sequencing of the amplified T. cruzi satellite DNA PCR fragment from the horse was homologous with various clones of T. cruzi in GenBank. While canine Chagas disease cases have been widely reported in southern Texas, this is the first report of clinical T. cruzi infection in an equid with demonstrable amastigotes in the spinal cord. In contrast to previous instances of Chagas disease in the central nervous system (CNS) of dogs and humans, no inflammation or T. cruzi amastigotes were detected in the heart of the horse. Based on clinical signs, there is a potential for misdiagnosis of Chagas disease with other infectious diseases that affect the equine CNS. T. cruzi should be considered as a differential diagnosis in horses with neurologic clinical signs and histologic evidence of meningomyelitis that originate in areas where Chagas disease is present. The prevalence of T. cruzi in horses and the role of equids in the parasite life cycle require further study. Copyright © 2015 Elsevier B.V. All rights reserved.

  11. Identification of risk factors for neurological deficits in patients with pelvic fractures.

    Science.gov (United States)

    Schmal, Hagen; Hauschild, Oliver; Culemann, Ulf; Pohlemann, Tim; Stuby, Fabian; Krischak, Gert; Südkamp, Norbert P

    2010-08-11

    This multicenter register study was performed to define injury and fracture constellations that are at risk to develop pelvic associated neural lesions. Data of 3607 patients treated from 2004 to 2009 for pelvic fractures were evaluated for neurological deficits depending on Tile classification, pelvic injury configuration, and treatment.In 223 patients (6.5%), neurological lesions were diagnosed on the day of discharge from the hospital. The degree of instability of the pelvic fracture correlated with occurrence of nerve lesions. Rate of neurological dysfunction increased from 1.5% in type A fractures to 14.4% in type C fractures (P<.001). As the most endangered anatomical regions in pelvic fractures, the roots L5 (18.3%) and S1 (15.6%) and isolated peripheral nerves (19.2%) were identified. Patients sustaining complex pelvic trauma (7.85%) suffered from significantly more neurological dysfunctions (33.5%) compared to patients without peripelvic organ or soft tissue injuries (P<.001). Whereas stable type A3 sacral fractures were not associated with a different risk to develop neurological deficits (3.8%), unstable sacral fractures with the need for operative fixation showed an increased rate of accompanying nerve lesions (15.4%; P<.001). Twenty-one (11.5%) operative sacral stabilizations were supplemented with nerve root decompression (mainly S1). Neurological complications in the course of treatment were seen in 69 cases (1.9%).A high degree of instability, complex pelvic trauma, and unstable sacral fractures predispose for additional neurological deficits in patients with pelvic fractures. Copyright 2010, SLACK Incorporated.

  12. Neurological Deficits After Long-term Pyrethroid Exposure

    DEFF Research Database (Denmark)

    Hansen, Martin Rune Hassan; Jørs, Erik; Lander, Flemming

    2017-01-01

    Pyrethroid pesticides have been suggested to be a cause of Parkinson disease and other neurodegenerative diseases. To investigate this, a cross-sectional study was conducted among 120 Bolivian public health vector program spray men, primarily exposed to pyrethroids. Pesticide exposure and central...... nervous system (CNS) symptoms were determined by a structured interview, whereas neuromotor and neurocognitive performance was assessed using the computerized Behavioral Assessment and Research System and CATSYS system. Individuals exposed to higher levels reported significantly more CNS symptoms...... quintile = -0.405 [-0.660 to -0.150]), and workers only exposed to pyrethroids performed worse than workers also exposed to other pesticides (adjusted β = -1.344 [-2.224 to -0.464]). Chronic pyrethroid exposure may cause deterioration in neurocognitive performance, and exposure control is recommended....

  13. Neonatal Meningitis: Risk Factors, Causes, and Neurologic Complications

    OpenAIRE

    KHALESSI, Nasrin; AFSHARKHAS, Ladan

    2014-01-01

    How to Cite This Article: Khalessi N, Afsharkhas L. Neonatal Meningitis: Risk Factors, Causes and Neurologic Complications.Iran J Child Neurol. 2014 Autumn;8(4): 46-50.AbstractObjectiveNeonates are at greater risk for sepsis and meningitis than other ages and in spite of rapid diagnoses of pathogens and treatments, they still contribute to complications and mortality. This study determines risk factors, causes, andneurologic complications of neonatal meningitis in  ospitalized neonates.Materi...

  14. Traumatic Posterior Atlantoaxial Dislocation Without Associated Fracture but With Neurological Deficit

    Science.gov (United States)

    Xu, Yong; Li, Feng; Guan, Hanfeng; Xiong, Wei

    2015-01-01

    Abstract Posterior atlantoaxial dislocation without odontoid fracture is extremely rare and often results in fatal spinal cord injury. According to the reported literature, all cases presented mild or no neurologic deficit, with no definite relation to upper spinal cord injury. Little is reported about traumatic posterior atlantoaxial dislocation, with incomplete quadriplegia associated with a spinal cord injury. We present a case of posterior atlantoaxial dislocation without associated fracture, but with quadriplegia, and accompanying epidural hematoma and subarachnoid hemorrhage. The patient underwent gentle traction in the neutral position until repeated cranial computed tomography revealed no progression of the epidural hematoma. Thereafter, the atlantoaxial dislocation was reduced by using partial odontoidectomy via a video-assisted transcervical approach and maintained with posterior polyaxial screw-rod constructs and an autograft. Neurological status improved immediately after surgery, and the patient recovered completely after 1 year. Posterior fusion followed by closed reduction is the superior strategy for posterior atlantoaxial dislocation without odontoid fracture, according to literature. But for cases with severe neurological deficit, open reduction may be the safest choice to avoid the lethal complication of overdistraction of the spinal cord. Also, open reduction and posterior srew-rod fixation are safe and convenient strategies in dealing with traumatic posterior atlantoaxial dislocation patients with neurological deficit. PMID:26512572

  15. Radiological findings correlate with neurological deficits but not with pain after operatively treated sacral fractures

    Science.gov (United States)

    Tötterman, Anna; Hellund, Johan C; Glott, Thomas; Madsen, Jan Erik; Røise, Olav

    2014-01-01

    Background and purpose Neurological deficits and pain are common after displaced sacral fractures. However, little is known about the association between the long-term clinical outcomes and radiological findings. We examined the long-term radiological findings and their correlations with lumbosacral pain and neurological deficits in the lower extremities after surgery for sacral fractures. Methods 28 consecutive patients with operatively treated displaced sacral fractures were followed for mean 11 (8–13) years. Sensorimotor impairments of the lower extremities were classified according to the American Spinal Injury Association (ASIA). Pain was assessed using a visual analog scale (VAS). All patients underwent conventional radiographic examination and CT, and the images were scrutinized for nonunion, residual displacement, narrowing of the sacral foramina, and post-foraminal encroachment of the L5 and S1 nerves. Results There was residual displacement of ≥ 10 mm in 16 of the 28 patients. 26 patients had narrowing of 1 or more neural root foramina in L5-S4. 8 patients reported having no pain, 11 had pain only in the lumbosacral area, and 9 had pain in combination with radiating leg pain. Statistically significant correlations were found between narrowing of the sacral foramina and neurological deficits in the corresponding dermatomes. Significant correlations were also found between post-foraminal encroachment of L5 nerves and both sensory and motor deficits. No correlations were found between pain and radiological findings. Interpretation Pathological radiological findings are common 11 years after operatively treated displaced sacral fractures. Sacral foraminal and L5 post-foraminal bony encroachments were common findings and correlated with neurological deficits. However, lumbosacral pain did not correlate with radiological sequelae after fracture healing. PMID:24694272

  16. Systemic administration of urocortin after intracerebral hemorrhage reduces neurological deficits and neuroinflammation in rats

    Directory of Open Access Journals (Sweden)

    Liew Hock-Kean

    2012-01-01

    Full Text Available Abstract Background Intracerebral hemorrhage (ICH remains a serious clinical problem lacking effective treatment. Urocortin (UCN, a novel anti-inflammatory neuropeptide, protects injured cardiomyocytes and dopaminergic neurons. Our preliminary studies indicate UCN alleviates ICH-induced brain injury when administered intracerebroventricularly (ICV. The present study examines the therapeutic effect of UCN on ICH-induced neurological deficits and neuroinflammation when administered by the more convenient intraperitoneal (i.p. route. Methods ICH was induced in male Sprague-Dawley rats by intrastriatal infusion of bacterial collagenase VII-S or autologous blood. UCN (2.5 or 25 μg/kg was administered i.p. at 60 minutes post-ICH. Penetration of i.p. administered fluorescently labeled UCN into the striatum was examined by fluorescence microscopy. Neurological deficits were evaluated by modified neurological severity score (mNSS. Brain edema was assessed using the dry/wet method. Blood-brain barrier (BBB disruption was assessed using the Evans blue assay. Hemorrhagic volume and lesion volume were assessed by Drabkin's method and morphometric assay, respectively. Pro-inflammatory cytokine (TNF-α, IL-1β, and IL-6 expression was evaluated by enzyme-linked immunosorbent assay (ELISA. Microglial activation and neuronal loss were evaluated by immunohistochemistry. Results Administration of UCN reduced neurological deficits from 1 to 7 days post-ICH. Surprisingly, although a higher dose (25 μg/kg, i.p. also reduced the functional deficits associated with ICH, it is significantly less effective than the lower dose (2.5 μg/kg, i.p.. Beneficial results with the low dose of UCN included a reduction in neurological deficits from 1 to 7 days post-ICH, as well as a reduction in brain edema, BBB disruption, lesion volume, microglial activation and neuronal loss 3 days post-ICH, and suppression of TNF-α, IL-1β, and IL-6 production 1, 3 and 7 days post

  17. A novel porcine model of ataxia telangiectasia reproduces neurological features and motor deficits of human disease.

    Science.gov (United States)

    Beraldi, Rosanna; Chan, Chun-Hung; Rogers, Christopher S; Kovács, Attila D; Meyerholz, David K; Trantzas, Constantin; Lambertz, Allyn M; Darbro, Benjamin W; Weber, Krystal L; White, Katherine A M; Rheeden, Richard V; Kruer, Michael C; Dacken, Brian A; Wang, Xiao-Jun; Davis, Bryan T; Rohret, Judy A; Struzynski, Jason T; Rohret, Frank A; Weimer, Jill M; Pearce, David A

    2015-11-15

    Ataxia telangiectasia (AT) is a progressive multisystem disorder caused by mutations in the AT-mutated (ATM) gene. AT is a neurodegenerative disease primarily characterized by cerebellar degeneration in children leading to motor impairment. The disease progresses with other clinical manifestations including oculocutaneous telangiectasia, immune disorders, increased susceptibly to cancer and respiratory infections. Although genetic investigations and physiological models have established the linkage of ATM with AT onset, the mechanisms linking ATM to neurodegeneration remain undetermined, hindering therapeutic development. Several murine models of AT have been successfully generated showing some of the clinical manifestations of the disease, however they do not fully recapitulate the hallmark neurological phenotype, thus highlighting the need for a more suitable animal model. We engineered a novel porcine model of AT to better phenocopy the disease and bridge the gap between human and current animal models. The initial characterization of AT pigs revealed early cerebellar lesions including loss of Purkinje cells (PCs) and altered cytoarchitecture suggesting a developmental etiology for AT and could advocate for early therapies for AT patients. In addition, similar to patients, AT pigs show growth retardation and develop motor deficit phenotypes. By using the porcine system to model human AT, we established the first animal model showing PC loss and motor features of the human disease. The novel AT pig provides new opportunities to unmask functions and roles of ATM in AT disease and in physiological conditions. © The Author 2015. Published by Oxford University Press. All rights reserved. For Permissions, please email: journals.permissions@oup.com.

  18. Seat belt syndrome with unstable Chance fracture dislocation of the second lumbar vertebra without neurological deficits.

    Science.gov (United States)

    Onu, David O; Hunn, Andrew W; Bohmer, Robert D

    2014-01-08

    The seat belt syndrome is a recognised complication of seat belt use in vehicles. Unstable Chance fractures of the spine without neurological deficits have been reported infrequently. We describe a young woman with completely disrupted Chance fracture of the second lumbar vertebra in association with left hemidiaphragmatic rupture/hernia, multiple bowel perforations, splenic capsular tear, left humeral shaft and multiple rib fractures. These injuries which resulted from high-speed vehicle collision and led to death of one of the occupants were readily detected by trauma series imaging. The patient was successfully treated by a dedicated multidisciplinary team which adopted a staged surgical approach and prioritisation of care. There were no manifested neurological or other deficits after 1 year of follow-up. To the authors' knowledge, this is the first report of such a case in Australasia. We discuss the challenging surgical management, highlighting the role of radiological imaging in such cases and provide a literature review.

  19. Delayed Postoperative Neurologic Deficit After Spine Deformity Surgery: Analysis of 5377 Cases at 1 Institution.

    Science.gov (United States)

    Qiao, Jun; Xiao, Liangyan; Zhu, Zezhang; Xu, Leilei; Qian, Bangping; Liu, Zhen; Sun, Xu; Qiu, Yong

    2017-12-15

    To our knowledge, few studies have focused on delayed postoperative neurologic deficit (DPND) after spine deformity surgery. This study was intended to investigate the incidence, risk factors, treatments, and outcomes of DPND after corrective surgery for spinal deformity in a single spine center. The database of a single spine center was queried for dates from 2002 to 2014 to identify all spinal deformity cases. The variables extracted included patient age, diagnosis, procedure, whether neuromonitoring was used and if so which methods were used, whether neuromonitoring abnormalities were detected, whether new neurologic deficits occurred, whether implants were used, and the degree of recovery from new neurologic deficits (none, partial, complete). The patients were classified as pediatric (<21 years old) or adult (≥21 years old). The rates of DPND were tabulated and stratified on the basis of age, diagnosis, and surgical features. A total of 5377 cases were investigated from 2002 through 2014. Seven cases of DPND were reported (incidence, 0.13%). For adult patients, the overall incidence of DPND was 0.17%, and for pediatric patients, it was 0.10%. The incidence of DPND was 0.35% when osteotomies were performed and 0.05% without osteotomies. After the onset of neurologic deficits, loss of somatosensory evoked potentials occurred in 1 patient, and loss of motor evoked potentials occurred in all 7 patients. Revision surgery was performed for 3 patients. At the last follow-up visit, 1 patient experienced no recovery, 2 partial recovery, and 5 complete recovery. The incidence of DPND is low. Old age and osteotomies are risk factors for DPND. Most patients with DPND experience varying degrees of recovery. Copyright © 2017 Elsevier Inc. All rights reserved.

  20. Traumatic Posterior Atlantoaxial Dislocation Without Associated Fracture but With Neurological Deficit

    OpenAIRE

    Xu, Yong; Li, Feng; Guan, Hanfeng; Xiong, Wei

    2015-01-01

    Abstract Posterior atlantoaxial dislocation without odontoid fracture is extremely rare and often results in fatal spinal cord injury. According to the reported literature, all cases presented mild or no neurologic deficit, with no definite relation to upper spinal cord injury. Little is reported about traumatic posterior atlantoaxial dislocation, with incomplete quadriplegia associated with a spinal cord injury. We present a case of posterior atlantoaxial dislocation without associated fract...

  1. Quantitative Evaluation System of Soft Neurological Signs for Children with Attention Deficit Hyperactivity Disorder

    Directory of Open Access Journals (Sweden)

    Miki Kaneko

    2016-01-01

    Full Text Available Attention deficit hyperactivity disorder (ADHD is a neurodevelopmental disorder characterized by symptoms of inattention, hyperactivity, and impulsivity. Soft neurological signs (SNS are minor neurological abnormalities in motor performance, and are used as one evaluation method for neurodevelopmental delays in children with ADHD. Our aim is to establish a quantitative evaluation system for children with ADHD. We focused on the arm movement called pronation and supination, which is one such soft neurological sign. Thirty three children with ADHD aged 7–11 years (27 males, six females and twenty five adults participants aged 21–29 years old (19 males, six females participated in our experiments. Our results suggested that the pronation and supination function in children with ADHD has a tendency to lag behind that of typically developing children by several years. From these results, our system has a possibility to objectively evaluate the neurodevelopmental delay of children with ADHD.

  2. The effect of pre-nutrition of hydroalcoholic extractof Origanum vulgare on brain edema and neurologic deficits in a rat stroke model

    Directory of Open Access Journals (Sweden)

    Meysam Foroozandeh

    2015-10-01

    Full Text Available Background and Aim: Stroke is one of the most important factors of mortality and disability in the world. Free radicals are produced following ischemic stroke and they play a central role in breaking the blood-brain barrier and  causing brain edema formation. The aim of the current study was to evaluate the effect of hydro- alcoholic extract of Origanum vulgare on brain edema and neurologic deficit in a rat stroke model. Materials and Methods: In thisexperimental study, 35 male Wistar rats were randomly divided into 5 equal groups.  The first  two groups (control and Sham received distilled water, while three treatment groups received oral Origanum vulgare extract for 30days (50,75and 100 mg/kgdaily, respectively.  Two hours after the last dose of Origanum vulgare extract,each main group underwent  a 60 min middle cerebral artery occlusion.  Then, the assessment of blood brain edema, and neurologic deficits analysis were done . Brain edema (brain water content was analyzed by One-Way ANOVA using LSD method and neurologic deficits analysis by means of Mann-Whitney U, and P<0.05 was taken as the significant level. Results: Origanum vulgare extract reduced brain edema in the experimental groups of 50 (82.49±0.47, 75 (80.89±0.63 and 100 mg/kg/day (80.80±0.66 compared to the control group (84.46±0.67. The neurologic deficit scores in the experimental groups of 75and 100mg/kg/day, compared with control group, but neurologic deficit scores did not affect the group receiving the dose 50 mg/kg. Conclusion:  The obtained data indicate that Origanum vulgar extract via reduction of brain edema and neurologic deficits scorescan have a protective effect on the stroke model.

  3. One-stage posterior instrumentation surgery for the treatment of osteoporotic vertebral collapse with neurological deficits

    Science.gov (United States)

    Ito, Manabu; Abumi, Kuniyoshi; Kotani, Yoshihisa; Takahata, Masahiko; Hojo, Yoshihiro; Minami, Akio

    2010-01-01

    The number of reports describing osteoporotic vertebral fracture has increased as the number of elderly people has grown. Anterior decompression and fusion alone for the treatment of vertebral collapse is not easy for patients with comorbid medical problems and severe bone fragility. The purpose of the present study was to evaluate the efficacy of one-stage posterior instrumentation surgery for the treatment of osteoporotic vertebral collapse with neurological deficits. A consecutive series of 21 patients who sustained osteoporotic vertebral collapse with neurological deficits were managed with posterior decompression and short-segmental pedicle screw instrumentation augmented with ultra-high molecular weight polyethylene (UHMWP) cables with or without vertebroplasty using calcium phosphate cement. The mean follow-up was 42 months. All patients showed neurologic recovery. Segmental kyphotic angle at the instrumented level was significantly improved from an average preoperative kyphosis of 22.8–14.7 at a final follow-up. Spinal canal occupation was significantly reduced from an average before surgery of 40.4–19.1% at the final follow-up. Two patients experienced loosening of pedicle screws and three patients developed subsequent vertebral compression fractures within adjacent segments. However, these patients were effectively treated in a conservative fashion without any additional surgery. Our results indicated that one-stage posterior instrumentation surgery augmented with UHMWP cables could provide significant neurological improvement in the treatment of osteoporotic vertebral collapse. PMID:20157741

  4. Incidence and risk factors of neurological deficits of surgical correction for scoliosis: analysis of 1373 cases at one Chinese institution.

    Science.gov (United States)

    Qiu, Yong; Wang, Shoufeng; Wang, Bin; Yu, Yang; Zhu, Feng; Zhu, Zezhang

    2008-03-01

    A retrospective study. To investigate the incidence of neurologic deficits after scoliosis correction at 1 institution and identify the risk factors for such deficits in scoliosis correction. Neurologic deficit is one of the risks of surgical correction of scoliosis. Reports of the incidence of the neurologic deficits involving a large number of cases at 1 institution are rare. Statistical analysis of the neurologic deficits was performed in 1373 scoliosis cases treated at 1 institution by etiologies in light of the patients' sex, age, sagittal profile, surgical approach, Cobb's angle, and the type of surgery. The total incidence of neurologic deficits was 1.89% and that of serious and mild ones was 0.51% and 1.38%, respectively. The total incidence of neurologic deficits were 1.06% in adolescent idiopathic scoliosis patients and 2.89% in congenital scoliosis (CS) patients, 3.32% in scoliosis patients with hyperkyphosis (>40 degrees ) and 1.38% in those without hyperkyphosis, 3.43% for combined procedures and 1.24% for single posterior procedures, 3.69% in patients with Cobb's angle more than 90 degrees and 1.45% in those with an angle less than 90 degrees , 1.68% with primary surgery and 5.97% with revision surgery, the difference between them was significant (P hyperkyphosis and 0.61% without hyperkyphosis, the difference between them was significant (P hyperkyphosis, scoliosis correction by combined procedures, scoliosis with a Cobb's angle more than 90 degrees , and a revision surgery.

  5. Syndrome of transient headache and neurologic deficits with cerebrospinal fluid lymphocytosis (HaNDL): a pediatric case report.

    Science.gov (United States)

    Gonçalves, Daniel; Meireles, Joana; Rocha, Ruben; Sampaio, Mafalda; Leão, Miguel

    2013-12-01

    The syndrome of transient headache and neurologic deficits associated with cerebrospinal fluid lymphocytosis (HaNDL) is characterized by 1 or more episodes of severe headache, transient neurologic deficits, and lymphocytic pleocytosis in the cerebrospinal fluid. It is a benign and self limited disorder seldom reported in pediatric age. We report the case of a 14-year-old girl who suffered from 2 episodes of headache with transient focal neurologic deficits and pleocytosis consistent with the syndrome of HaNDL. This entity should be taken into account as a differential diagnosis in otherwise healthy children presenting with recurrent headache and acute neurologic deficits. Repeated use of invasive and expensive laboratory and imaging investigations can be avoided when the diagnosis of the syndrome of HaNDL is correctly established.

  6. Posterior atlantoaxial dislocation without fracture and neurologic deficit: a case report and the review of literature.

    Science.gov (United States)

    Jiang, Lei-Sheng; Shen, Lei; Wang, Wei; Wu, Hao; Dai, Li-Yang

    2010-07-01

    Traumatic posterior atlantoaxial dislocation without related fracture of the odontoid process is very rare, and only ten cases have been previously reported. The objective of this paper was to describe a case of traumatic posterior atlantoaxial dislocation without related fracture of the odontoid process, and its management with atlantoaxial transarticular screw fixation and bony fusion through an anterior retropharyngeal approach, and to review the relevant literature. The patient's medical and radiographic history is reviewed as well as the relevant medical literature. Posterior atlantoaxial dislocation was confirmed in a 48-year-old male struck by an automobile through conventional radiography, computed tomography and magnetic resonance imaging. No related fracture of the odontoid process or neurological deficit was found in this patient. Transarticular screw fixation of the atlantoaxial articulation through anterior retropharyngeal approach was performed after several unsuccessful attempts of closed reduction. At the latest follow-up, the lateral cervical spine radiography in flexion and extension demonstrated no instability of the atlantoaxial complex 21 months after the operation. In conclusion, patients with posterior atlantoaxial dislocation without fracture may survive with few or no-long term neurological deficit. Routine CT and MRI of the cervical spine should be carried out in patients with head or neck trauma to prevent missing of this rare clinical entity. Transarticular screw fixation of the atlantoaxial articulation through anterior retropharyngeal approach is safe and useful in case the management of dislocation is unsuccessful under closed reduction.

  7. Effects of mTOR on neurological deficits after transient global ischemia

    Directory of Open Access Journals (Sweden)

    Xing Jihong

    2017-04-01

    Full Text Available Mammalian target of rapamycin (mTOR is a serine/threonine protein kinase and activation of its signal pathway plays an important role in regulating protein growth and synthesis as well as cell proliferation and survival. In the present study, we examined the contribution of mTOR and its downstream products to brain injuries and neurological deficiencies after cardiac arrest (CA induced-transient global ischemia. CA was induced by asphyxia followed by cardiopulmonary resuscitation (CPR in rats. Our results showed that expression of p-mTOR, mTOR-mediated phosphorylation of 4E-binding protein 4 (4E-BP1 and p70 ribosomal S6 protein kinase 1 (S6K1 pathways were amplified in CA rats compared to their controls. Blocking mTOR using rapamycin attenuated upregulation of pro-inflammatory cytokines (namely IL-1β, IL-6 and TNF-α, and Caspase-3, indicating cell apoptosis and also promoting the levels of vascular endothelial growth factor (VEGF and its subtype receptor VEGFR-2 in the hippocampus. Moreover, the effects of rapamycin were linked to improvement of neurological deficits and increased brain water content observed in CA rats. In conclusion, activation of mTOR signal is engaged in pathophysiological process during CA-induced transient global ischemia and blocking mTOR pathway plays a beneficial role in regulating injured neuronal tissues and neurological deficits via PIC, apoptotic Caspase-3 and VEGF mechanisms. Targeting one or more of these specific mTOR pathways and its downstream signaling molecules may present new opportunities for neural dysfunction and vulnerability related to transient global ischemia.

  8. Electrical Burn Causing a Unique Pattern of Neurological Injury

    Directory of Open Access Journals (Sweden)

    Nathan R. Schaefer, BExSc, MBBS (Hons

    2015-04-01

    Full Text Available Summary: Neurological involvement is not uncommon in patients who sustain electrical injury. The exact mechanism of nervous system damage following electrical trauma is not fully understood. The gamut of possible neurologic manifestations following electrical injury is diverse. This case report describes a young man with a unique pattern of neurological injury following an electrical burn. The combination of brachial plexopathy, partial Horner’s syndrome, and phrenic nerve palsy secondary to electrical injury has not been previously described in the literature.

  9. A pilot evaluation of the role of bracing in stable thoracolumbar burst fractures without neurological deficit.

    Science.gov (United States)

    Shamji, Mohammed F; Roffey, Darren M; Young, Darryl K; Reindl, Rudy; Wai, Eugene K

    2014-10-01

    Prospective, 2-center, observer-blinded, randomized controlled trial. Investigate clinical and radiologic outcomes of bracing versus no-bracing in the treatment of stable thoracolumbar burst fractures. Management of thoracolumbar burst fractures depends upon clinical presentation of neurological deficit and radiographic features of fracture severity. Neurologically intact patients with mild deformity and biomechanical stability may be treated with conservative therapy. Patients with stable (AO type A3), single level, thoracolumbar burst fractures between T12 and L2 with no neurological deficit were randomized to nonoperative treatment with a customized thoracolumbosacral orthosis (TLSO) or no-brace. Self-reported clinical outcomes of pain, disability, and health-related quality of life, and radiographic outcomes of kyphotic progression and loss of vertebral height, assessed by 2 independent reviewers blinded to treatment group, were measured at 6 months follow-up. Twenty-three consecutive eligible patients were included (TLSO: n=12; no-brace: n=11). There were no between-group differences regarding level of injury (P=0.75) and baseline spine geometry including fractional canal compromise (P=0.49), anterior loss of vertebral body height (P=0.28), and sagittal Cobb angle (P=0.13). In-hospital stay was significantly shorter in the no-brace group (mean: 2.8±3.0 d) compared with the TLSO group (mean: 6.3±2.1 d; P=0.004). At follow-up there were no differences in anterior loss of vertebral body height (TLSO: 12.5%±10.2% vs. no-brace: 11.9%±8.1%; P=0.88), kyphotic progression (TLSO: 5.3±4.4 degrees vs. no-brace 5.2±3.6 degrees; P=0.93), adverse events, or self-reported clinical outcomes. Neurologically intact patients with stable thoracolumbar burst fractures treated with or without bracing had similar radiographic and clinical outcomes at 6 months follow-up. The no-brace group had shorter in-hospital lengths of stay. Conservative therapy involving early

  10. Honey and propolis abrogate neurologic deficit and neuronal damage in the hippocampus and cerebral cortex of ischemic stroke rats

    OpenAIRE

    Mark Joseph M. Desamero; Mikaela Angelica Villablanca; Jussiaea V. Bariuan; Therese Marie A. Collantes; Delia T. Ang Gobonseng; Mary Jasmin C. Ang; Alejandro C. Fajardo Jr; Cleofas R. Cervancia; Maria Amelita C. Estacio

    2017-01-01

    Summary. The effect of honey and propolis on the neurologic deficit and neural damage in extracranial internal carotid artery occlusion ischemic stroke was investigated using male Sprague-Dawley rats which were randomly allocated into distilled water, propolis and honey treated groups. Neurologic motor assessment was performed daily during the 7-day treatment period and brain samples were processed and analyzed by histopathological approach. Oral administration of honey and propolis from the ...

  11. Lack of mitochondrial ferritin aggravated neurological deficits via enhancing oxidative stress in a traumatic brain injury murine model.

    Science.gov (United States)

    Wang, Ligang; Wang, Libo; Dai, Zhibo; Wu, Pei; Shi, Huaizhang; Zhao, Shiguang

    2017-12-22

    Oxidative stress has been strongly implicated in the pathogenesis of traumatic brain injury (TBI). Mitochondrial ferritin (Ftmt) is reported to be closely related to oxidative stress. However, whether Ftmt is involved in TBI-induced oxidative stress and neurological deficits remains unknown. In the present study, the controlled cortical impact model was established in wild-type and Ftmt knockout mice as a TBI model. The Ftmt expression, oxidative stress, neurological deficits, and brain injury were measured. We found that Ftmt expression was gradually decreased from 3 to 14 days post-TBI, while oxidative stress was gradually increased, as evidenced by reduced GSH and superoxide dismutase levels and elevated malondialdehyde and nitric oxide levels. Interestingly, the extent of reduced Ftmt expression in the brain was linearly correlated with oxidative stress. Knockout of Ftmt significantly exacerbated TBI-induced oxidative stress, intracerebral hemorrhage, brain infarction, edema, neurological severity score, memory impairment, and neurological deficits. However, all these effects in Ftmt knockout mice were markedly mitigated by pharmacological inhibition of oxidative stress using an antioxidant, N-acetylcysteine. Taken together, these results reveal an important correlation between Ftmt and oxidative stress after TBI. Ftmt deficiency aggravates TBI-induced brain injuries and neurological deficits, which at least partially through increasing oxidative stress levels. Our data suggest that Ftmt may be a promising molecular target for the treatment of TBI. © 2017 The Author(s).

  12. Scalp acupuncture attenuates neurological deficits in a rat model of hemorrhagic stroke.

    Science.gov (United States)

    Liu, Hao; Sun, Xiaowei; Zou, Wei; Leng, Mengtong; Zhang, Beng; Kang, Xiaoyu; He, Tao; Wang, Hui

    2017-06-01

    Hemorrhagic stroke accounts for approximately 15% of all stroke cases, and is associated with high morbidity and mortality. Limited human studies suggested that scalp acupuncture could facilitate functional recovery after cerebral hemorrhage. In the current study, we used an animal model of cerebral hemorrhage to examine the potential effects of scalp acupuncture. Adult male Sprague-Dawley rats received autologous blood (50μL) into the right caudate nucleus on the right side under pentobarbital anesthesia, and then received scalp acupuncture (DU20 through GB7 on the lesion side) or sham acupuncture (1cm to the right side of the acupoints) (n=10 per group). A group of rats receiving autologous blood into the caudate nucleus but no other intervention, as well as a group of rats receiving anesthesia but no blood injection to the brain (n=10 per group) were included as additional controls. Composite neuroscore, corner turn test, forelimb placing test, wire hang task and beam walking were used to evaluate the behavior of rats. Hematoxylin and Eosin (HE) staining was used to observe the histopathological changes. Western blot was used to detect the content of tumor necrosis factor alpha (TNF-α) and nuclear factor-KappaB (NFκB) protein expression. Scalp acupuncture attenuated neurological deficits (pvs. sham acupuncture using a variety of behavioral tests) at 1-7days after the treatment. The brain content of TNF-α and NFκB was decreased (pacupuncture could improve neurological deficits in a rat model of hemorrhagic stroke. Copyright © 2017 Elsevier Ltd. All rights reserved.

  13. a rare but treatable cause of rapid neurological deterioration in ...

    African Journals Online (AJOL)

    Pneumocephalus is a frequent complication following head injury and craniotomies. It can become an acute neurosurgical emergency when associated with raised intracranial pressure and neurological deterioration. Early diagnosis and timely appropriate intervention will reduce morbidity and unnecessary mortality from a ...

  14. Abnormal MRI in a patient with 'headache with neurological deficits and CSF lymphocytosis (HaNDL)'.

    Science.gov (United States)

    Yilmaz, A; Kaleagasi, H; Dogu, O; Kara, E; Ozge, A

    2010-05-01

    A 27-year-old woman was admitted to the Emergency Department with right upper-extremity numbness and mild weakness followed by a bifrontal throbbing headache for 30 min, which was similar to a headache lasting for 12 h that had occurred 3 days ago. Laboratory tests were unremarkable except for cerebrospinal fluid (CSF) lymphocytic pleocytosis. On the following day, a headache episode with left hemiparesis and hemihypoaesthesia, left hemifield visio-spatial inattention, anosagnosia and confusion recurred. The headache was diagnosed as headache and neurological deficits with cerebrospinal fluid lymphocytosis (HaNDL) syndrome according to the criteria of the second edition of the International Classification of Headache Disorders. Simultaneously performed magnetic resonance imaging (MRI) revealed swelling of the grey matter, CSF enhancement in the sulci of the right temporal and occipital regions and hypoperfusion of the same brain regions. During the following 10 days two more similar episodes recurred and during the ensuing 12 months the patient remained headache free. Neuroimaging findings of the HaNDL syndrome are always thought as virtually normal. MRI abnormalities in our patient have not been reported in HaNDL syndrome previously, although they have been reported in hemiplegic migraine patients before. The findings in our case suggest that hemiplegic migraine and HaNDL syndrome may share a common pathophysiological pathway resulting in similar imaging findings and neurological symptoms.

  15. Blood Brain Barrier Dysfunction and Delayed Neurological Deficits in Mild Traumatic Brain Injury Induced by Blast Shock Waves

    Directory of Open Access Journals (Sweden)

    Ashok K Shetty

    2014-08-01

    Full Text Available Mild traumatic brain injury (mTBI resulting from exposure to blast shock waves (BSWs is one of the most predominant causes of illnesses among veterans who served in the recent Iraq and Afghanistan wars. Such mTBI can also happen to civilians if exposed to shock waves of bomb attacks by terrorists. While cognitive problems, memory dysfunction, depression, anxiety and diffuse white matter injury have been observed at both early and/or delayed time-points, an initial brain pathology resulting from exposure to BSWs appears to be the dysfunction or disruption of the blood-brain barrier (BBB. Studies in animal models suggest that exposure to relatively milder BSWs (123 kPa initially induces free radical generating enzymes in and around brain capillaries, which enhances oxidative stress resulting in loss of tight junction proteins, edema formation, and leakiness of BBB with disruption or loss of its components pericytes and astrocyte end-feet. On the other hand, exposure to more intense BSWs (145-323 kPa causes acute disruption of the BBB with vascular lesions in the brain. Both of these scenarios lead to apoptosis of endothelial and neural cells and neuroinflammation in and around capillaries, which may progress into chronic traumatic encephalopathy and/or a variety of neurological impairments, depending on brain regions that are afflicted with such lesions. This review discusses studies that examined alterations in the brain milieu causing dysfunction or disruption of the BBB and neuroinflammation following exposure to different intensities of BSWs. Furthermore, potential of early intervention strategies capable of easing oxidative stress, repairing the BBB or blocking inflammation for minimizing delayed neurological deficits resulting from exposure to BSWs is conferred.

  16. Blood brain barrier dysfunction and delayed neurological deficits in mild traumatic brain injury induced by blast shock waves.

    Science.gov (United States)

    Shetty, Ashok K; Mishra, Vikas; Kodali, Maheedhar; Hattiangady, Bharathi

    2014-01-01

    Mild traumatic brain injury (mTBI) resulting from exposure to blast shock waves (BSWs) is one of the most predominant causes of illnesses among veterans who served in the recent Iraq and Afghanistan wars. Such mTBI can also happen to civilians if exposed to shock waves of bomb attacks by terrorists. While cognitive problems, memory dysfunction, depression, anxiety and diffuse white matter injury have been observed at both early and/or delayed time-points, an initial brain pathology resulting from exposure to BSWs appears to be the dysfunction or disruption of the blood-brain barrier (BBB). Studies in animal models suggest that exposure to relatively milder BSWs (123 kPa) initially induces free radical generating enzymes in and around brain capillaries, which enhances oxidative stress resulting in loss of tight junction (TJ) proteins, edema formation, and leakiness of BBB with disruption or loss of its components pericytes and astrocyte end-feet. On the other hand, exposure to more intense BSWs (145-323 kPa) causes acute disruption of the BBB with vascular lesions in the brain. Both of these scenarios lead to apoptosis of endothelial and neural cells and neuroinflammation in and around capillaries, which may progress into chronic traumatic encephalopathy (CTE) and/or a variety of neurological impairments, depending on brain regions that are afflicted with such lesions. This review discusses studies that examined alterations in the brain milieu causing dysfunction or disruption of the BBB and neuroinflammation following exposure to different intensities of BSWs. Furthermore, potential of early intervention strategies capable of easing oxidative stress, repairing the BBB or blocking inflammation for minimizing delayed neurological deficits resulting from exposure to BSWs is conferred.

  17. Rescue of neurological deficits in a mouse model for Angelman Syndrome by reduction of αCaMKII inhibitory phosphorylation

    NARCIS (Netherlands)

    G.M. van Woerden (Geeske); K.D. Harris; M.R. Hojjati (Mohammed Reza); R.M. Gustin; S. Qiu; R. de Avila Freire (Rogerio); Y. Jiang; Y. Elgersma (Ype); E.J. Weeber

    2007-01-01

    textabstractAngelman Syndrome (AS) is a severe neurological disorder characterized by mental retardation, motor dysfunction and epilepsy. We now show that the molecular and cellular deficits of an AS mouse model can be rescued by introducing an additional mutation at the inhibitory phosphorylation

  18. Asymmetrical focal neurological deficits in dogs and cats with naturally occurring tick paralysis (Ixodes holocyclus): 27 cases (1999-2006).

    Science.gov (United States)

    Holland, C T

    2008-10-01

    To describe basic epidemiological features, clinical characteristics and outcomes of asymmetrical focal neurological deficits identified in dogs and cats with naturally occurring tick paralysis (Ixodes holocyclus). A retrospective study. Computer records were reviewed for all dogs and cats treated for tick paralysis between July 1999 and June 2006 at a suburban veterinary hospital in Newcastle, New South Wales. Neurological deficits were identified in 17/197 dogs and 10/89 cats and included unilateral facial paralysis (14 dogs; 2 cats), anisocoria (4 dogs; 7 cats), unilateral loss of the cutaneous trunci reflex (1 dog; 1 cat) and Horner's syndrome in 2 cats with anisocoria. Occurrence of deficits was not linked to season, severity of tick paralysis, breed, age, sex or body weight. With facial paralysis and anisocoria, the site of tick attachment was invariably on the head or neck and always ipsilateral to the facial paralysis. By contrast, with anisocoria alone, no consistent relationship was noted between any one pupillary dimension and the side of tick attachment. With cutaneous trunci deficits the site of tick attachment was the ipsilateral caudal axilla. Compared with recovery times from generalised signs of tick paralysis, those for facial paralysis were significantly longer (days to weeks; P neurological deficits are a consistent finding in a proportion of dogs and cats with naturally occurring tick paralysis due to I. holocylcus.

  19. Predictive value of ischemic lesion volume assessed with magnetic resonance imaging for neurological deficits and functional outcome poststroke: A critical review of the literature.

    NARCIS (Netherlands)

    Schiemanck, S.K.; Kwakkel, G.; Post, M.W.; Prevo, A.J.

    2006-01-01

    OBJECTIVE: Ischemic lesion volume is assumed to be an important predictor of poststroke neurological deficits and functional outcome. This critical review examines the methodological quality of MRI studies and the predictive value of hemispheric infarct volume for neurological deficits (at body

  20. Phrenic nerve deficits and neurological immunopathology associated with acute West Nile virus infection in mice and hamsters.

    Science.gov (United States)

    Zukor, Katherine; Wang, Hong; Hurst, Brett L; Siddharthan, Venkatraman; Van Wettere, Arnaud; Pilowsky, Paul M; Morrey, John D

    2017-04-01

    Neurological respiratory deficits are serious outcomes of West Nile virus (WNV) disease. WNV patients requiring intubation have a poor prognosis. We previously reported that WNV-infected rodents also appear to have respiratory deficits when assessed by whole-body plethysmography and diaphragmatic electromyography. The purpose of this study was to determine if the nature of the respiratory deficits in WNV-infected rodents is neurological and if deficits are due to a disorder of brainstem respiratory centers, cervical spinal cord (CSC) phrenic motor neuron (PMN) circuitry, or both. We recorded phrenic nerve (PN) activity and found that in WNV-infected mice, PN amplitude is reduced, corroborating a neurological basis for respiratory deficits. These results were associated with a reduction in CSC motor neuron number. We found no dramatic deficits, however, in brainstem-mediated breathing rhythm generation or responses to hypercapnia. PN frequency and pattern parameters were normal, and all PN parameters changed appropriately upon a CO 2 challenge. Histological analysis revealed generalized microglia activation, astrocyte reactivity, T cell and neutrophil infiltration, and mild histopathologic lesions in both the brainstem and CSC, but none of these were tightly correlated with PN function. Similar results in PN activity, brainstem function, motor neuron number, and histopathology were seen in WNV-infected hamsters, except that histopathologic lesions were more severe. Taken together, the results suggest that respiratory deficits in acute WNV infection are primarily due to a lower motor neuron disorder affecting PMNs and the PN rather than a brainstem disorder. Future efforts should focus on markers of neuronal dysfunction, axonal degeneration, and myelination.

  1. Edaravone Reduces Hyperperfusion-Related Neurological Deficits in Adult Moyamoya Disease: Historical Control Study.

    Science.gov (United States)

    Uchino, Haruto; Nakayama, Naoki; Kazumata, Ken; Kuroda, Satoshi; Houkin, Kiyohiro

    2016-07-01

    Postoperative hyperperfusion-related transient neurological deficits (TNDs) are frequently observed in adult patients with moyamoya disease who undergo direct bypass procedures. The present study evaluated the effect of the free radical scavenger edaravone on postoperative hyperperfusion in adult moyamoya disease. This study included 92 hemispheres in 72 adult patients who underwent direct bypass for moyamoya disease. Serial measurements of cerebral blood flow were conducted immediately after surgery and on postoperative days 2 and 7. In 40 hemispheres for 36 patients, edaravone (60 mg/d) was administered from the day of surgery to postsurgical day 7. The incidence of postoperative hyperperfusion and associated TNDs were compared with a control group that included 52 hemispheres in 36 patients. Radiological hyperperfusion was observed in 28 of 40 (70.0%) and 39 of 52 (75.0%) hemispheres in the edaravone and control groups, respectively (P=0.30). Hyperperfusion-related TND incidences were significantly lower in the edaravone group compared with the control group (12.5% versus 32.7%; P=0.024). Multivariate analysis demonstrated that edaravone administration (P=0.009) and left-sided surgery (P=0.037) were significantly correlated with hyperperfusion-related TNDs (odds ratios, 0.3 and 4.2, respectively). Perioperative administration of edaravone reduced the incidence of hyperperfusion-related TNDs after direct bypass procedures in adult patients with moyamoya disease. © 2016 American Heart Association, Inc.

  2. Traumatic Posterior Atlantoaxial Dislocation Without Associated Fracture but With Neurological Deficit: A Case Report and Literature Review.

    Science.gov (United States)

    Xu, Yong; Li, Feng; Guan, Hanfeng; Xiong, Wei

    2015-10-01

    Posterior atlantoaxial dislocation without odontoid fracture is extremely rare and often results in fatal spinal cord injury. According to the reported literature, all cases presented mild or no neurologic deficit, with no definite relation to upper spinal cord injury. Little is reported about traumatic posterior atlantoaxial dislocation, with incomplete quadriplegia associated with a spinal cord injury.We present a case of posterior atlantoaxial dislocation without associated fracture, but with quadriplegia, and accompanying epidural hematoma and subarachnoid hemorrhage.The patient underwent gentle traction in the neutral position until repeated cranial computed tomography revealed no progression of the epidural hematoma. Thereafter, the atlantoaxial dislocation was reduced by using partial odontoidectomy via a video-assisted transcervical approach and maintained with posterior polyaxial screw-rod constructs and an autograft. Neurological status improved immediately after surgery, and the patient recovered completely after 1 year.Posterior fusion followed by closed reduction is the superior strategy for posterior atlantoaxial dislocation without odontoid fracture, according to literature. But for cases with severe neurological deficit, open reduction may be the safest choice to avoid the lethal complication of overdistraction of the spinal cord. Also, open reduction and posterior srew-rod fixation are safe and convenient strategies in dealing with traumatic posterior atlantoaxial dislocation patients with neurological deficit.

  3. An exploratory study of the relationship between neurological soft signs and theory of mind deficits in schizophrenia.

    Science.gov (United States)

    Romeo, Stefano; Chiandetti, Alessio; Siracusano, Alberto; Troisi, Alfonso

    2014-08-15

    Indirect evidence suggests partially common pathogenetic mechanisms for Neurological Soft Signs (NSS), neurocognition, and social cognition in schizophrenia. However, the possible association between NSS and mentalizing impairments has not yet been examined. In the present study, we assessed the ability to attribute mental states to others in patients with schizophrenia and predicted that the presence of theory of mind deficits would be significantly related to NSS. Participants were 90 clinically stable patients with a DSM-IV diagnosis of schizophrenia. NSS were assessed using the Neurological Evaluation Scale (NES). Theory of mind deficits were assessed using short verbal stories designed to measure false belief understanding. The findings of the study confirmed our hypothesis. Impaired sequencing of complex motor acts was the only neurological abnormality correlated with theory of mind deficits. By contrast, sensory integration, motor coordination and the NES Others subscale had no association with patients׳ ability to pass first- or second-order false belief tasks. If confirmed by future studies, the current findings provide the first preliminary evidence for the claim that specific NSS and theory of mind deficits may reflect overlapping neural substrates. Copyright © 2014 Elsevier Ireland Ltd. All rights reserved.

  4. Opsoclonus-ataxia caused by childhood neuroblastoma: developmental and neurologic sequelae.

    Science.gov (United States)

    Mitchell, Wendy G; Davalos-Gonzalez, Yolanda; Brumm, Virdette L; Aller, Sonia K; Burger, Elvira; Turkel, Susan B; Borchert, Mark S; Hollar, Susan; Padilla, Sonia

    2002-01-01

    Opsoclonus-ataxia, also called "dancing eye syndrome," is a serious neurologic condition that is often a paraneoplastic manifestation of occult neuroblastoma in early childhood. Despite resection of tumor and immunosuppressive therapy, outcome generally includes significant developmental and behavioral sequelae. There is controversy about how treatment alters outcome. The goals of this study were to understand the ongoing neurologic and developmental deficits of children who are treated for opsoclonus-ataxia with associated neuroblastoma; to relate treatment history to outcome; and to quantify objectively the acute changes in motor function, speech, mood, and behavior related to intravenous immunoglobulin (IVIg) treatment. Patients were children with opsoclonus-ataxia caused by neuroblastoma, regardless of interval since diagnosis. Records were reviewed, and children underwent comprehensive evaluations, including neurologic examination and tests of cognitive and adaptive function, speech and language, and fine and gross motor abilities. Psychiatric interview and questionnaires were used to assess current and previous behavior. In 6 children, a videotaped standardized examination of eye movements was performed. Additional examinations were performed immediately before and 2 to 3 days after treatment with IVIg in 5 children. Seventeen children, ages 1.75 to 12.62 years, were examined. All had a stage I or II neuroblastoma resected 3 months to 11 years previously. None received any other treatment for the tumor. All but 1 had received at least 1 year of either oral corticosteroids or corticotropin (ACTH); 12 had received 1 or more courses of IVIg, 2 g/kg. Three had received other immunosuppressive treatment, including cyclophosphamide. Cognitive development and adaptive behavior were delayed or abnormal in nearly all children. Expressive language was more impaired than receptive language. Speech was impaired, including both intelligibility and overall output. Fine and

  5. Neurological sequelae of bacterial meningitis.

    Science.gov (United States)

    Lucas, Marjolein J; Brouwer, Matthijs C; van de Beek, Diederik

    2016-07-01

    We reported on occurrence and impact of neurological sequelae after bacterial meningitis. We reviewed occurrence of neurological sequelae in children and adults after pneumococcal and meningococcal meningitis. Most frequently reported sequelae are focal neurological deficits, hearing loss, cognitive impairment and epilepsy. Adults with pneumococcal meningitis have the highest risk of developing focal neurological deficits, which are most commonly caused by cerebral infarction, but can also be due to cerebritis, subdural empyema, cerebral abscess or intracerebral bleeding. Focal deficits may improve during clinical course and even after discharge, but a proportion of patients will have persisting focal neurological deficits that often interfere in patient's daily life. Hearing loss occurs in a high proportion of patients with pneumococcal meningitis and has been associated with co-existing otitis. Children and adults recovering from bacterial meningitis without apparent neurological deficits are at risk for long-term cognitive deficits. Early identification of neurological sequelae is important for children to prevent additional developmental delay, and for adults to achieve successful return in society after the disease. Neurological sequelae occur in a substantial amount of patients following bacterial meningitis. Most frequently reported sequelae are focal neurological deficits, hearing loss, cognitive impairment and epilepsy. Copyright © 2016 The British Infection Association. Published by Elsevier Ltd. All rights reserved.

  6. The Most Common Causes of Eye Pain at 2 Tertiary Ophthalmology and Neurology Clinics.

    Science.gov (United States)

    Bowen, Randy C; Koeppel, Jan N; Christensen, Chance D; Snow, Karisa B; Ma, Junjie; Katz, Bradley J; Krauss, Howard R; Landau, Klara; Warner, Judith E A; Crum, Alison V; Straumann, Dominik; Digre, Kathleen B

    2018-01-12

    Eye pain is a common complaint, but no previous studies have determined the most common causes of this presenting symptom. Our objective was to determine the most common causes of eye pain in 2 ophthalmology and neurology departments at academic medical centers. This was a retrospective cross-sectional analysis and chart review at the departments of ophthalmology and neurology at the University Hospital Zurich (USZ), University of Zürich, Switzerland, and the University of Utah (UU), USA. Data were analyzed from January 2012 to December 2013. We included patients aged 18 years or older presenting with eye pain as a major complaint. Two thousand six hundred three patient charts met inclusion criteria; 742 were included from USZ and 1,861 were included from UU. Of these, 2,407 had been seen in an ophthalmology clinic and 196 had been seen in a neurology clinic. Inflammatory eye disease (conjunctivitis, blepharitis, keratitis, uveitis, dry eye, chalazion, and scleritis) was the underlying cause of eye pain in 1,801 (69.1%) of all patients analyzed. Although only 71 (3%) of 2,407 patients had migraine diagnosed in an ophthalmology clinic as the cause of eye pain, migraine was the predominant cause of eye pain in the neurology clinics (100/196; 51%). Other causes of eye pain in the neurology clinics included optic neuritis (44 patients), trigeminal neuralgia, and other cranial nerve disorders (8 patients). Eye pain may be associated with a number of different causes, some benign and others sight- or life-threatening. Because patients with eye pain may present to either a neurology or an ophthalmology clinic and because the causes of eye pain may be primarily ophthalmic or neurologic, the diagnosis and management of these patients often requires collaboration and consultation between the 2 specialties.

  7. Exercise attenuates neurological deficits by stimulating a critical HSP70/NF-κB/IL-6/synapsin I axis in traumatic brain injury rats.

    Science.gov (United States)

    Chio, Chung-Ching; Lin, Hung-Jung; Tian, Yu-Feng; Chen, Yu-Chieh; Lin, Mao-Tsun; Lin, Cheng-Hsien; Chang, Ching-Ping; Hsu, Chien-Chin

    2017-04-24

    Despite previous evidence for a potent inflammatory response after a traumatic brain injury (TBI), it is unknown whether exercise preconditioning (EP) improves outcomes after a TBI by modulating inflammatory responses. We performed quantitative real-time PCR (qPCR) to quantify the genes encoding 84 cytokines and chemokines in the peripheral blood and used ELISA to determine both the cerebral and blood levels of interleukin-6 (IL-6). We also performed the chromatin immunoprecipitation (ChIP) assay to evaluate the extent of nuclear factor kappa-B (NF-κB) binding to the DNA elements in the IL-6 promoter regions. Also, we adopted the Western blotting assay to measure the cerebral levels of heat shock protein (HSP) 70, synapsin I, and β-actin. Finally, we performed both histoimmunological and behavioral assessment to measure brain injury and neurological deficits, respectively. We first demonstrated that TBI upregulated nine pro-inflammatory and/or neurodegenerative messenger RNAs (mRNAs) in the peripheral blood such as CXCL10, IL-18, IL-16, Cd-70, Mif, Ppbp, Ltd, Tnfrsf 11b, and Faslg. In addition to causing neurological injuries, TBI also upregulated the following 14 anti-inflammatory and/or neuroregenerative mRNAs in the peripheral blood such as Ccl19, Ccl3, Cxcl19, IL-10, IL-22, IL-6, Bmp6, Ccl22, IL-7, Bmp7, Ccl2, Ccl17, IL-1rn, and Gpi. Second, we observed that EP inhibited both neurological injuries and six pro-inflammatory and/or neurodegenerative genes (Cxcl10, IL-18, IL-16, Cd70, Mif, and Faslg) but potentiated four anti-inflammatory and/or neuroregenerative genes (Bmp6, IL-10, IL-22, and IL-6). Prior depletion of cerebral HSP70 with gene silence significantly reversed the beneficial effects of EP in reducing neurological injuries and altered gene profiles after a TBI. A positive Pearson correlation exists between IL-6 and HSP70 in the peripheral blood or in the cerebral levels. In addition, gene silence of cerebral HSP70 significantly reduced the

  8. Symptomatic intracranial hypertension during recovery from the syndrome of headache with neurologic deficits and cerebrospinal fluid lymphocytosis (HANDL).

    Science.gov (United States)

    Mulroy, Eoin; Yap, Joel; Danesh-Meyer, Helen; Anderson, Neil

    2017-04-01

    The syndrome of headache with neurologic deficits and cerebrospinal fluid lymphocytosis (HANDL) is rare; it comprises migrainous headaches (generally in headache-naïve people), fluctuating neurological symptoms and cerebrospinal fluid (CSF) lymphocytosis. The syndrome generally runs a benign, self-limiting course over weeks. A small proportion of patients develop intracranial hypertension as a consequence of the illness. Recurrence of headaches or development of visual symptoms following apparent recovery from HANDL should prompt urgent re-evaluation for elevated intracranial pressure. Short-to-medium term management with CSF drainage and acetazolamide may be necessary to prevent visual loss. © Article author(s) (or their employer(s) unless otherwise stated in the text of the article) 2017. All rights reserved. No commercial use is permitted unless otherwise expressly granted.

  9. Posterior atlantoaxial dislocation complicating odontoid fracture without neurologic deficit: a case report and review of the literature.

    Science.gov (United States)

    Meng, Hao; Gao, Yuan; Li, Mo; Luo, Zhuojing; Du, Junjie

    2014-07-01

    Traumatic posterior atlantoaxial dislocation associated with odontoid fracture is extremely rare, with only eight cases reported thus far in the English literature. This report concerns a 47-year-old female who presented with considerable pain and stiffness in the neck without a neurologic deficit after injury due to a fall. Radiographs, computed tomography, and magnetic resonance imaging demonstrated a posterior dislocation of the atlas with respect to the axis with an odontoid fracture. No cord compression or intramedullary cord signal abnormalities were detected at the level of the atlantoaxial dislocation. A pedicle screw fixation/fusion was performed via a posterior approach following successful closed reduction.

  10. Navigated transcranial magnetic stimulation for glioma removal: prognostic value in motor function recovery from postsurgical neurological deficits.

    Science.gov (United States)

    Takakura, Tomokazu; Muragaki, Yoshihiro; Tamura, Manabu; Maruyama, Takashi; Nitta, Masayuki; Niki, Chiharu; Kawamata, Takakazu

    2017-10-01

    OBJECTIVE The aim of the present study was to evaluate the usefulness of navigated transcranial magnetic stimulation (nTMS) as a prognostic predictor for upper-extremity motor functional recovery from postsurgical neurological deficits. METHODS Preoperative and postoperative nTMS studies were prospectively applied in 14 patients (mean age 39 ± 12 years) who had intraparenchymal brain neoplasms located within or adjacent to the motor eloquent area in the cerebral hemisphere. Mapping by nTMS was done 3 times, i.e., before surgery, and 1 week and 3 weeks after surgery. To assess the response induced by nTMS, motor evoked potential (nTMS-MEP) was recorded using a surface electromyography electrode attached to the abductor pollicis brevis (APB). The cortical locations that elicited the largest electromyography response by nTMS were defined as hotspots. Hotspots for APB were confirmed as positive responsive sites by direct electrical stimulation (DES) during awake craniotomy. The distances between hotspots and lesions (DHS-L) were measured. Postoperative neurological deficits were assessed by manual muscle test and dynamometer. To validate the prognostic value of nTMS in recovery from upper-extremity paresis, the following were investigated: 1) the correlation between DHS-L and the serial grip strength change, and 2) the correlation between positive nTMS-MEP at 1 week after surgery and the serial grip strength change. RESULTS From the presurgical nTMS study, MEPs from targeted muscles were identified in 13 cases from affected hemispheres. In one case, MEP was not evoked due to a huge tumor. Among 9 cases from which intraoperative DES mapping for hand motor area was available, hotspots for APB identified by nTMS were concordant with DES-positive sites. Compared with the adjacent group (DHS-L motor recovery at 1 week, 3 weeks, and 3 months after surgery (r = 0.87, 0.88, and 0.77, respectively). CONCLUSIONS Navigated TMS is a useful tool for identifying motor eloquent

  11. Effects of the cyclooxygenase-2 inhibitor nimesulide on cerebral infarction and neurological deficits induced by permanent middle cerebral artery occlusion in the rat

    Directory of Open Access Journals (Sweden)

    Muñoz Eduardo

    2005-01-01

    Full Text Available Abstract Background Previous studies suggest that the cyclooxygenase-2 (COX-2 inhibitor nimesulide has a remarkable protective effect against different types of brain injury including ischemia. Since there are no reports on the effects of nimesulide on permanent ischemic stroke and because most cases of human stroke are caused by permanent occlusion of cerebral arteries, the present study was conducted to assess the neuroprotective efficacy of nimesulide on the cerebral infarction and neurological deficits induced by permanent middle cerebral artery occlusion (pMCAO in the rat. Methods Ischemia was induced by permanent occlusion of the middle cerebral artery in rats, via surgical insertion of a nylon filament into the internal carotid artery. Infarct volumes (cortical, subcortical and total and functional recovery, assessed by neurological score evaluation and rotarod performance test, were performed 24 h after pMCAO. In initial experiments, different doses of nimesulide (3, 6 and 12 mg/kg; i.p or vehicle were administered 30 min before pMCAO and again at 6, 12 and 18 h after stroke. In later experiments we investigated the therapeutic time window of protection of nimesulide by delaying its first administration 0.5–4 h after the ischemic insult. Results Repeated treatments with nimesulide dose-dependently reduced cortical, subcortical and total infarct volumes as well as the neurological deficits and motor impairment resulting from permanent ischemic stroke, but only the administration of the highest dose (12 mg/kg was able to significantly (P Conclusions These data show that nimesulide protects against permanent focal cerebral ischemia, even with a 2 h post-treatment delay. These findings have important implications for the therapeutic potential of using COX-2 inhibitors in the treatment of stroke.

  12. Immediate effects of cerebral ischemia: evolution and resolution of neurological deficits after experimental occlusion of one middle cerebral artery in conscious cats.

    Science.gov (United States)

    Hayakawa, T; Waltz, A G

    1975-01-01

    Acute occlusion of the left middle cerebral artery (MCA) was accomplished without anesthesia and inside an intact cranium containing cerebrospinal fluid (CSF) in ten cats five to nine days after implantation of an occlusive device through the orbit. Immediate neurological deficits included forced ambuxlation, circling, and tonic deviation of the head and neck toward the side of the occluded artery; weakness of the opposite limbs; and an apathetic or akinetic state. Two cats died within 24 hours. The other eight cats improved but secondary deficits developed in two, causing death. In two of the remaining six cats no deficits were apparent seven days later. The cerbral infarcts regularly involved the basal ganglia, internal capsule, and cortical regions, and were larger and less variable than those produced by MCA occlusion through and open optic foramen or craniectomy with cranial decompression by drainage of CSF. This model of acute focal cerebral ischemia may be of value for studies of physiological and biochemical factors uninfluenced by sedatives, anesthesia, or recent surgical procedures.

  13. [Neurological features of decision-making deficit: Korinai syndrome in Parkinson disease and fearlessness in dementia].

    Science.gov (United States)

    Iwata, Makoto

    2012-10-01

    For patients with Parkinson disease, falls are generally attributed to postural instability. However, closer examination often shows that parkinsonian patients tend to keep falling at the same spot in their home on performing the same actions such as standing up from a chair, starting to walk, or turning at the corner and hitting the same part of the head. Each time the patients fall, their treating physicians explain the reasons for falling and tell them how to avoid falls in daily life. In spite of the repeated advice given by physicians, these patients fall in the same manner and location. When physicians question them regarding the reason for repeating the same risky actions that they had been asked to avoid, the patients answer that they clearly remembered their physician's advice but had thought that they would be able to successfully accomplish the risky actions at that time. Thus, it seems that this type of fall is partly caused by decision-making deficit. Negative-reward motor learning is known to be defective in parkinsonian patients who are being treated with dopamine agonists and are liable to indulge in risky behavior and tend to be involved in pathological gambling. The behavioral abnormalities that are caused by defective decision making and are common to pathological gambling and repeated falling in parkinsonian patients could be termed as "Korinai syndrome, " which means "syndrome involving the inability to learn by experience." In contrast, patients with dementia often show loss of fear reaction, which may result in the life-threatening inability to perceive crises. The present author performed a series of studies just after the Great East Japan Earthquake in March 2011; these studies were based on the behavior of patients with dementia during this large earthquake. The results showed that both intellectually normal elderly people and patients with mild dementia had shown evident fear reactions and could remember their own fearful experience

  14. Recent onset neck pain with associated neurological deficit--Pott's disease remains an important differential diagnosis.

    LENUS (Irish Health Repository)

    Bourke, M G

    2010-11-05

    The incidence of spinal tuberculosis is increasing in developed nations. In Ireland, half of all cases seen in the most recent decade for which figures are available were diagnosed in 2005-2007, the three most recent years for which there is complete data. We discuss a patient who presented with neurological complications due to destructive spinal tuberculous disease affecting the sixth cervical vertebra.

  15. Diagnosis of Attention-Deficit/Hyperactivity Disorder and Its Behavioral, Neurological, and Genetic Roots

    Science.gov (United States)

    Mueller, Kathryn L.; Tomblin, J. Bruce

    2012-01-01

    Attention-deficit/hyperactivity disorder (ADHD) is a common developmental disorder often associated with other developmental disorders including speech, language, and reading disorders. Here, we review the principal features of ADHD and current diagnostic standards for the disorder. We outline the ADHD subtypes, which are based upon the dimensions…

  16. Minimal epicondylectomy improves neurologic deficits in moderate to severe cubital tunnel syndrome.

    Science.gov (United States)

    Kim, Kang Wook; Lee, Hyuk Jin; Rhee, Seung Hwan; Baek, Goo Hyun

    2012-05-01

    Previous studies of minimal medial epicondylectomy for cubital tunnel syndrome included patients with mild disease, making it difficult to determine how much this procedure improved sensory and motor impairments in patients with moderate to severe disease. We asked if minimal epicondylectomy improved sensory and motor impairments in patients with moderate to severe cubital tunnel syndrome. We retrospectively reviewed 25 patients treated with minimal medial epicondylectomy for advanced cubital tunnel syndrome involving motor weakness between January 2003 and February 2009. Preoperatively, five patients had Medical Research Council (MRC) Grade 4 motor strength without atrophy (McGowan Grade IIA), nine had MRC Grade 3 motor strength with detectable atrophy (McGowan Grade IIB), and 11 had MRC Grade 3 or less motor strength with severe atrophy (McGowan Grade III). Postoperatively we obtained DASH scores and evaluated improvement of sensory impairment and motor impairment: excellent with minimal sensory deficit and motor deficit, good with mild deficits, fair with improved but persistent deficit(s), and poor with no improvement. The minimum followup was 13 months (mean, 46 months; range, 13-86 months). The mean DASH score was 14 points (range, 2-47 points). Of the 25 patients, sensory improvement and motor improvement were excellent in 16 patients, good in five, fair in two, and poor in two. Twenty-three of the 25 patients improved at least one McGowan grade. There were no complications, such as medial elbow instability. Minimal medial epicondylectomy can improve sensory and motor impairments for patients with moderate to severe cubital tunnel syndrome. Level IV, therapeutic study. See the guidelines for authors for a complete description of levels of evidence.

  17. Postpartum cerebral angiopathy presenting with non-aneurysmal subarachnoid hemorrhage and interval development of neurological deficits: a case report and review of literature.

    Science.gov (United States)

    Yang, Li; Bai, Harrison X; Zhao, Xin; Xiao, Yanqiao; Tan, Liming

    2013-01-01

    Postpartum cerebral angiopathy (PCA) is a cerebrovascular disease that occurs during the postpartum period. It is characterized by reversible multifocal vasoconstriction of the cerebral arteries. We report a patient with PCA proven by cerebral angiography that revealed multifocal, segmental narrowing of the cerebral arteries and non-aneurysmal subarachnoid hemorrhage. The patient suddenly deteriorated with focal neurological deficits on the 5 th day of hospitalization. She was treated with calcium-channel blockers and monitored with daily transcranial Doppler ultrasound. Her symptoms gradually improved and she was discharged on the 11 th day of hospitalization. At 1-month follow-up, patient was completely symptom-free with no neurological deficits.

  18. Sex Difference in Oxidative Stress Parameters in Spinal Cord of Rats with Experimental Autoimmune Encephalomyelitis: Relation to Neurological Deficit.

    Science.gov (United States)

    Dimitrijević, Mirjana; Kotur-Stevuljević, Jelena; Stojić-Vukanić, Zorica; Vujnović, Ivana; Pilipović, Ivan; Nacka-Aleksić, Mirjana; Leposavić, Gordana

    2017-02-01

    The study examined (a) whether there is sex difference in spinal cord and plasma oxidative stress profiles in Dark Agouti rats immunised for experimental autoimmune encephalomyelitis (EAE), the principal experimental model of multiple sclerosis, and (b) whether there is correlation between the oxidative stress in spinal cord and neurological deficit. Regardless of rat sex, with the disease development xanthine oxidase (XO) activity and inducible nitric oxide synthase (iNOS) mRNA expression increased in spinal cord, whereas glutathione levels decreased. This was accompanied by the rise in spinal cord malondialdehyde level. On the other hand, with EAE development superoxide dismutase (SOD) activity decreased, while O2(-) concentration increased only in spinal cord of male rats. Consequently, SOD activity was lower, whereas O2(-) concentration was higher in spinal cord of male rats with clinically manifested EAE. XO activity and iNOS mRNA expression were also elevated in their spinal cord. Consistently, in the effector phase of EAE the concentration of advanced oxidation protein product (AOPP) was higher in spinal cord of male rats, which exhibit more severe neurological deficit than their female counterparts. In as much as data obtained in the experimental models could be translated to humans, the findings may be relevant for designing sex-specific antioxidant therapeutic strategies. Furthermore, the study indicated that the increased pro-oxidant-antioxidant balance in plasma may be an early indicator of EAE development. Moreover, it showed that plasma AOPP level may indicate not only actual activity of the disease, but also serve to predict severity of its course.

  19. EFFECT OF KINESIO TAPING AND SOFT ORTHOSIS APPLICATION ON THE PAIN AND FUNCTIONAL DISABILITY IN LUMBAR REGION PATHOLOGIES WITHOUT NEUROLOGICAL DEFICITS: A RANDOMIZED CONTROLLED EXPERIMENTAL STUDY

    Directory of Open Access Journals (Sweden)

    Burcu TALU

    2016-12-01

    Full Text Available Background: Back pain caused by lumbar region pathologies is a condition that leads to loss of productivity and physical disability, with high costs of diagnosis and treatment. This study was planned to investigate the effect of taping and soft orthosis application on the pain and functional disability in the pathology of lumbar region without neurological deficit. Methods: This study is randomized controlled trial. Sixty-three volunteer patients were randomly divided into three groups of 21 people. Group I, soft orthotics and stabilization exercise program; Group II, Kinesio taping and stabilization exercise program; Group III, stabilization exercise program was applied. After obtaining demographic data of the participants; patients were evaluated in terms of range of motion and muscle strength. We used visual analog scale for pain level assessment, sit and reach test for flexibility assessment, timed up and go test (TUG for functional ambulation and balance, modified Schober test for lumbar spine flexibility, Oswestry Disability Index in the assessment of functional disability. They were assessed at the pretreatment, third (post treatment and six week (home programs and follow-up. Results: The results showed that significant differences (p<0.05 occurred over time in the study parameters such as functional ambulation, flexibility, lumbar flexibility, functional disability, pain, strength, range of motion in all groups. In comparisons between groups, there was a difference mainly in favor of Group II (p<0.05. Conclusions: We have concluded that in lumbar region pathologies without neurological deficits, stabilization exercises combined with orthotics and Kinesio taping applications reduces pain and functional disability.

  20. Vanishing bone disease of chest wall and spine with kyphoscoliosis and neurological deficit: A case report and review of literature

    Directory of Open Access Journals (Sweden)

    Sudhir Kumar Srivastava

    2017-01-01

    Full Text Available Vanishing bone disease is an extremely rare disorder of unknown etiology characterized by idiopathic osteolysis of bone. We describe a case of vanishing bone disease of chest wall and spine with kyphoscoliosis and neurological deficit. A 17-year-old male presented with gradually progressive deformity of back and dorsal compressive myelopathy with nonambulatory power in lower limbs. Radiographs revealed absent 4 th-7 th ribs on the right side with dorsal kyphoscoliosis and severe canal narrowing at the apex. The patient was given localized radiotherapy and started on a monthly infusion of 4 mg zoledronic acid. Posterior instrumented fusion with anterior reconstruction via posterolateral approach was performed. The patient had a complete neurological recovery at 5 weeks following surgery. At 1 year, anterior nonunion was noted for which transthoracic tricortical bone grafting was done. Bone graft from the patient′s mother was used both times. At 7 months following anterior grafting, the alignment was maintained and the patient was asymptomatic; however, fusion at graft-host interface was not achieved. Bisphosphonates and radiotherapy were successful in halting the progress of osteolysis.

  1. Memory outcomes following cognitive interventions in children with neurological deficits: A review with a focus on under-studied populations.

    Science.gov (United States)

    Schaffer, Yael; Geva, Ronny

    2016-01-01

    Given the primary role of memory in children's learning and well-being, the aim of this review was to examine the outcomes of memory remediation interventions in children with neurological deficits as a function of the affected memory system and intervention method. Fifty-seven studies that evaluated the outcome of memory interventions in children were identified. Thirty-four studies met the inclusion criteria, and were included in a systematic review. Diverse rehabilitation methods for improving explicit and implicit memory in children were reviewed. The analysis indicates that teaching restoration strategies may improve, and result in the generalisation of, semantic memory and working memory performance in children older than 7 years with mild to moderate memory deficits. Factors such as longer protocols, emotional support, and personal feedback contribute to intervention efficacy. In addition, the use of compensation aids seems to be highly effective in prospective memory tasks. Finally, the review unveiled a lack of studies with young children and the absence of group interventions. These findings point to the importance of future evidence-based intervention protocols in these areas.

  2. Frequency of screening magnetic resonance imaging to detect occult spinal cord compromise and to prevent neurological deficit in metastatic castration-resistant prostate cancer.

    Science.gov (United States)

    Venkitaraman, R; Sohaib, S A; Barbachano, Y; Parker, C C; Huddart, R A; Horwich, A; Dearnaley, D

    2010-03-01

    Neurological deficit from malignant spinal cord compression (SCC) is a major complication of metastatic castration-resistant prostate cancer (CRPC). The aims of the present study were to determine the incidence of neurological deficit in metastatic prostate cancer patients and to determine the optimal frequency of screening magnetic resonance imaging (MRI) spine required to detect clinically occult radiological SCC (rSCC). A retrospective analysis of the clinical data of 130 consecutive patients with CRPC, with no functional neurological deficit, who had screening MRI spine from January 2001 to May 2005, was undertaken. Patients found to have rSCC received radiotherapy. All patients were followed-up to document the incidence of neurological deficit. Thirty-seven (28.4%) patients had rSCC on MRI. The proportion of patients free from neurological deficit at 3, 6, 12, 18 and 24 months was 94, 80, 59 and 43%, respectively, in patients who had rSCC on initial MRI and 97.5, 89, 75 and 63%, respectively, in patients who had no rSCC. A high prostate-specific antigen (PSA) level at initial MRI (P = 0.035) and a short PSA doubling time neurological deficit on univariate analysis, whereas back pain (P = 0.059), although an important predictive factor, did not attain statistical significance. On multivariate analysis, only rapid PSA doubling time (neurological deficit (P = 0.042). MRI spine can be used to detect asymptomatic rSCC in patients with CRPC and serial estimations are required to maintain a low incidence of clinical SCC. If serial screening MRI spine is used to detect rSCC in 90% of patients before the development of neurological signs, the optimum frequency depends on the subset of patients studied. The results of our study suggest that the optimum frequency would be every 4-6 months for patients with previous SCC, rapid or high PSA or back pain and annually for asymptomatic patients. 2009 The Royal College of Radiologists. Published by Elsevier Ltd. All rights

  3. Use of Machine Learning Classifiers and Sensor Data to Detect Neurological Deficit in Stroke Patients.

    Science.gov (United States)

    Park, Eunjeong; Chang, Hyuk-Jae; Nam, Hyo Suk

    2017-04-18

    The pronator drift test (PDT), a neurological examination, is widely used in clinics to measure motor weakness of stroke patients. The aim of this study was to develop a PDT tool with machine learning classifiers to detect stroke symptoms based on quantification of proximal arm weakness using inertial sensors and signal processing. We extracted features of drift and pronation from accelerometer signals of wearable devices on the inner wrists of 16 stroke patients and 10 healthy controls. Signal processing and feature selection approach were applied to discriminate PDT features used to classify stroke patients. A series of machine learning techniques, namely support vector machine (SVM), radial basis function network (RBFN), and random forest (RF), were implemented to discriminate stroke patients from controls with leave-one-out cross-validation. Signal processing by the PDT tool extracted a total of 12 PDT features from sensors. Feature selection abstracted the major attributes from the 12 PDT features to elucidate the dominant characteristics of proximal weakness of stroke patients using machine learning classification. Our proposed PDT classifiers had an area under the receiver operating characteristic curve (AUC) of .806 (SVM), .769 (RBFN), and .900 (RF) without feature selection, and feature selection improves the AUCs to .913 (SVM), .956 (RBFN), and .975 (RF), representing an average performance enhancement of 15.3%. Sensors and machine learning methods can reliably detect stroke signs and quantify proximal arm weakness. Our proposed solution will facilitate pervasive monitoring of stroke patients.

  4. Patients with Blunt Traumatic Spine Injuries with Neurological Deficits Presenting to an Urban Tertiary Care Centre in Mumbai: An Epidemiological Study

    Directory of Open Access Journals (Sweden)

    Anoop C Dhamangaonkar

    2013-03-01

    Full Text Available INTRODUCTION: Traumatic spine injuries are on the rise. The literature is sparse regarding epidemiology of patients with traumatic spine injuries from this part of the world. OBJECTIVES: To analyse the following in patients with traumatic spine injuries with neurological deficits: demographic and social profile, common modes of injury, pre-hospitalisation practices, region of spine affected, severity of neurological deficit and the lay individuals’ awareness about traumatic spine injuries. METHODS: The study sample comprised 52 adult patients with traumatic spine injuries with neurological deficits. We collected data on demographic and social characteristics, mode of injury, pre-hospitalisation treatment, interval between injury and presentation, spine region affected and severity of neurological deficits and patient's knowledge about such injuries. RESULTS: The average patient age was 31.32y. The male: female ratio was 2.25:1, and the most common modes of injury were fall from height, followed by traffic accident. More than half of the patients suffered cervical spine injuries, followed by dorsolumbar spine injuries. Only 9.61% of patients received pre-hospitalisation treatment. All patients understood there could be complete functional recovery after treatment for traumatic spine injuries. CONCLUSION: There is a growing need to improve railway and roadway safety equipment and to make it accessible and affordable to the susceptible economically weaker population. Attempts should be made to increase awareness regarding traumatic spine injuries.

  5. Dumping syndrome: an unusual cause of severe hyperinsulinemic hypoglycemia in neurologically impaired children with gastrostomy.

    Science.gov (United States)

    Bizzarri, C; Cervoni, M; Crea, F; Cutrera, R; Schiavino, A; Schiaffini, R; Cappa, M

    2011-02-01

    This paper describes severe hyperinsulinemic hypoglycemia during bolus enteral feeding in two neurologically impaired children. Both children were affected by dysphagia with swallowing difficulties; caloric intake was inadequate. For these reasons, percutaneous endoscopic gastrostomy had been positioned during the first months of life. In one patient due to persisting vomiting, after a few months, a gastrojejunal tube (PEG-J) was inserted. Hypoglycemia was revealed by routine blood tests, without evidence of specific symptoms. Continuous subcutaneous glucose monitoring showed wide glucose excursions, ranging from hypoglycemia to hyperglycemia. Extremely high levels of insulin were detected at the time of hypoglycemia. A diagnosis of dumping syndrome (DS) was suspected in both children. In the child with PEG, the tip of the gastrostomy catheter was found to be lying in the bulbus duodeni. Once this had been pulled back, hypoglycemic episodes disappeared. The child with PEG-J needed continuous enteral feeding to reach a normal glucose balance. DS is a relatively common complication in children with gastrostomy, but extremely irregular glucose levels, ranging from hypoglycemia to hyperglycemia, and increased insulin secretion had not been previously demonstrated. The incidence of DS is probably underestimated in children receiving enteral feeding for neurological impairment. In these patients intensive monitoring of blood glucose levels should be performed to calibrate meals. Repeated underestimated hypoglycemic episodes could worsen neurological damage and cause a deterioration in clinical conditions.

  6. Traumatic high-grade spondylolisthesis at C7-T1 with no neurological deficits: Case series, literature review, and biomechanical implications

    Directory of Open Access Journals (Sweden)

    Ha Son Nguyen

    2017-01-01

    Full Text Available Traumatic high-grade spondylolisthesis in subaxial cervical spine is frequently associated with acute spinal cord injury and quadriparesis. There have been rare cases where such pathology demonstrates minimal to no neurological deficits. Assessment of the underlying biomechanics may provide insight into the mechanism of injury and associated neurological preservation. Patient 1 is a 63-year-old female presenting after a motor vehicle collision with significant right arm pain without neurological deficits. Imaging demonstrated C7/T1 spondyloptosis, associated with a locked facet on the left at C6/7 and a locked facet on the right at C7/T1, with a fracture of the left C7 pedicle and right C7 lamina. Patient 2 is a 60-year-old male presenting after a bicycle collision with transient bilateral upper extremity paresthesias without neurological deficits. Imaging demonstrated C7/T1 spondyloptosis, with fractures of bilateral C7 pedicles, C7/T1 facets, and C7 lamina. Patient 3 is a 36-year-old male presenting after a motor vehicle collision with diffuse tingling sensation throughout all extremities. His neurological examination was nonfocal. Imaging demonstrated a grade 4 spondylolithesis at C7/T1, associated with bilateral C7/T1 locked facets. From literature, most cases were noted to be dislocations resulting from fractures of the posterior elements. A minority of cases has been found to involve facet dislocations without fractures. Further biomechanical studies are needed to understand the underlying mechanisms.

  7. The risk factors of neurologic deficits of one-stage posterior vertebral column resection for patients with severe and rigid spinal deformities.

    Science.gov (United States)

    Xie, Jing-Ming; Zhang, Ying; Wang, Ying-Song; Bi, Ni; Zhao, Zhi; Li, Tao; Yang, Hua

    2014-01-01

    To determine the risk factors of neurologic deficits during PVCR correction, so as to help improve safety during and after surgery. A consecutive series of 76 patients with severe and rigid spinal deformities who were treated with PVCR at a single institution between October 2004 and July 2011 were included in our study. Of the 76 patients, 37 were male and 39 female, with an average age of 17.5 years (range 10-48 years). There were 52 adolescent patients (with an age hyperkyphosis (X 5), level of vertebral column resected (X 6), number of segmental vessels ligated (X 7), preexisting neurologic dysfunction (X 8), and associated with intraspinal and brain stem anomalies (X 9). The multi-factor unconditional logistic regression analysis revealed that X 8 (OR = 49.322), X 9 (OR = 18.423), X 5 (OR = 11.883), and X 6 (OR = 8.769) were independent and positively correlated with the neurologic deficit. Preexisting neurologic dysfunction, associated with intraspinal and brain stem anomalies, scoliosis associated with thoracic hyperkyphosis and level of vertebral column resected are independent risk factors for neurologic deficits during PVCR procedure.

  8. Acute flaccid paralysis in South African children: Causes, respiratory complications and neurological outcome.

    Science.gov (United States)

    van der Pijl, Jolanda; Wilmshurst, Jo M; van Dijk, Monique; Argent, Andrew; Booth, Jane; Zampoli, Marco

    2017-09-28

    To describe the causes, clinical presentation and neurological outcome of acute flaccid paralysis in children. A retrospective study in a tertiary paediatric hospital in South Africa. Data on clinical presentation, respiratory complications and long-term neurological outcomes of children presenting with acute flaccid paralysis were collected. Logistic regression analysis was applied to determine predictors for the need of mechanical ventilation. The study included 119 patients, 99 of whom had Guillain-Barré syndrome (GBS); 47 patients (39.5%) required mechanical ventilation. Backward logistic regression analysis revealed that bulbar dysfunction (P < 0.001), autonomic dysfunction (P = 0.003) and upper limb paralysis (P = 0.038) significantly predicted the need for mechanical ventilation. EuroQol-5D scores of self-care problems and usual activities after discharge significantly declined over time. In this large series from Africa, GBS was the main cause of acute flaccid paralysis in children and was associated with significant morbidity. Other causes of acute flaccid paralysis mimicking GBS were not uncommon and should be excluded in this setting. © 2017 Paediatrics and Child Health Division (The Royal Australasian College of Physicians).

  9. Pretreatment with intravenous FGF-13 reduces infarct volume and ameliorates neurological deficits following focal cerebral ischemia in rats.

    Science.gov (United States)

    Yao, D L; Masonic, K; Petullo, D; Li, L Y; Lincoln, C; Wibberley, L; Alderson, R F; Antonaccio, M

    1999-02-06

    Fibroblast growth factor-13 (FGF-13), novel member of FGF family has recently been molecularly cloned as a result of high throughput sequencing of a ovarian cancer cell, hippocampal, and kidney cDNA libraries. The human gene encodes for a protein with a molecular weight of 22 kDa that is most homologous to FGF-8 (70% similarity). In the current study, we tested the effects of intravenously administered FGF-13 in a model of permanent focal cerebral ischemia in Sprague-Dawley rats. FGF-13 or the vehicle was administered systematically via the tail vein 30 min prior, and 30 min and 24 h after the occlusion of the left middle cerebral artery (MCAo). Animals were weighed and evaluated behaviorally prior to and at 24 and 48 h after MCAo. The volume of cerebral infarct and swelling were determined using an image analysis system (BioQuant) and cresyl violet stained sequential sections from the forebrain region. Histopathology was evaluated to compare the therapeutic effects. We found a 63% reduction in infarct volume in FGF-13- vs. vehicle-treated animals (infarct volume was 21.9+/-3.8% in vehicle- and 8.1+/-1.6% in FGF-13-treated rats, p=0.0016) and a moderate inhibition of brain swelling by FGF-13. The reduction in infarct volume and brain swelling were associated with improvement of clinical deficits in FGF-13 treated animals (p<0.001). Histopathological examination determined that nervous tissue was better preserved in FGF-13 treated rats than those of controls. These data show that pretreatment with intravenous FGF-13 reduces infarct size and ameliorates neurological deficits following permanent focal cerebral ischemia in rats. Copyright 1999 Elsevier Science B.V.

  10. Sleep deprivation causes memory deficits by negatively impacting neuronal connectivity in hippocampal area CA1

    National Research Council Canada - National Science Library

    Havekes, Robbert; Park, Alan J; Tudor, Jennifer C; Luczak, Vincent G; Hansen, Rolf T; Ferri, Sarah L; Bruinenberg, Vibeke M; Poplawski, Shane G; Day, Jonathan P; Aton, Sara J; Radwańska, Kasia; Meerlo, Peter; Houslay, Miles D; Baillie, George S; Abel, Ted

    2016-01-01

    .... Recovery sleep normalizes these structural alterations. Suppression of cofilin function prevents spine loss, deficits in hippocampal synaptic plasticity, and impairments in long-term memory caused by sleep deprivation...

  11. Methamphetamine treatment during development attenuates the dopaminergic deficits caused by subsequent high-dose methamphetamine administration

    OpenAIRE

    McFadden, Lisa M.; Hoonakker, Amanda J.; Vieira-Brock, Paula L.; Stout, Kristen A.; Sawada, Nicole M; Ellis, Jonathan D; Allen, Scott C.; Walters, Elliot T.; Nielsen, Shannon M.; Gibb, James W.; Alburges, Mario E.; Wilkins, Diana G.; Hanson, Glen R.; Fleckenstein, Annette E.

    2011-01-01

    Administration of high doses of methamphetamine (METH) causes persistent dopaminergic deficits in both nonhuman preclinical models and METH-dependent persons. Noteworthy, adolescent (i.e., postnatal day (PND) 40) rats are less susceptible to this damage than young adult (PND90) rats. In addition, biweekly treatment with METH, beginning at PND40 and continuing throughout development, prevents the persistent dopaminergic deficits caused by a “challenge” high-dose METH regimen when administered ...

  12. [Pseudomigraine with cerebrospinal fluid pleocytosis or syndrome of headache, temporary neurological deficit and cerebrospinal fluid. A historical review].

    Science.gov (United States)

    Martin-Balbuena, S; Arpa-Gutierrez, F J

    The pseudomigraine syndrome with cerebrospinal fluid (CSF) and pleocytosis (PMP) or headache with neurologic deficits and CSF lymphocytosis (HaNDL) is an entity that they have been realized multiple contributions to their etiophysiopathology in the 25 years of their discovery. The PMP is described in 1980 by Swanson, Bartleson and Whisnant, and parallelly for Marti-Masso, and from then on there have been contributions of new cases, ones some atypical for mild headache, prolonged recurrence, symptomatic intracranial hypertension or infections for citomegalovirus that simulates PMP. They have carried out several approaches diagnoses along the years being established at the moment in the year 2004 by the International Classification of Headache Disorders. They have carried out contributions to their knowledge thanks to the realization of electroencephalograms, single photon emission computed tomography brain imaging, transcranial Doppler, evoked potentials, brain magnetic resonance imaging diffusion... giving place to the existence of numerous theories like the infectious-autoimmune, dysfunction of the blood brain barrier, spread cortical depression, trigeminous-vascular activation. The PMP or HaNDL is a benign entity with even unknown etiophysiopathology and where it is important the differential diagnosis with other entities potentially more dangerous.

  13. Prenatal Mercuric Chloride Exposure Causes Developmental Deficits in Rat Cortex

    Directory of Open Access Journals (Sweden)

    Tayebeh Rastegar

    2011-09-01

    Full Text Available Introduction: Environmental pollution with heavy metals such as mercury is a major health problem. Growing studies on the field have shown the deleterious effects of mercury on human and nonhuman nervous system, especially in infants, however the effects of prenatal exposure to mercuricchloride on cortical development are not yet well understood. The aim of this study was to investigate the effect of prenatal exposure to mercuric chloride on morphological characteristics of brain cortex. Methods: Mercuric chloride (2 mg/kg or normal saline were injected (I.P. to 36 Sprague – dawley rats in the 8th, 9th or 10th day of gestation. The embryos were surgically removed in the 15th day of gestation, and brain cortices were studied by histological techniques. Results: Histological studies showed that embryos of mercuric chloride treated rats hadcortical neuronal disarrangement withdifferent orientations of nuclei, increased diameter of cortex, increased mitosis of cells, increased cell death, decreased cellular density and increased intracellular space. Conclusion: These findings suggest some micro structural abnormalities in cortical regions after prenatal exposure to mercuric chloride. These structural abnormalities may underliesome neurologic disturbances following mercury intoxication.

  14. Absent CNKSR2 causes seizures and intellectual, attention, and language deficits.

    Science.gov (United States)

    Vaags, Andrea K; Bowdin, Sarah; Smith, Mary-Lou; Gilbert-Dussardier, Brigitte; Brocke-Holmefjord, Katja S; Sinopoli, Katia; Gilles, Cindy; Haaland, Tove B; Vincent-Delorme, Catherine; Lagrue, Emmanuelle; Harbuz, Radu; Walker, Susan; Marshall, Christian R; Houge, Gunnar; Kalscheuer, Vera M; Scherer, Stephen W; Minassian, Berge A

    2014-11-01

    Synaptic function is central to brain function. Understanding the synapse is aided by studies of patients lacking individual synaptic proteins. Common neurological diseases are genetically complex. Their understanding is likewise simplified by studies of less common monogenic forms. We detail the disease caused by absence of the synaptic protein CNKSR2 in 8 patients ranging from 6 to 62 years old. The disease is characterized by intellectual disability, attention problems, and abrupt lifelong language loss following a brief early childhood epilepsy with continuous spike-waves in sleep. This study describes the phenotype of CNKSR2 deficiency and its involvement in systems underlying common neurological disorders. © 2014 American Neurological Association.

  15. Developmental lead exposure causes startle response deficits in zebrafish.

    Science.gov (United States)

    Rice, Clinton; Ghorai, Jugal K; Zalewski, Kathryn; Weber, Daniel N

    2011-10-01

    Lead (Pb(2+)) exposure continues to be an important concern for fish populations. Research is required to assess the long-term behavioral effects of low-level concentrations of Pb(2+) and the physiological mechanisms that control those behaviors. Newly fertilized zebrafish embryos (max) and escape time. With increasing exposure concentrations, a larger number of larvae failed to respond to even the initial tap and, for those that did respond, ceased responding earlier than control larvae. These differences were more pronounced at a frequency of 4 taps/s. (2) Response to a visual stimulus: Fish, exposed as embryos (2-24 hpf) to Pb(2+) (0-10 μM) were tested as adults under low light conditions (≈ 60 μW/m(2)) for visual responses to a rotating black bar. Visual responses were significantly degraded at Pb(2+) concentrations of 30 nM. These data suggest that zebrafish are viable models for short- and long-term sensorimotor deficits induced by acute, low-level developmental Pb(2+) exposures. Copyright © 2011 Elsevier B.V. All rights reserved.

  16. Dysregulation of gene expression as a cause of Cockayne syndrome neurological disease.

    Science.gov (United States)

    Wang, Yuming; Chakravarty, Probir; Ranes, Michael; Kelly, Gavin; Brooks, Philip J; Neilan, Edward; Stewart, Aengus; Schiavo, Giampietro; Svejstrup, Jesper Q

    2014-10-07

    Cockayne syndrome (CS) is a multisystem disorder with severe neurological symptoms. The majority of CS patients carry mutations in Cockayne syndrome group B (CSB), best known for its role in transcription-coupled nucleotide excision repair. Indeed, because various repair pathways are compromised in patient cells, CS is widely considered a genome instability syndrome. Here, we investigate the connection between the neuropathology of CS and dysregulation of gene expression. Transcriptome analysis of human fibroblasts revealed that even in the absence of DNA damage, CSB affects the expression of thousands of genes, many of which are neuronal genes. CSB is present in a significant subset of these genes, suggesting that regulation is direct, at the level of transcription. Importantly, reprogramming of CS fibroblasts to neuron-like cells is defective unless an exogenous CSB gene is introduced. Moreover, neuroblastoma cells from which CSB is depleted show defects in gene expression programs required for neuronal differentiation, and fail to differentiate and extend neurites. Likewise, neuron-like cells cannot be maintained without CSB. Finally, a number of disease symptoms may be explained by marked gene expression changes in the brain of patients with CS. Together, these data point to dysregulation of gene regulatory networks as a cause of the neurological symptoms in CS.

  17. Secondary causes of attention deficit and hyperactivity in Nigerian ...

    African Journals Online (AJOL)

    Although much is known about this disorder the cause of ADHD remains unknown. In this report, we have described 4 children with features of inattention and hyperactivity/impulsivity following cerebral infections. In all 4 children, they had a history of illness characterized by fever and convulsion, suggestive of meningitis or ...

  18. Percutaneous versus traditional and paraspinal posterior open approaches for treatment of thoracolumbar fractures without neurologic deficit: a meta-analysis.

    Science.gov (United States)

    Sun, Xiang-Yao; Zhang, Xi-Nuo; Hai, Yong

    2017-05-01

    This study evaluated differences in outcome variables between percutaneous, traditional, and paraspinal posterior open approaches for traumatic thoracolumbar fractures without neurologic deficit. A systematic review of PubMed, Cochrane, and Embase was performed. In this meta-analysis, we conducted online searches of PubMed, Cochrane, Embase using the search terms "thoracolumbar fractures", "lumbar fractures", ''percutaneous'', "minimally invasive", ''open", "traditional", "posterior", "conventional", "pedicle screw", "sextant", and "clinical trial". The analysis was performed on individual patient data from all the studies that met the selection criteria. Clinical outcomes were expressed as risk difference for dichotomous outcomes and mean difference for continuous outcomes with 95 % confidence interval. Heterogeneity was assessed using the χ 2 test and I 2 statistics. There were 4 randomized controlled trials and 14 observational articles included in this analysis. Percutaneous approach was associated with better ODI score, less Cobb angle correction, less Cobb angle correction loss, less postoperative VBA correction, and lower infection rate compared with open approach. Percutaneous approach was also associated with shorter operative duration, longer intraoperative fluoroscopy, less postoperative VAS, and postoperative VBH% in comparison with traditional open approach. No significant difference was found in Cobb angle correction, postoperative VBA, VBA correction loss, Postoperative VBH%, VBH correction loss, and pedicle screw misplacement between percutaneous approach and open approach. There was no significant difference in operative duration, intraoperative fluoroscopy, postoperative VAS, and postoperative VBH% between percutaneous approach and paraspianl approach. The functional and the radiological outcome of percutaneous approach would be better than open approach in the long term. Although trans-muscular spatium approach belonged to open fixation methods

  19. Deficit

    CERN Multimedia

    2002-01-01

    UCL's former provost, Sir Derek Roberts, has been drafted in for a year to run the college. UCL is expected to have a 6 million pounds deficit this year and up to a 10 million pounds deficit next year. Sir Christopher Llewellyn-Smith took over at UCL nearly 4 years ago and decided then that the finanical situation was serious enough to warrant a reduction in the vast expansion policy undertaken by his predecessor (1 page).

  20. Prevalence of thoracic vertebral malformations in French bulldogs, Pugs and English bulldogs with and without associated neurological deficits.

    Science.gov (United States)

    Ryan, R; Gutierrez-Quintana, R; Ter Haar, G; De Decker, Steven

    2017-03-01

    Congenital vertebral malformations are common incidental findings in small breed dogs. This retrospective observational study evaluated the type and prevalence of thoracic vertebral malformations in 171 neurologically normal and 10 neurologically abnormal screw-tailed brachycephalic dogs. Neurologically normal dogs underwent CT for reasons unrelated to spinal disease, while affected dogs underwent MRI. Imaging studies were reviewed and vertebral malformations including hemivertebrae, block vertebrae, transitional vertebrae, and spina bifida were documented. The group of clinically normal dogs consisted of 62 French bulldogs, 68 Pugs and 41 English bulldogs. The group of affected dogs consisted of one French bulldog and nine Pugs. Overall, 80.7% of neurologically normal animals were affected by at least one vertebral malformation. There was a significant influence of breed, with thoracic vertebral malformations occurring more often in neurologically normal French bulldogs (P neurologically normal French bulldogs (93.5%; P neurologically normal Pugs (17.6%; P = 0.004 vs. English bulldogs). Neurologically normal Pugs were more often diagnosed with transitional vertebrae and spina bifida compared to other breeds (P neurologically normal screw-tailed brachycephalic dogs. While hemivertebrae are often interpreted as incidental diagnostic findings, they appear to be of greater clinical importance in Pugs compared to other screw-tailed brachycephalic breeds. Copyright © 2017 Elsevier Ltd. All rights reserved.

  1. Traumatic spondylolisthesis and spondyloptosis of the subaxial cervical spine without neurological deficits: closed re-alignment, surgical options and literature review.

    Science.gov (United States)

    Ramieri, Alessandro; Domenicucci, Maurizio; Cellocco, Paolo; Lenzi, Jacopo; Dugoni, Demo Eugenio; Costanzo, Giuseppe

    2014-10-01

    Cervical subaxial malalignment due to complete or partial post-traumatic dislocation is generally associated to neurological impairment of ranging severity. Literature lacks reporting this entity in patients with no neurological issues. Cervical traction is not widely accepted in treating this kind of injury, due to its potential for neurological damage, although surgery seems to represent the gold standard. We studied in detail 18 cervical subaxial severe dislocations and ptosis, especially analyzing 2 personal cases plus 5 from the literature without neurological impairment. We discuss the role of pre-operative cervical traction and its influence on the overall surgical planning and outcome. Sixteen cases of anterior complete luxation were described in detail by literature. Five patients were reported having no associated neurological impairment and three were treated by pre-operative traction. Our two cases of cervical subaxial dislocation due to bi-pedicular fractures without neurological deficits were treated by traction and surgical fixation. Subaxial bi-pedicular fracture is a highly unstable condition of the cervical spine. Complete or incomplete dislocation requires instrumented fixation. An intact neurological status is very rare. Pathological canal enlargement seems to be able to protect the spinal cord, during trauma and/or traction. For these findings, cervical traction could be applied with no excessive worrying. We prefer a progressive traction up to 20 lb, administered in 7-10 days with no intubation and close neuro-vascular status monitoring. Good pre-operative realignment can be properly achieved in the majority of cervical dislocations, thus avoiding three-stage surgery and somatectomy.

  2. Protective effect of ascorbic acid and Ginkgo biloba against learning and memory deficits caused by fluoride.

    Science.gov (United States)

    Jetti, Raghu; Raghuveer, C V; Mallikarjuna, Rao C

    2016-01-01

    Fluoride is present in the ground water, World Health Organization permitted level of fluoride in the ground water is 0.5 ppm. Tooth pastes, mouth washes, tea and sea fish are the sources of fluoride. Exposure to these multiple sources results in several adverse effects in addition to the fluorosis. The present study aimed to test the effect of vitamin C and Ginkgo biloba against the behavioural deficits caused by fluoride. Rats were divided into five groups with six animals in each group (n = 6). Control group received ordinary tap water with 0.5 ppm of fluoride, the remaining groups received 100 ppm of fluoride for 30 days prior to fluoride exposure. Two groups of animals received 100 mg/kg body weight of vitamin C and G. biloba for 15 days prior to fluoride exposure. After 45 days, behavioural studies (T-Maze, passive avoidance) were conducted on the experimental animals. The results of the present study showed no behavioural deficits in the control group of animals however, the rats that received fluoride water exhibited impairment in their spatial learning and memory deficits. The deficits are not marked in the vitamin C and G. biloba groups. To conclude chronic exposure to high levels of fluoride causes severe impairment in the spatial learning and memory, these deficits can be ameliorated with the vitamin C and G. biloba. © The Author(s) 2013.

  3. Methamphetamine treatment during development attenuates the dopaminergic deficits caused by subsequent high-dose methamphetamine administration.

    Science.gov (United States)

    McFadden, Lisa M; Hoonakker, Amanda J; Vieira-Brock, Paula L; Stout, Kristen A; Sawada, Nicole M; Ellis, Jonathan D; Allen, Scott C; Walters, Elliot T; Nielsen, Shannon M; Gibb, James W; Alburges, Mario E; Wilkins, Diana G; Hanson, Glen R; Fleckenstein, Annette E

    2011-08-01

    Administration of high doses of methamphetamine (METH) causes persistent dopaminergic deficits in both nonhuman preclinical models and METH-dependent persons. Noteworthy, adolescent [i.e., postnatal day (PND) 40] rats are less susceptible to this damage than young adult (PND90) rats. In addition, biweekly treatment with METH, beginning at PND40 and continuing throughout development, prevents the persistent dopaminergic deficits caused by a "challenge" high-dose METH regimen when administered at PND90. Mechanisms underlying this "resistance" were thus investigated. Results revealed that biweekly METH treatment throughout development attenuated both the acute and persistent deficits in VMAT2 function, as well as the acute hyperthermia, caused by a challenge METH treatment. Pharmacokinetic alterations did not appear to contribute to the protection afforded by the biweekly treatment. Maintenance of METH-induced hyperthermia abolished the protection against both the acute and persistent VMAT2-associated deficits suggesting that alterations in thermoregulation were caused by exposure of rats to METH during development. These findings suggest METH during development prevents METH-induced hyperthermia and the consequent METH-related neurotoxicity. Copyright © 2011 Wiley-Liss, Inc.

  4. Neuronopathic Gaucher disease in the mouse: viable combined selective saposin C deficiency and mutant glucocerebrosidase (V394L) mice with glucosylsphingosine and glucosylceramide accumulation and progressive neurological deficits.

    Science.gov (United States)

    Sun, Ying; Liou, Benjamin; Ran, Huimin; Skelton, Matthew R; Williams, Michael T; Vorhees, Charles V; Kitatani, Kazuyuki; Hannun, Yusuf A; Witte, David P; Xu, You-Hai; Grabowski, Gregory A

    2010-03-15

    Gaucher disease is caused by defective acid beta-glucosidase (GCase) function. Saposin C is a lysosomal protein needed for optimal GCase activity. To test the in vivo effects of saposin C on GCase, saposin C deficient mice (C-/-) were backcrossed to point mutated GCase (V394L/V394L) mice. The resultant mice (4L;C*) began to exhibit CNS abnormalities approximately 30 days: first as hindlimb paresis, then progressive tremor and ataxia. Death occurred approximately 48 days due to neurological deficits. Axonal degeneration was evident in brain stem, spinal cord and white matter of cerebellum accompanied by increasing infiltration of the brain stem, cortex and thalamus by CD68 positive microglial cells and activation of astrocytes. Electron microscopy showed inclusion bodies in neuronal processes and degenerating cells. Accumulation of p62 and Lamp2 were prominent in the brain suggesting the impairment of autophagosome/lysosome function. This phenotype was different from either V394L/V394L or C-/- alone. Relative to V394L/V394L mice, 4L;C* mice had diminished GCase protein and activity. Marked increases (20- to 30-fold) of glucosylsphingosine (GS) and moderate elevation (1.5- to 3-fold) of glucosylceramide (GC) were in 4L;C* brains. Visceral tissues had increases of GS and GC, but no storage cells were found. Neuronal cells in thick hippocampal slices from 4L;C* mice had significantly attenuated long-term potentiation, presumably resulting from substrate accumulation. The 4L;C* mouse mimics the CNS phenotype and biochemistry of some type 3 (neuronopathic) variants of Gaucher disease and is a unique model suitable for testing pharmacological chaperone and substrate reduction therapies, and investigating the mechanisms of neuronopathic Gaucher disease.

  5. ‘Smoke in the air’: a rare cerebrovascular cause of neurological signs and symptoms in a young adult

    Directory of Open Access Journals (Sweden)

    Imtiaz Ismail

    2015-06-01

    Full Text Available Moyamoya disease is a rare neurological condition that affects children and adults of all ages. It is characterized by chronic, progressive stenosis of the circle of Willis that ultimately leads to the development of extensive collateral vessels. Presenting symptoms are usually due to cerebral ischemia or hemorrhage. The Japanese term moyamoya (meaning puffy or obscure was coined to describe the characteristic ‘smoke in the air’ appearance of these vessels on cerebral angiography. Moyamoya has the highest recorded incidence in Japan (0.28 per 100,000. In the west it is an extremely rare condition with an overall incidence of (0.086 per 100,000 in the Western United States. Etiology for the most part is unknown; however, genetic susceptibility related to RNF213 gene on chromosome 17q25.3 has been suggested. Moyamoya is being diagnosed more frequently in all races with varying clinical manifestations. Moyamoya disease is a rare progressive neurologic condition characterized by occlusion of the cerebral circulation with extensive collaterals recruitment in children and adults. Distinguished radiological findings confirm the diagnosis. Early recognition and swift institution of therapy is vital in order to minimize neurological deficits. We present the case of a 19-year-old African American female who presented with left-sided parastheia, weakness, and headache for 2 days duration.

  6. Prior Methamphetamine Self-Administration Attenuates the Dopaminergic Deficits Caused by a Subsequent Methamphetamine Exposure

    OpenAIRE

    McFadden, Lisa M.; Vieira-Brock, Paula L.; Hanson, Glen R.; Fleckenstein, Annette E.

    2015-01-01

    Others and we have reported that prior methamphetamine (METH) exposure attenuates the persistent striatal dopaminergic deficits caused by a subsequent high-dose “binge” METH exposure. The current study investigated intermediate neurochemical changes that may contribute to, or serve to predict, this resistance. Rats self-administered METH or saline for 7 d. On the following day (specifically, 16 h after the conclusion of the final METH self-administration session), rats received a binge exposu...

  7. Posterior leukoencephalopathy syndrome: Postpartum focal neurologic deficits: A report of three cases and review of the literature

    Directory of Open Access Journals (Sweden)

    Genaro Maggi

    2013-01-01

    Full Text Available Posterior reversible encephalopathy syndrome presents with a variety of neurologic features, which, although devastating at some point, are potentially reversible on prompt recognition and institution of appropriated treatment. We report the management of three cases occurring in the last 4 years in our tertiary university hospital.

  8. Relationship between intracellular Na+ concentration and reduced Na+ affinity in Na+,K+-ATPase mutants causing neurological disease

    DEFF Research Database (Denmark)

    Toustrup-Jensen, Mads Schak; Einholm, Anja P.; Schack, Vivien

    2014-01-01

    The neurological disorders familial hemiplegic migraine type 2 (FHM2), alternating hemiplegia of childhood (AHC), and rapid-onset dystonia parkinsonism (RDP) are caused by mutations of Na+,K+-ATPase α2- and α3-isoforms, expressed in glial and neuronal cells, respectively. Although these disorders...... mutations that increase Na+ affinity were found to reduce [Na+]i. It is concluded that the Na+ affinity of the Na+,K+-ATPase is an important determinant of [Na+]i....

  9. The microstructural status of the corpus callosum is associated with the degree of motor function and neurological deficit in stroke patients.

    Science.gov (United States)

    Li, Yongxin; Wu, Ping; Liang, Fanrong; Huang, Wenhua

    2015-01-01

    Human neuroimaging studies and animal models have suggested that white matter damage from ischemic stroke leads to the functional and structural reorganization of perilesional and remote brain regions. However, the quantitative relationship between the transcallosal tract integrity and clinical motor performance score after stroke remains unexplored. The current study employed a tract-based spatial statistics (TBSS) analysis on diffusion tensor imaging (DTI) to investigate the relationship between white matter diffusivity changes and the clinical scores in stroke patients. Probabilistic fiber tracking was also used to identify structural connectivity patterns in the patients. Thirteen ischemic stroke patients and fifteen healthy control subjects participated in this study. TBSS analyses showed that the corpus callosum (CC) and bilateral corticospinal tracts (CST) in the stroke patients exhibited significantly decreased fractional anisotropy and increased axial and radial diffusivity compared with those of the controls. Correlation analyses revealed that the motor and neurological deficit scores in the stroke patients were associated with the value of diffusivity indices in the CC. Compared with the healthy control group, probabilistic fiber tracking analyses revealed that significant changes in the inter-hemispheric fiber connections between the left and right motor cortex in the stroke patients were primarily located in the genu and body of the CC, left anterior thalamic radiation and inferior fronto-occipital fasciculus, bilateral CST, anterior/superior corona radiate, cingulum and superior longitudinal fasciculus, strongly suggesting that ischemic induces inter-hemispheric network disturbances and disrupts the white matter fibers connecting motor regions. In conclusion, the results of the present study show that DTI-derived measures in the CC can be used to predict the severity of motor skill and neurological deficit in stroke patients. Changes in structural

  10. Acute, transient hemorrhagic hypotension does not aggravate structural damage or neurologic motor deficits but delays the long-term cognitive recovery following mild to moderate traumatic brain injury

    Science.gov (United States)

    Schütz, Christian; Stover, John F.; Thompson, Hilaire J.; Hoover, Rachel C.; Morales, Diego M.; Schouten, Joost W.; McMillan, Asenia; Soltesz, Kristie; Motta, Melissa; Spangler, Zachery; Neugebauer, Edmund; McIntosh, Tracy K.

    2008-01-01

    Objectives Posttraumatic hypotension is believed to increase morbidity and mortality in traumatically brain-injured patients. Using a clinically relevant model of combined traumatic brain injury with superimposed hemorrhagic hypotension in rats, the present study evaluated whether a reduction in mean arterial blood pressure aggravates regional brain edema formation, regional cell death, and neurologic motor/cognitive deficits associated with traumatic brain injury. Design Experimental prospective, randomized study in rodents. Setting Experimental laboratory at a university hospital. Subjects One hundred nineteen male Sprague-Dawley rats weighing 350-385 g. Interventions Experimental traumatic brain injury of mild to moderate severity was induced using the lateral fluid percussion brain injury model in anesthetized rats (n = 89). Following traumatic brain injury, in surviving animals one group of animals was subjected to pressure-controlled hemorrhagic hypotension, maintaining the mean arterial blood pressure at 50-60 mm Hg for 30 mins (n = 47). The animals were subsequently either resuscitated with lactated Ringer’s solution (three times shed blood volume, n = 18) or left uncompensated (n = 29). Other groups of animals included those with isolated traumatic brain injury (n = 34), those with isolated hemorrhagic hypotension (n = 8), and sham-injured control animals receiving anesthesia and surgery alone (n = 22). Measurements and Main Results The withdrawal of 6-7 mL of arterial blood significantly reduced mean arterial blood pressure by 50% without decreasing arterial oxygen saturation or Pao2. Brain injury induced significant cerebral edema (p hypotension. Brain injury-induced neurologic deficits persisted up to 20 wks after injury and were also not aggravated by the hemorrhagic hypotension. Cognitive dysfunction persisted for up to 16 wks postinjury. The superimposition of hemorrhagic hypotension significantly delayed the time course of cognitive recovery

  11. Injury mechanism of midfacial fractures in football causes in over 40% typical neurological symptoms of minor brain injuries.

    Science.gov (United States)

    Krutsch, Volker; Gesslein, Markus; Loose, Oliver; Weber, Johannes; Nerlich, Michael; Gaensslen, Axel; Bonkowsky, Viktor; Krutsch, Werner

    2017-02-08

    The injury mechanisms of midfacial fractures may be typical causes of concussion, but hardly any scientific data on midfacial injuries sustained in football are available. Head and brain trauma represent frequent injuries in athletes of different sports that require appropriate treatment by sports and trauma physicians. This study investigated the management of midfacial fractures in football and the association of such fractures with concomitant brain injury. In a prospective cohort study lasting 24 months (2012 to 2013), midfacial injuries of football players were analysed with regard to the injury mechanisms, first aid procedures on the field, treatment and return-to-play. To analyse concomitant and potentially overlooked minor brain injuries due to the trauma, we retrospectively investigated the neurological symptoms of the study population. The study included 132 football players (37 semi-professionals and 95 amateurs) with midfacial fractures. The main injury mechanisms were head-to-head and head-to-elbow trauma. The mean period of return-to-play after trauma was 33.5 days, which was significantly shortened if a protective face mask was worn (mean 10.4 days earlier, p = 0.0006). Semi-professional football players returned to play earlier (p = 0.009) and more often used protective face masks (p = 0.001). 55 players (41.6%) had neurological symptoms immediately after trauma as a possible sign of concomitant minor brain injury. 5 of 132 players with concussion had been hospitalised for 24 h, but no persistent neurological symptoms were detected. In football, midfacial fractures represent moderate-to-severe injuries with time away from sports of more than 4 weeks. Over 40% of athletes with a midfacial fracture showed concomitant neurological symptoms as a sign of minor brain injury. Therefore, sports physicians and other staff supervising athletes in daily practice should be aware of the presence of neurological symptoms. Level III.

  12. Prenatal ethanol exposure does not cause neurological alterations in adult CD1 mice.

    Science.gov (United States)

    Wei, Suli; Xu, Zhiqiang; Gao, Junying; Ding, Jiong; Xiao, Ming

    2013-03-06

    Genetic factors are involved in variation in fetal alcohol spectrum disorders (FASD), which is also observed among various inbred mouse strains. The CD1 mouse strain is often used in toxicological and genetic experiments. However, there is little literature using this strain to study long-term neurologic abnormalities of FASD. In the present study, we addressed the effect of prenatal ethanol exposure on neurological alterations in adult CD1 mice. The female CD1 mice received exposure to ethanol solution (10 vol%) starting from 2 weeks before mating up to pups born (postnatal day 1). At 24 weeks after the birth, the prenatal ethanol-exposed mice and control mice showed no difference in spatial learning and memory performance in a Morris water maze. Consistently, pathological changes, such as increased neuronal apoptosis, decreased synaptic protein synaptophysin expression, synaptic loss and reactive astrogliosis, were not observed in the hippocampus of mice prenatally exposed to ethanol. These results suggest that CD1 mice are highly resistant to prenatal alcohol exposure and may serve as genetic modification models of FASD.

  13. Reprint of "Neurocysticercosis-related mortality in Brazil, 2000-2011: Epidemiology of a neglected neurologic cause of death".

    Science.gov (United States)

    Martins-Melo, Francisco Rogerlândio; Ramos, Alberto Novaes; Cavalcanti, Marta Guimarães; Alencar, Carlos Henrique; Heukelbach, Jorg

    2017-01-01

    Neurocysticercosis (NCC) is an important cause of severe neurological disease mainly in low- and middle-income countries, but data on NCC mortality from endemic areas are scarce. Here we analysed the epidemiological patterns of NCC-related mortality in Brazil. We included all deaths recorded in Brazil between 2000 and 2011, in which NCC was mentioned on death certificates, either as underlying or as associated cause of death. NCC was identified in 1829/12,491,280 deaths (0.015%), 1130 (61.8%) as underlying cause, and 699 (38.2%) as associated cause. Overall age-adjusted mortality rate for the period was 0.97 deaths/1,000,000 inhabitants (95% confidence interval [CI]: 0.83-1.12). The highest NCC-related mortality rates were found in males, elderly, white race/colour and residents in endemic states/regions. Age-adjusted mortality rates at national level decreased significantly over time (annual percent change [APC]: -4.7; 95% CI: -6.0 to -3.3), with a decrease in the Southeast, South and Central-West regions, and a non-significant increasing trend in the North and Northeast regions. We identified spatial and spatiotemporal high-risk mortality clusters located mainly in NCC-endemic areas. Conditions related to the nervous system were the most commonly associated causes of death when NCC was mentioned as an underlying cause, and HIV/AIDS was the main underlying cause when NCC was an associated cause. NCC is a neglected and preventable cause of severe neurologic disease and death with high public health impact in Brazil. There is a clear need to strengthen nationwide epidemiological surveillance and control for the taeniasis/cysticercosis complex. Copyright © 2015 Elsevier B.V. All rights reserved.

  14. Neurocysticercosis-related mortality in Brazil, 2000-2011: Epidemiology of a neglected neurologic cause of death.

    Science.gov (United States)

    Martins-Melo, Francisco Rogerlândio; Ramos, Alberto Novaes; Cavalcanti, Marta Guimarães; Alencar, Carlos Henrique; Heukelbach, Jorg

    2016-01-01

    Neurocysticercosis (NCC) is an important cause of severe neurological disease mainly in low- and middle-income countries, but data on NCC mortality from endemic areas are scarce. Here we analysed the epidemiological patterns of NCC-related mortality in Brazil. We included all deaths recorded in Brazil between 2000 and 2011, in which NCC was mentioned on death certificates, either as underlying or as associated cause of death. NCC was identified in 1829/12,491,280 deaths (0.015%), 1130 (61.8%) as underlying cause, and 699 (38.2%) as associated cause. Overall age-adjusted mortality rate for the period was 0.97 deaths/1,000,000 inhabitants (95% confidence interval [CI]: 0.83-1.12). The highest NCC-related mortality rates were found in males, elderly, white race/colour and residents in endemic states/regions. Age-adjusted mortality rates at national level decreased significantly over time (annual percent change [APC]: -4.7; 95% CI: -6.0 to -3.3), with a decrease in the Southeast, South and Central-West regions, and a non-significant increasing trend in the North and Northeast regions. We identified spatial and spatiotemporal high-risk mortality clusters located mainly in NCC-endemic areas. Conditions related to the nervous system were the most commonly associated causes of death when NCC was mentioned as an underlying cause, and HIV/AIDS was the main underlying cause when NCC was an associated cause. NCC is a neglected and preventable cause of severe neurologic disease and death with high public health impact in Brazil. There is a clear need to strengthen nationwide epidemiological surveillance and control for the taeniasis/cysticercosis complex. Copyright © 2015 Elsevier B.V. All rights reserved.

  15. Too Little and Too Much: Hypoactivation and Disinhibition of Medial Prefrontal Cortex Cause Attentional Deficits

    Science.gov (United States)

    McGarrity, Stephanie; Mason, Rob; Fone, Kevin C.

    2014-01-01

    Attentional deficits are core symptoms of schizophrenia, contributing strongly to disability. Prefrontal dysfunction has emerged as a candidate mechanism, with clinical evidence for prefrontal hypoactivation and disinhibition (reduced GABAergic inhibition), possibly reflecting different patient subpopulations. Here, we tested in rats whether imbalanced prefrontal neural activity impairs attention. To induce prefrontal hypoactivation or disinhibition, we microinfused the GABA-A receptor agonist muscimol (C4H6N2O2; 62.5, 125, 250 ng/side) or antagonist picrotoxin (C30H34O13; 75, 150, 300 ng/side), respectively, into the medial prefrontal cortex. Using the five-choice serial reaction time (5CSRT) test, we showed that both muscimol and picrotoxin impaired attention (reduced accuracy, increased omissions). Muscimol also impaired response control (increased premature responses). In addition, muscimol dose dependently reduced open-field locomotor activity, whereas 300 ng of picrotoxin caused locomotor hyperactivity; sensorimotor gating (startle prepulse inhibition) was unaffected. Therefore, infusion effects on the 5CSRT test can be dissociated from sensorimotor effects. Combining microinfusions with in vivo electrophysiology, we showed that muscimol inhibited prefrontal firing, whereas picrotoxin increased firing, mainly within bursts. Muscimol reduced and picrotoxin enhanced bursting and both drugs changed the temporal pattern of bursting. Picrotoxin also markedly enhanced prefrontal LFP power. Therefore, prefrontal hypoactivation and disinhibition both cause attentional deficits. Considering the electrophysiological findings, this suggests that attention requires appropriately tuned prefrontal activity. Apart from attentional deficits, prefrontal disinhibition caused additional neurobehavioral changes that may be relevant to schizophrenia pathophysiology, including enhanced prefrontal bursting and locomotor hyperactivity, which have been linked to psychosis

  16. Is the emotion recognition deficit associated with frontotemporal dementia caused by selective inattention to diagnostic facial features?

    Science.gov (United States)

    Oliver, Lindsay D; Virani, Karim; Finger, Elizabeth C; Mitchell, Derek G V

    2014-07-01

    Frontotemporal dementia (FTD) is a debilitating neurodegenerative disorder characterized by severely impaired social and emotional behaviour, including emotion recognition deficits. Though fear recognition impairments seen in particular neurological and developmental disorders can be ameliorated by reallocating attention to critical facial features, the possibility that similar benefits can be conferred to patients with FTD has yet to be explored. In the current study, we examined the impact of presenting distinct regions of the face (whole face, eyes-only, and eyes-removed) on the ability to recognize expressions of anger, fear, disgust, and happiness in 24 patients with FTD and 24 healthy controls. A recognition deficit was demonstrated across emotions by patients with FTD relative to controls. Crucially, removal of diagnostic facial features resulted in an appropriate decline in performance for both groups; furthermore, patients with FTD demonstrated a lack of disproportionate improvement in emotion recognition accuracy as a result of isolating critical facial features relative to controls. Thus, unlike some neurological and developmental disorders featuring amygdala dysfunction, the emotion recognition deficit observed in FTD is not likely driven by selective inattention to critical facial features. Patients with FTD also mislabelled negative facial expressions as happy more often than controls, providing further evidence for abnormalities in the representation of positive affect in FTD. This work suggests that the emotional expression recognition deficit associated with FTD is unlikely to be rectified by adjusting selective attention to diagnostic features, as has proven useful in other select disorders. Copyright © 2014 Elsevier Ltd. All rights reserved.

  17. Manual versus Automated Rodent Behavioral Assessment: Comparing Efficacy and Ease of Bederson and Garcia Neurological Deficit Scores to an Open Field Video-Tracking System

    Directory of Open Access Journals (Sweden)

    Fiona A. Desland

    2014-01-01

    Full Text Available Animal models of stroke have been crucial in advancing our understanding of the pathophysiology of cerebral ischemia. Currently, the standards for determining neurological deficit in rodents are the Bederson and Garcia scales, manual assessments scoring animals based on parameters ranked on a narrow scale of severity. Automated open field analysis of a live-video tracking system that analyzes animal behavior may provide a more sensitive test. Results obtained from the manual Bederson and Garcia scales did not show significant differences between pre- and post-stroke animals in a small cohort. When using the same cohort, however, post-stroke data obtained from automated open field analysis showed significant differences in several parameters. Furthermore, large cohort analysis also demonstrated increased sensitivity with automated open field analysis versus the Bederson and Garcia scales. These early data indicate use of automated open field analysis software may provide a more sensitive assessment when compared to traditional Bederson and Garcia scales.

  18. Tree stand falls: A persistent cause of neurological injury in hunting.

    Science.gov (United States)

    Pierre, Clifford A; Plog, Benjamin A; Srinivasan, Vasisht; Srinivasan, Kaushik; Petraglia, Anthony L; Huang, Jason H

    2014-08-16

    To characterize and compare our current series of patients to prior reports in order to identify any changes in the incidence of neurological injury related to hunting accidents in Rochester, New York. All tree stand-related injuries referred to our regional trauma center from September 2003 through November 2011 were reviewed. Information was obtained from the hospital's trauma registry and medical records were retrospectively reviewed for data pertaining to the injuries. Fifty-four patients were identified. Ninety-six percent of patients were male with a mean age of 47.9 years (range 15-69). The mean Injury Severity Score was 12.53 ± 1.17 (range 2-34). The average height of fall was 18.2 feet (range 4-40 feet). All patients fell to the ground with the exception of one who landed on rocks, and many hit the tree or branches on the way down. A reason for the fall was documented in only 13 patients, and included tree stand construction (3), loss of balance (3), falling asleep (3), structural failure (2), safety harness breakage (3) or light-headedness (1). The most common injuries were spinal fractures (54%), most commonly in the cervical spine (69%), followed by the thoracic (38%) and lumbar (21%) spine. Eight patients required operative repair. Head injuries occurred in 22%. Other systemic injuries include rib/clavicular fractures (47%), pelvic fractures (11%), solid organ injury (23%), and pneumothorax or hemothorax (19%). No patient deaths were reported. The average hospital length of stay was 6.56 ± 1.07 d. Most patients were discharged home without (72%) or with (11%) services and 17% required rehabilitation. Falls from hunting tree stands are still common, with a high rate of neurological injury. Compared to a decade ago we have made no progress in preventing these neurological injuries, despite an increase in safety advances. Neurosurgeons must continue to advocate for increased safety awareness and participate in leadership roles to improve outcomes for

  19. Combined lithium and valproate treatment delays disease onset, reduces neurological deficits and prolongs survival in an amyotrophic lateral sclerosis mouse model.

    Science.gov (United States)

    Feng, H-L; Leng, Y; Ma, C-H; Zhang, J; Ren, M; Chuang, D-M

    2008-08-26

    Lithium and valproic acid (VPA) are two primary drugs used to treat bipolar disorder, and have been shown to have neuroprotective properties in vivo and in vitro. A recent study demonstrated that combined treatment with lithium and VPA elicits synergistic neuroprotective effects against glutamate excitotoxicity in cultured brain neurons, and the synergy involves potentiated inhibition of glycogen synthase kinase-3 (GSK-3) activity through enhanced GSK-3 serine phosphorylation [Leng Y, Liang MH, Ren M, Marinova Z, Leeds P, Chuang DM (2008) Synergistic neuroprotective effects of lithium and valproic acid or other histone deacetylase inhibitors in neurons: roles of glycogen synthase kinase-3 inhibition. J Neurosci 28:2576-2588]. We therefore investigated the effects of lithium and VPA cotreatment on the disease symptom onset, survival time and neurological deficits in cooper zinc superoxide dismutase (SOD1) G93A mutant mice, a commonly used mouse model of amyotrophic lateral sclerosis (ALS). The G93A ALS mice received twice daily i.p. injections with LiCl (60 mg/kg), VPA (300 mg/kg) or lithium plus VPA, starting from the 30(th) day after birth and continuing until death. We found that combined treatment with lithium and VPA produced a greater and more consistent effect in delaying the onset of disease symptoms, prolonging the lifespan and decreasing the neurological deficit scores, compared with the results of monotreatment with lithium or VPA. Moreover, lithium in conjunction with VPA was more effective than lithium or VPA alone in enhancing the immunostaining of phospho-GSK-3beta(Ser9) in brain and lumbar spinal cord sections. To our knowledge, this is the first demonstration of enhanced neuroprotection by a combinatorial approach using mood stabilizers in a mouse ALS model. Our results suggest that clinical trials using lithium and VPA in combination for ALS patients are a rational strategy.

  20. Contractures in orthopaedic and neurological conditions: a review of causes and treatment.

    Science.gov (United States)

    Farmer, S E; James, M

    2001-09-10

    To examine the techniques used for the treatment of contracture in the context of current scientific knowledge of muscle. Synthesis of data available from MEDLINE, RECAL, EMBASE, the Cochrane Library and relevant texts. The development of contractures through immobilisation, muscle weakness and spasticity is described. The effects of passive stretching, continuous passive movement, serial plastering, splinting, electrical stimulation, botulinum injections and surgical tenotomies in the treatment of contractures in persons with neurological and orthopaedic conditions are identified. The strengths and weaknesses of these modalities are discussed. Predisposing factors persist after treatment of contractures thus for treatment to be effective long-term management programmes need to be developed. New treatment techniques, used in series or combined, offer the prospect of improved management of contracture. Scientific and clinical research is needed to investigate the effect of contracture treatment.

  1. Alterations in the brain adenosine metabolism cause behavioral and neurological impairment in ADA-deficient mice and patients

    Science.gov (United States)

    Sauer, Aisha V.; Hernandez, Raisa Jofra; Fumagalli, Francesca; Bianchi, Veronica; Poliani, Pietro L.; Dallatomasina, Chiara; Riboni, Elisa; Politi, Letterio S.; Tabucchi, Antonella; Carlucci, Filippo; Casiraghi, Miriam; Carriglio, Nicola; Cominelli, Manuela; Forcellini, Carlo Alberto; Barzaghi, Federica; Ferrua, Francesca; Minicucci, Fabio; Medaglini, Stefania; Leocani, Letizia; la Marca, Giancarlo; Notarangelo, Lucia D.; Azzari, Chiara; Comi, Giancarlo; Baldoli, Cristina; Canale, Sabrina; Sessa, Maria; D’Adamo, Patrizia; Aiuti, Alessandro

    2017-01-01

    Adenosine Deaminase (ADA) deficiency is an autosomal recessive variant of severe combined immunodeficiency (SCID) caused by systemic accumulation of ADA substrates. Neurological and behavioral abnormalities observed in ADA-SCID patients surviving after stem cell transplantation or gene therapy represent an unresolved enigma in the field. We found significant neurological and cognitive alterations in untreated ADA-SCID patients as well as in two groups of patients after short- and long-term enzyme replacement therapy with PEG-ADA. These included motor dysfunction, EEG alterations, sensorineural hypoacusia, white matter and ventricular alterations in MRI as well as a low mental development index or IQ. Ada-deficient mice were significantly less active and showed anxiety-like behavior. Molecular and metabolic analyses showed that this phenotype coincides with metabolic alterations and aberrant adenosine receptor signaling. PEG-ADA treatment corrected metabolic adenosine-based alterations, but not cellular and signaling defects, indicating an intrinsic nature of the neurological and behavioral phenotype in ADA deficiency. PMID:28074903

  2. Sulforaphane preconditioning of the Nrf2/HO-1 defense pathway protects the cerebral vasculature against blood-brain barrier disruption and neurological deficits in stroke.

    Science.gov (United States)

    Alfieri, Alessio; Srivastava, Salil; Siow, Richard C M; Cash, Diana; Modo, Michel; Duchen, Michael R; Fraser, Paul A; Williams, Steven C R; Mann, Giovanni E

    2013-12-01

    Disruption of the blood-brain barrier (BBB) and cerebral edema are the major pathogenic mechanisms leading to neurological dysfunction and death after ischemic stroke. The brain protects itself against infarction via activation of endogenous antioxidant defense mechanisms, and we here report the first evidence that sulforaphane-mediated preactivation of nuclear factor erythroid 2-related factor 2 (Nrf2) and its downstream target heme oxygenase-1 (HO-1) in the cerebral vasculature protects the brain against stroke. To induce ischemic stroke, Sprague-Dawley rats were subjected to 70 min middle cerebral artery occlusion (MCAo) followed by 4, 24, or 72 h reperfusion. Nrf2 and HO-1 protein expression was upregulated in cerebral microvessels of peri-infarct regions after 4-72 h, with HO-1 preferentially associated with perivascular astrocytes rather than the cerebrovascular endothelium. In naïve rats, treatment with sulforaphane increased Nrf2 expression in cerebral microvessels after 24h. Upregulation of Nrf2 by sulforaphane treatment prior to transient MCAo (1h) was associated with increased HO-1 expression in perivascular astrocytes in peri-infarct regions and cerebral endothelium in the infarct core. BBB disruption, lesion progression, as analyzed by MRI, and neurological deficits were reduced by sulforaphane pretreatment. As sulforaphane pretreatment led to a moderate increase in peroxynitrite generation, we suggest that hormetic preconditioning underlies sulforaphane-mediated protection against stroke. In conclusion, we propose that pharmacological or dietary interventions aimed to precondition the brain via activation of the Nrf2 defense pathway in the cerebral microvasculature provide a novel therapeutic approach for preventing BBB breakdown and neurological dysfunction in stroke. Crown Copyright © 2013. Published by Elsevier Inc. All rights reserved.

  3. Sleep deprivation causes memory deficits by negatively impacting neuronal connectivity in hippocampal area CA1

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    Havekes, Robbert; Park, Alan J; Tudor, Jennifer C; Luczak, Vincent G; Hansen, Rolf T; Ferri, Sarah L; Bruinenberg, Vibeke M; Poplawski, Shane G; Day, Jonathan P; Aton, Sara J; Radwańska, Kasia; Meerlo, Peter; Houslay, Miles D; Baillie, George S; Abel, Ted

    2016-01-01

    Brief periods of sleep loss have long-lasting consequences such as impaired memory consolidation. Structural changes in synaptic connectivity have been proposed as a substrate of memory storage. Here, we examine the impact of brief periods of sleep deprivation on dendritic structure. In mice, we find that five hours of sleep deprivation decreases dendritic spine numbers selectively in hippocampal area CA1 and increased activity of the filamentous actin severing protein cofilin. Recovery sleep normalizes these structural alterations. Suppression of cofilin function prevents spine loss, deficits in hippocampal synaptic plasticity, and impairments in long-term memory caused by sleep deprivation. The elevated cofilin activity is caused by cAMP-degrading phosphodiesterase-4A5 (PDE4A5), which hampers cAMP-PKA-LIMK signaling. Attenuating PDE4A5 function prevents changes in cAMP-PKA-LIMK-cofilin signaling and cognitive deficits associated with sleep deprivation. Our work demonstrates the necessity of an intact cAMP-PDE4-PKA-LIMK-cofilin activation-signaling pathway for sleep deprivation-induced memory disruption and reduction in hippocampal spine density. DOI: http://dx.doi.org/10.7554/eLife.13424.001 PMID:27549340

  4. Sleep deprivation causes memory deficits by negatively impacting neuronal connectivity in hippocampal area CA1.

    Science.gov (United States)

    Havekes, Robbert; Park, Alan J; Tudor, Jennifer C; Luczak, Vincent G; Hansen, Rolf T; Ferri, Sarah L; Bruinenberg, Vibeke M; Poplawski, Shane G; Day, Jonathan P; Aton, Sara J; Radwańska, Kasia; Meerlo, Peter; Houslay, Miles D; Baillie, George S; Abel, Ted

    2016-08-23

    Brief periods of sleep loss have long-lasting consequences such as impaired memory consolidation. Structural changes in synaptic connectivity have been proposed as a substrate of memory storage. Here, we examine the impact of brief periods of sleep deprivation on dendritic structure. In mice, we find that five hours of sleep deprivation decreases dendritic spine numbers selectively in hippocampal area CA1 and increased activity of the filamentous actin severing protein cofilin. Recovery sleep normalizes these structural alterations. Suppression of cofilin function prevents spine loss, deficits in hippocampal synaptic plasticity, and impairments in long-term memory caused by sleep deprivation. The elevated cofilin activity is caused by cAMP-degrading phosphodiesterase-4A5 (PDE4A5), which hampers cAMP-PKA-LIMK signaling. Attenuating PDE4A5 function prevents changes in cAMP-PKA-LIMK-cofilin signaling and cognitive deficits associated with sleep deprivation. Our work demonstrates the necessity of an intact cAMP-PDE4-PKA-LIMK-cofilin activation-signaling pathway for sleep deprivation-induced memory disruption and reduction in hippocampal spine density.

  5. The Retrospective Analysis of Posterior Short-Segment Pedicle Instrumentation without Fusion for Thoracolumbar Burst Fracture with Neurological Deficit

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    Zhouming Deng

    2014-01-01

    Full Text Available This study aims to investigate the efficacy of posterior short-segment pedicle instrumentation without fusion in curing thoracolumbar burst fracture. All of the 53 patients were treated with short-segment pedicle instrumentation and laminectomy without fusion, and the restoration of retropulsed bone fragments was conducted by a novel custom-designed repositor (RRBF. The mean operation time and blood loss during surgery were analyzed; the radiological index and neurological status were compared before and after the operation. The mean operation time was 93 min (range: 62–110 min and the mean intraoperative blood loss was 452 mL in all cases. The average canal encroachment was 50.04% and 10.92% prior to the surgery and at last followup, respectively (P<0.01. The preoperative kyphotic angle was 17.2 degree (±6.87 degrees, whereas it decreased to 8.42 degree (±4.99 degrees at last followup (P<0.01. Besides, the mean vertebral body height increased from 40.15% (±9.40% before surgery to 72.34% (±12.32% at last followup (P<0.01. 45 patients showed 1-2 grades improvement in Frankel’s scale at last followup. This technique allows for satisfactory canal clearance and restoration of vertebral body height and kyphotic angle, and it may promote the recovery of neurological function. However, further research is still necessary to confirm the efficacy of this treatment.

  6. Transcranial Doppler Ultrasound Examination in Dogs with Suspected Intracranial Hypertension Caused by Neurologic Diseases.

    Science.gov (United States)

    Sasaoka, K; Nakamura, K; Osuga, T; Morita, T; Yokoyama, N; Morishita, K; Sasaki, N; Ohta, H; Takiguchi, M

    2017-12-19

    Transcranial Doppler ultrasound examination (TCD) is a rapid, noninvasive technique used to evaluate cerebral blood flow and is useful for the detection of intracranial hypertension in humans. However, the clinical usefulness of TCD in diagnosing intracranial hypertension has not been demonstrated for intracranial diseases in dogs. To determine the association between the TCD variables and intracranial hypertension in dogs with intracranial diseases. Fifty client-owned dogs with neurologic signs. Cross-sectional study. All dogs underwent TCD of the basilar artery under isoflurane anesthesia after magnetic resonance imaging (MRI). Dogs were classified into 3 groups based on MRI findings: no structural diseases (group I), structural disease without MRI evidence of intracranial hypertension (group II), and structural disease with MRI evidence of intracranial hypertension (group III). The TCD vascular resistance variables (resistive index [RI], pulsatility index [PI], and the ratio of systolic to diastolic mean velocity [Sm/Dm]) were measured. Fifteen, 22, and 13 dogs were classified into groups I, II, and III, respectively. Dogs in group III had significantly higher Sm/Dm (median, 1.78; range, 1.44-2.58) than those in group I (median, 1.63; range, 1.43-1.75) and group II (median, 1.62; range, 1.27-2.10). No significant differences in RI and PI were identified among groups. Our findings suggest that increased Sm/Dm is associated with MRI findings of suspected intracranial hypertension in dogs with intracranial diseases and that TCD could be a useful tool to help to diagnose intracranial hypertension. Copyright © 2017 The Authors. Journal of Veterinary Internal Medicine published by Wiley Periodicals, Inc. on behalf of the American College of Veterinary Internal Medicine.

  7. [Hematological and neurological compromise due to vitamin B12 deficit in infant of a vegetarian mother: case report].

    Science.gov (United States)

    Bravo J, Paulina; Ibarra C, Judith; Paredes M, Marcela

    2014-06-01

    Vitamin B12 deficiency is extremely common in strict vegetarians and their variants. Infants of vegetarian mothers have a higher risk of deficiency and are more prone to its effects. To report a case in order to warn people about the importance of suspected vitamin B12 deficiency in children of vegetarian mothers. A 12-month old infant, daughter of a longtime vegetarian woman, who presented neurological and hematological compromise due to vitamin B12 deficiency, is discussed. After a short period of parenteral administration of cyanocobalamin and enteral nutrition, the patient evolved with clinical and laboratory improvement, although she still had residual development delay. Vitamin B12 deficiency is often not suspected by the pediatrician in healthy infants. Clinical manifestations can be nonspecific, such as apathy, food refusal and progressive impairment of psychomotor development. A nutritional anamnesis performed on the mother (with great emphasis on those strict vegetarians) to estimate her reserves in the period prior to, during and after delivery can be critical to detect the risk of this vitamin deficiency in young children.

  8. Dysmyelination not demyelination causes neurological symptoms in preweaned mice in a murine model of Cockayne syndrome

    Science.gov (United States)

    Revet, Ingrid; Feeney, Luzviminda; Tang, Amy A.; Huang, Eric J.; Cleaver, James E.

    2012-01-01

    Cockayne syndrome (CS) is a rare autosomal recessive neurodegenerative disease that is associated with mutations in either of two transcription-coupled DNA repair genes, CSA or CSB. Mice with a targeted mutation in the Csb gene (Cs-bm/m) exhibit a milder phenotype compared with human patients with mutations in the orthologous CSB gene. Mice mutated in Csb were crossed with mice lacking Xpc (Xp-c−/−), the global genome repair gene, to enhance the pathological symptoms. These Cs-bm/m.Xp-c−/− mice were normal at birth but exhibited progressive failure to thrive, whole-body wasting, and ataxia and died at approximately postnatal day 21. Characterization of Cs-bm/m.Xp-c−/− brains at postnatal stages demonstrated widespread reduction of myelin basic protein (MBP) and myelin in the sensorimotor cortex, the stratum radiatum, the corpus callosum, and the anterior commissure. Quantification of individual axons by electron microscopy showed a reduction in both the number of myelinated axons and the average diameter of myelin surrounding the axons. There were no significant differences in proliferation or oligodendrocyte differentiation between Cs-bm/m.Xp-c−/− and Cs-bm/+.Xp-c−/− mice. Rather, Cs-bm/m.Xp-c−/− oligodendrocytes were unable to generate sufficient MBP or to maintain the proper myelination during early development. Csb is a multifunctional protein regulating both repair and the transcriptional response to reactive oxygen through its interaction with histone acetylase p300 and the hypoxia-inducible factor (HIF)1 pathway. On the basis of our results, combined with that of others, we suggest that in Csb the transcriptional response predominates during early development, whereas a neurodegenerative response associated with repair deficits predominates in later life. PMID:22393014

  9. Does Fiscal Deficit Granger Cause Impulsiveness in Inflation Rate in Nigeria?

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    Oseni Isiaq Olasunkanmi

    2016-08-01

    Full Text Available This study examines the direction of causality between fiscal policy and inflation volatility in Nigeria for the periods 1981 to 2014. Studies have examined the relationship between fiscal policy and inflation volatility without taking cognizant of the direction of relationship that exist between the two variables, hence this study. The study employs quarterly time series data on fiscal deficit and consumer price index (measure of inflation rate from 1981:1 to 2013:3 and obtains from the central bank of Nigeria statistical bulletin 2014 while the volatility data is generated through GARCH (1,1 method and analyze using the Pairwise Granger Causality Test. The results of the study showed that there is bi-directional causality between fiscal deficit ( − = 5.86 & 3.96; < 0.05 and inflation volatility. The implication of this result is that volatility in inflation rate is traceable to the persistent nature of the excess government expenditure over revenue of the Nigerian economy and vice versa; this will inform the government, policy makers and individual the reasons for continuous fluctuation in the prices of goods and services in the country. The paper contributes to knowledge by providing information on the causes of fluctuation in inflation rate in Nigeria.

  10. Variables That Best Differentiate In-Patient Acute Stroke from Stroke-Mimics with Acute Neurological Deficits

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    P. Natteru

    2016-01-01

    Full Text Available Introduction. Strokes and stroke-mimics have been extensively studied in the emergency department setting. Although in-hospital strokes are less studied in comparison to strokes in the emergency department, they are a source of significant direct and indirect costs. Differentiating in-hospital strokes from stroke-mimics is important. Thus, our study aimed to identify variables that can differentiate in-hospital strokes from stroke-mimics. Methods. We present here a retrospective analysis of 93 patients over a one-year period (2009 to 2010, who were evaluated for a concern of in-hospital strokes. Results. About two-thirds (57 of these patients were determined to have a stroke, and the remaining (36 were stroke-mimics. Patients with in-hospital strokes were more likely to be obese (p=0.03, have been admitted to the cardiology service (p=0.01, have atrial fibrillation (p=0.03, have a weak hand or hemiparesis (p=0.03, and have a prior history of stroke (p=0.05, whereas, when the consults were called for “altered mental status” but no other deficits (p<0.0001, it is likely a stroke-mimic. Conclusion. This study demonstrates that in-hospital strokes are a common occurrence, and knowing the variables can aid in their timely diagnosis and treatment.

  11. An Acute Respiratory Infection of a Physiologically Anemic Infant is a More Likely Cause of SIDS than Neurological Prematurity

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    E. Maria Donner

    2016-08-01

    Full Text Available Introduction: The cause of the Sudden Infant Death Syndrome (SIDS is perhaps the oldest of unsolved mysteries of medicine, possibly dating back to Exodus in Biblical times when Egyptian children died in their sleep as if from a plague. It occurs when infants die unexpectedly with no sufficient cause of death found in a forensic autopsy including death scene investigation and review of medical history. That SIDS is an X-linked recessive death from infectious respiratory disease of a physiologically anemic infant and not a simple anomalous cardiac or neurological condition is an extraordinary claim that requires extraordinary evidence. If it were by a simple cause it would have been solved already with over 11,000 papers on SIDS listed now in PUBMED. Any proposed cause of SIDS must explain: 1 its 50% excess male death rate; 2 its 4-parameter lognormal distribution of ages at death; 3 its winter maxima and summer minima; and 4 its increasing rate with livebirth order.Methods: From extensive SIDS vital statistics data and published epidemiologic studies, we developed probability models to explain the mathematical behavior of SIDS meeting the four constraints mentioned above. We then compare these SIDS properties to infant death from Acute Respiratory Infection (ARI, and infant death from Encephalopathy, Unspecified (EU.Results: Comparisons show that SIDS are congruent with ARI and are not consistent with EU, and that these probability models not only fit the SIDS data but they also predict and fit the male fraction of all infant and child mortality from birth through the first 5 years of their life.Conclusions: SIDS are not rejected as an X-linked disease involving ARI and are not explained by a triple risk model that has been commonly accepted by the SIDS medical community as implicating a neurological causation process in a subset of SIDS.

  12. DRα1-MOG-35-55 treatment reduces lesion volumes and improves neurological deficits after traumatic brain injury.

    Science.gov (United States)

    Yang, Liu; Liu, Zhijia; Ren, Honglei; Zhang, Lei; Gao, Siman; Ren, Li; Chai, Zhi; Meza-Romero, Roberto; Benedek, Gil; Vandenbark, Arthur A; Offner, Halina; Li, Minshu

    2017-10-01

    Traumatic brain injury (TBI) results in severe neurological impairments without effective treatments. Inflammation appears to be an important contributor to key pathogenic events such as secondary brain injury following TBI and therefore serves as a promising target for novel therapies. We have recently demonstrated the ability of a molecular construct comprised of the human leukocyte antigen (HLA)-DRα1 domain linked covalently to mouse (m)MOG-35-55 peptide (DRα1-MOG-35-55 construct) to reduce CNS inflammation and tissue injury in animal models of multiple sclerosis and ischemic stroke. The aim of the current study was to determine if DRα1-MOG-35-55 treatment of a fluid percussion injury (FPI) mouse model of TBI could reduce the lesion size and improve disease outcome measures. Neurodeficits, lesion size, and immune responses were determined to evaluate the therapeutic potential and mechanisms of neuroprotection induced by DRα1-MOG-35-55 treatment. The results demonstrated that daily injections of DRα1-MOG-35-55 given after FPI significantly reduced numbers of infiltrating CD74(+) and CD86(+) macrophages and increased numbers of CD206(+) microglia in the brain concomitant with smaller lesion sizes and improvement in neurodeficits. Conversely, DRα1-MOG-35-55 treatment of TBI increased numbers of circulating CD11b(+) monocytes and their expression of CD74 but had no detectable effect on cell numbers or marker expression in the spleen. These results demonstrate that DRα1-MOG-35-55 therapy can reduce CNS inflammation and significantly improve histological and clinical outcomes after TBI. Future studies will further examine the potential of DRα1-MOG-35-55 for treatment of TBI.

  13. Modulation of Neurological Deficits and Expression of Glutamate Receptors during Experimental Autoimmune Encephalomyelitis after Treatment with Selected Antagonists of Glutamate Receptors

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    Grzegorz Sulkowski

    2013-01-01

    Full Text Available The aim of our investigation was to characterize the role of group I mGluRs and NMDA receptors in pathomechanisms of experimental autoimmune encephalomyelitis (EAE, the rodent model of MS. We tested the effects of LY 367385 (S-2-methyl-4-carboxyphenylglycine, a competitive antagonist of mGluR1, MPEP (2-methyl-6-(phenylethynyl-pyridine, an antagonist of mGluR5, and the uncompetitive NMDA receptor antagonists amantadine and memantine on modulation of neurological deficits observed in rats with EAE. The neurological symptoms of EAE started at 10-11 days post-injection (d.p.i. and peaked after 12-13 d.p.i. The protein levels of mGluRs and NMDA did not increase in early phases of EAE (4 d.p.i., but starting from 8 d.p.i. to 25 d.p.i., we observed a significant elevation of mGluR1 and mGluR5 protein expression by about 20% and NMDA protein expression by about 10% over the control at 25 d.p.i. The changes in protein levels were accompanied by changes in mRNA expression of group I mGluRs and NMDARs. During the late disease phase (20–25 d.p.i., the mRNA expression levels reached 300% of control values. In contrast, treatment with individual receptor antagonists resulted in a reduction of mRNA levels relative to untreated animals.

  14. 163 Microstructural MRI Quantifies Tract-Specific Injury and Correlates With Global Disability and Focal Neurological Deficits in Degenerative Cervical Myelopathy.

    Science.gov (United States)

    Martin, Allan R; De Leener, Benjamin; Cohen-Adad, Julien; Aleksanderek, Izabela; Cadotte, David W; Kalsi-Ryan, Sukhvinder; Tetreault, Lindsay; Crawley, Adrian; Ginsberg, Howard J; Fehlings, Michael G

    2016-08-01

    Diffusion tensor imaging (DTI), magnetization transfer (MT), and T2*-weighted imaging measure aspects of spinal cord microstructure. This study investigates if these techniques can quantify injury to individual white matter (WM) tracts and correlate with focal neurological impairments in degenerative cervical myelopathy (DCM). Fifty-seven DCM patients (age 56.7; 61% male; 32 mild, 16 moderate, 9 severe) underwent comprehensive clinical assessments and multimodal MRI (3T GE). Analysis with Spinal Cord Toolbox extracted fractional anisotropy (FA), MT ratio (MTR), and T2* WM/gray matter (GM) ratio (representing gray-white contrast) from regions of interest including: total WM, lateral corticospinal tracts (LCSTs), dorsal columns (DCs), and spinothalamic tracts (STTs) at C1-C2. Spearman correlations were calculated between total WM and global disability (mJOA), and between metrics in unilateral/bilateral WM tracts and measures of focal neurological impairment: mJOA upper/lower extremity (UE/LE) motor scores, UE strength, JAMAR grip force, and UE sensation. DCM subjects showed reduced FA (P < .001), decreased MTR (P < .001), and increased T2*-WM/GM ratio (P < .001) vs 32 healthy subjects (MANOVA P < .001). FA of the WM correlated well with mJOA (r = 0.69, P < .01), whereas the other metrics showed weaker relationships (T2*-WM/GM: r = 0.46, P = .01; MTR: r = 0.39, P = .02). FA provided the strongest correlations with focal neurological deficits (all P < .05): FA of bilateral LCSTs correlated with mJOA motor scores (r = 0.65); FA of ipsilateral LCST predicted arm power (left: r = 0.64, right: r = 0.62) and grip strength (left: r = 0.55, right: r = 0.54); FA of the DCs correlated well with ipsilateral hand sensation (left: r = 0.61, right: r = 0.66), while contralateral STTs showed a weaker association (left: r = 0.38, right: r = 0.36). Microstructural MRI successfully measures WM injury rostral to cord compression in DCM, reflecting global and focal impairment. The DTI

  15. Gain-of-function SAMD9L mutations cause a syndrome of cytopenia, immunodeficiency, MDS, and neurological symptoms.

    Science.gov (United States)

    Tesi, Bianca; Davidsson, Josef; Voss, Matthias; Rahikkala, Elisa; Holmes, Tim D; Chiang, Samuel C C; Komulainen-Ebrahim, Jonna; Gorcenco, Sorina; Rundberg Nilsson, Alexandra; Ripperger, Tim; Kokkonen, Hannaleena; Bryder, David; Fioretos, Thoas; Henter, Jan-Inge; Möttönen, Merja; Niinimäki, Riitta; Nilsson, Lars; Pronk, Cornelis Jan; Puschmann, Andreas; Qian, Hong; Uusimaa, Johanna; Moilanen, Jukka; Tedgård, Ulf; Cammenga, Jörg; Bryceson, Yenan T

    2017-04-20

    Several monogenic causes of familial myelodysplastic syndrome (MDS) have recently been identified. We studied 2 families with cytopenia, predisposition to MDS with chromosome 7 aberrations, immunodeficiency, and progressive cerebellar dysfunction. Genetic studies uncovered heterozygous missense mutations in SAMD9L, a tumor suppressor gene located on chromosome arm 7q. Consistent with a gain-of-function effect, ectopic expression of the 2 identified SAMD9L mutants decreased cell proliferation relative to wild-type protein. Of the 10 individuals identified who were heterozygous for either SAMD9L mutation, 3 developed MDS upon loss of the mutated SAMD9L allele following intracellular infections associated with myeloid, B-, and natural killer (NK)-cell deficiency. Five other individuals, 3 with spontaneously resolved cytopenic episodes in infancy, harbored hematopoietic revertant mosaicism by uniparental disomy of 7q, with loss of the mutated allele or additional in cisSAMD9L truncating mutations. Examination of 1 individual indicated that somatic reversions were postnatally selected. Somatic mutations were tracked to CD34(+) hematopoietic progenitor cell populations, being further enriched in B and NK cells. Stimulation of these cell types with interferon (IFN)-α or IFN-γ induced SAMD9L expression. Clinically, revertant mosaicism was associated with milder disease, yet neurological manifestations persisted in 3 individuals. Two carriers also harbored a rare, in trans germ line SAMD9L missense loss-of-function variant, potentially counteracting the SAMD9L mutation. Our results demonstrate that gain-of-function mutations in the tumor suppressor SAMD9L cause cytopenia, immunodeficiency, variable neurological presentation, and predisposition to MDS with -7/del(7q), whereas hematopoietic revertant mosaicism commonly ameliorated clinical manifestations. The findings suggest a role for SAMD9L in regulating IFN-driven, demand-adapted hematopoiesis. © 2017 by The American

  16. Choline and Working Memory Training Improve Cognitive Deficits Caused by Prenatal Exposure to Ethanol

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    Jaylyn Waddell

    2017-09-01

    Full Text Available Prenatal ethanol exposure is associated with deficits in executive function such as working memory, reversal learning and attentional set shifting in humans and animals. These behaviors are dependent on normal structure and function in cholinergic brain regions. Supplementation with choline can improve many behaviors in rodent models of fetal alcohol spectrum disorders and also improves working memory function in normal rats. We tested the hypothesis that supplementation with choline in the postnatal period will improve working memory during adolescence in normal and ethanol-exposed animals, and that working memory engagement during adolescence will transfer to other cognitive domains and have lasting effects on executive function in adulthood. Male and female offspring of rats fed an ethanol-containing liquid diet (ET; 3% v/v or control dams given a non-ethanol liquid diet (CT were injected with choline (Cho; 100 mg/kg or saline (Sal once per day from postnatal day (P 16–P30. Animals were trained/tested on a working memory test in adolescence and then underwent attentional set shifting and reversal learning in young adulthood. In adolescence, ET rats required more training to reach criterion than CT-Sal. Choline improved working memory performance for both CT and ET animals. In young adulthood, ET animals also performed poorly on the set shifting and reversal tasks. Deficits were more robust in ET male rats than female ET rats, but Cho improved performance in both sexes. ET male rats given a combination of Cho and working memory training in adolescence required significantly fewer trials to achieve criterion than any other ET group, suggesting that early interventions can cause a persistent improvement.

  17. Choline and Working Memory Training Improve Cognitive Deficits Caused by Prenatal Exposure to Ethanol.

    Science.gov (United States)

    Waddell, Jaylyn; Mooney, Sandra M

    2017-09-29

    Prenatal ethanol exposure is associated with deficits in executive function such as working memory, reversal learning and attentional set shifting in humans and animals. These behaviors are dependent on normal structure and function in cholinergic brain regions. Supplementation with choline can improve many behaviors in rodent models of fetal alcohol spectrum disorders and also improves working memory function in normal rats. We tested the hypothesis that supplementation with choline in the postnatal period will improve working memory during adolescence in normal and ethanol-exposed animals, and that working memory engagement during adolescence will transfer to other cognitive domains and have lasting effects on executive function in adulthood. Male and female offspring of rats fed an ethanol-containing liquid diet (ET; 3% v / v ) or control dams given a non-ethanol liquid diet (CT) were injected with choline (Cho; 100 mg/kg) or saline (Sal) once per day from postnatal day (P) 16-P30. Animals were trained/tested on a working memory test in adolescence and then underwent attentional set shifting and reversal learning in young adulthood. In adolescence, ET rats required more training to reach criterion than CT-Sal. Choline improved working memory performance for both CT and ET animals. In young adulthood, ET animals also performed poorly on the set shifting and reversal tasks. Deficits were more robust in ET male rats than female ET rats, but Cho improved performance in both sexes. ET male rats given a combination of Cho and working memory training in adolescence required significantly fewer trials to achieve criterion than any other ET group, suggesting that early interventions can cause a persistent improvement.

  18. Prior methamphetamine self-administration attenuates the dopaminergic deficits caused by a subsequent methamphetamine exposure.

    Science.gov (United States)

    McFadden, Lisa M; Vieira-Brock, Paula L; Hanson, Glen R; Fleckenstein, Annette E

    2015-06-01

    Others and we have reported that prior methamphetamine (METH) exposure attenuates the persistent striatal dopaminergic deficits caused by a subsequent high-dose "binge" METH exposure. The current study investigated intermediate neurochemical changes that may contribute to, or serve to predict, this resistance. Rats self-administered METH or saline for 7 d. On the following day (specifically, 16 h after the conclusion of the final METH self-administration session), rats received a binge exposure of METH or saline (so as to assess the impact of prior METH self-administration), or were sacrificed without a subsequent METH exposure (i.e., to assess the status of the rats at what would have been the initiation of the binge METH treatment). Results revealed that METH self-administration per se decreased striatal dopamine (DA) transporter (DAT) function and DA content, as assessed 16 h after the last self-administration session. Exposure to a binge METH treatment beginning at this 16-h time point decreased DAT function and DA content as assessed 1 h after the binge METH exposure: this effect on DA content (but not DAT function) was attenuated if rats previously self-administered METH. In contrast, 24 h after the binge METH treatment prior METH self-administration: 1) attenuated deficits in DA content, DAT function and vesicular monoamine transporter-2 function; and 2) prevented increases in glial fibrillary acidic protein and DAT complex immunoreactivity. These data suggest that changes 24 h, but not 1 h, after binge METH exposure are predictive of tolerance against the persistence of neurotoxic changes following binge METH exposures. Copyright © 2015 Elsevier Ltd. All rights reserved.

  19. Unique paradoxical atlantoaxial dislocation with C1-C2 facet diastases and isolated ligamentous injury to the craniovertebral junction without neurological deficits: A case report

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    Aniruddha Thekkatte Jagannatha

    2013-01-01

    Full Text Available Study design: Retrospective review of the case file. Objective: The primary objective was to report this rare case and discuss the mechanism of dislocation and technique of manual closed reduction of C1-C2 vertebrae in such scenarios. Summary of background data: Posterior atlantoaxial dislocation (AAD is extremely rare and a few cases have been reported in English literature. This young man sustained a high speed car accident and survived an extreme hyperextension injury to the craniovertebral junction (CVJ without any neurological deficits. On evaluation for neck pain he was noted with a dislocated odontoid lying in front of Atlas. There was C1-C2 facet diastases. No bony injury was noted at CVJ. Transverse axial ligament (TAL was intact. He underwent a successful awake reduction of the dislocation. The joint had to be manually distracted, realigned, and released under the guidance of fluoroscopy. This was followed by single stage C1-C2 Goel′s fusion with awake prone positioning. This patient was able to go back to work at the end of 3 months (GOS 5. Conclusions: This condition is extremely rare, can be carefully reduced manually under adequate neuromonitoring, and requires C1-C2 fusion in the same sitting.

  20. Robotic psychophysics system for assessment, diagnosis and rehabilitation of the neurological causes of falls in the elderly.

    Science.gov (United States)

    Lin, Chin-Hsuan; Faisal, A Aldo

    2015-08-01

    Falls are the leading causes of unintentional injuries in the elderly and thus a pose a major hazard to our ageing society. We present the FOHEPO (FOot HEight POsitioning) system to measure, diagnose and eventually rehabilitate ageing-related neurological causes of falls. We hypothesise that both perceptual and motor variability is likely to increase with age and may lead to imprecise perception and movements causing trip overs, the major triggers of falls. Our robotic experimental system automatically measures and tracks different sources of noise in the nervous system: visual perception noise of obstacle height, proprioceptive noise of localising raising one's foot to a desired height, noise in the visual feedback of the foot movements. We developed age-appropriate psychophysical measurement protocols shorter than standard protocols for perceptual and motor accuracy. These quantify individual subjects perceptual and movement accuracy thresholds through their psychometric curves. Therefore, these platform measurements will enable us to estimate fall probabilities quantitatively, i.e. the chance that a foot will clip an obstacle because subjects did not add a sufficient safety factor when clearing it. Potentially, we can use our FOHEPO system in a game-ified setting to rehabilitate elderly users to move with larger safety factors so as to reduce their risks of trip-over.

  1. PINK1 defect causes mitochondrial dysfunction, proteasomal deficit and alpha-synuclein aggregation in cell culture models of Parkinson's disease.

    Directory of Open Access Journals (Sweden)

    Wencheng Liu

    Full Text Available Mutations in PTEN induced kinase 1 (PINK1, a mitochondrial Ser/Thr kinase, cause an autosomal recessive form of Parkinson's disease (PD, PARK6. Here, we report that PINK1 exists as a dimer in mitochondrial protein complexes that co-migrate with respiratory chain complexes in sucrose gradients. PARK6 related mutations do not affect this dimerization and its associated complexes. Using in vitro cell culture systems, we found that mutant PINK1 or PINK1 knock-down caused deficits in mitochondrial respiration and ATP synthesis. Furthermore, proteasome function is impaired with a loss of PINK1. Importantly, these deficits are accompanied by increased alpha-synclein aggregation. Our results indicate that it will be important to delineate the relationship between mitochondrial functional deficits, proteasome dysfunction and alpha-synclein aggregation.

  2. Multiattribute selection of acute stroke imaging software platform for Extending the Time for Thrombolysis in Emergency Neurological Deficits (EXTEND) clinical trial.

    Science.gov (United States)

    Churilov, Leonid; Liu, Daniel; Ma, Henry; Christensen, Soren; Nagakane, Yoshinari; Campbell, Bruce; Parsons, Mark W; Levi, Christopher R; Davis, Stephen M; Donnan, Geoffrey A

    2013-04-01

    The appropriateness of a software platform for rapid MRI assessment of the amount of salvageable brain tissue after stroke is critical for both the validity of the Extending the Time for Thrombolysis in Emergency Neurological Deficits (EXTEND) Clinical Trial of stroke thrombolysis beyond 4.5 hours and for stroke patient care outcomes. The objective of this research is to develop and implement a methodology for selecting the acute stroke imaging software platform most appropriate for the setting of a multi-centre clinical trial. A multi-disciplinary decision making panel formulated the set of preferentially independent evaluation attributes. Alternative Multi-Attribute Value Measurement methods were used to identify the best imaging software platform followed by sensitivity analysis to ensure the validity and robustness of the proposed solution. Four alternative imaging software platforms were identified. RApid processing of PerfusIon and Diffusion (RAPID) software was selected as the most appropriate for the needs of the EXTEND trial. A theoretically grounded generic multi-attribute selection methodology for imaging software was developed and implemented. The developed methodology assured both a high quality decision outcome and a rational and transparent decision process. This development contributes to stroke literature in the area of comprehensive evaluation of MRI clinical software. At the time of evaluation, RAPID software presented the most appropriate imaging software platform for use in the EXTEND clinical trial. The proposed multi-attribute imaging software evaluation methodology is based on sound theoretical foundations of multiple criteria decision analysis and can be successfully used for choosing the most appropriate imaging software while ensuring both robust decision process and outcomes. © 2012 The Authors. International Journal of Stroke © 2012 World Stroke Organization.

  3. Prenatal stress in rat causes long-term spatial memory deficit and hippocampus MRI abnormality: differential effects of postweaning enriched environment.

    Science.gov (United States)

    Lui, Chun Chung; Wang, Jia-Yi; Tain, You-Lin; Chen, Yu-Chieh; Chang, Kow-Aung; Lai, Ming-Chi; Huang, Li-Tung

    2011-02-01

    Prenatal stress (PS) can cause long-term hippocampus alternations in structure and plasticity in adult offspring. Enriched environment (EE) has an effect in rescuing a variety of neurological disorders. Pregnant dams were left undisturbed (prenatal control, PC) or restrained 6h per day from days 14 to 21 (prenatal stress, PS). Control and prenatal stressed offspring rats were subjected to a standard rearing environment (SE) or an EE on postnatal days 22-120 (PC/SE PC/EE, PS/SE, and PS/EE; n=5, each group). At ∼4 months of age, all rats underwent Morris water maze test and brain MRI examination. Hippocampi were then dissected for biochemical analyses, including, Western blot for NMDA receptor (NR) subunits and synaptophysin and RT-PCR forβ1 integrin and tissue-plasminogen activator (t-PA). MRI showed all 5 rats in the PS/SE group and 5 in the PS/EE group exhibited increased signals in bilateral hippocampus and increased T2 time in the PS/SE group. Exposure to EE treatment on postnatal days 22-120 counteracted the deficit in spatial memory and increased NR1 protein expression, but it did not affect the rate of high signals and increased T2 time, decreased NR2, synaptophysin, β1 integrin and t-PA mRNA expressions in PS adult offspring. The results of this study indicate PS in rats causes long-term spatial memory deficits and gross hippocampus pathology. Postnatal EE treatment has differential benefits in terms of spatial learning, signaling molecules, and gross hippocampus pathology. Copyright © 2011 Elsevier Ltd. All rights reserved.

  4. Recurrent water deficit causes epigenetic and hormonal changes in citrus plants.

    Science.gov (United States)

    Neves, Diana Matos; Almeida, Lucas Aragão da Hora; Santana-Vieira, Dayse Drielly Souza; Freschi, Luciano; Ferreira, Claudia Fortes; Soares Filho, Walter Dos Santos; Costa, Marcio Gilberto Cardoso; Micheli, Fabienne; Coelho Filho, Maurício Antônio; Gesteira, Abelmon da Silva

    2017-10-20

    The present study evaluated the physiological, molecular and hormonal parameters from scion/rootstock interaction of citrus plants during recurrent water deficit. Responses of the Valencia (VO) scion variety grafted on two rootstocks with different soil water extraction capacities, Rangpur Lime (RL) and Sunki Maravilha (SM), during three successive periods of water deficit: plants exposed to a single episode of water deficit (WD1) and plants exposed to two (WD2) and three (WD3) recurrent periods of WD were compared. The combinations VO/RL and VO/SM presented polymorphic alterations of epigenetic marks and hormonal (i.e. abscisic acid, auxins and salicylicacid) profiles, which were particularly prominent when VO/SM plantswere exposed toWD3 treatment. Upon successive drought events, the VO/SM combination presented acclimatization characteristics that enable higher tolerance to water deficit by increasing transpiration (E), stomatal conductance (g s ) and photosynthetic rate (A), which in turn may have facilitated the whole plant survival. Besides providing comprehensive data on the scion/rootstock interactions upon successive stress events, this study brings the first dataset suggesting that epigenetic alterations in citrus plants triggered by recurrent water deficit lead to improved drought tolerance in this crop species.

  5. Relationship between intracellular Na+ concentration and reduced Na+ affinity in Na+,K+-ATPase mutants causing neurological disease

    DEFF Research Database (Denmark)

    Toustrup-Jensen, Mads Schak; Einholm, Anja P.; Schack, Vivien

    The neurological disorders familial hemiplegic migraine type 2 (FHM2), alternating hemiplegia of childhood (AHC), and rapid-onset dystonia parkinsonism (RDP) are caused by mutations of Na+,K+-ATPase α2 and α3 isoforms, expressed in glial and neuronal cells, respectively. Although these disorders ...

  6. A case–control study examining whether neurological deficits and PTSD in combat veterans are related to episodes of mild TBI

    Science.gov (United States)

    Riechers, Ronald George; Wang, Xiao-Feng; Piero, Traci; Ruff, Suzanne Smith

    2012-01-01

    Background Mild traumatic brain injury (mTBI) is a common injury among military personnel serving in Iraq or Afghanistan. The impact of repeated episodes of combat mTBI is unknown. Objective To evaluate relationships among mTBI, post-traumatic stress disorder (PTSD) and neurological deficits (NDs) in US veterans who served in Iraq or Afghanistan. Methods This was a case–control study. From 2091 veterans screened for traumatic brain injury, the authors studied 126 who sustained mTBI with one or more episodes of loss of consciousness (LOC) in combat. Comparison groups: 21 combat veterans who had definite or possible episodes of mTBI without LOC and 21 veterans who sustained mTBI with LOC as civilians. Results Among combat veterans with mTBI, 52% had NDs, 66% had PTSD and 50% had PTSD and an ND. Impaired olfaction was the most common ND, found in 65 veterans. The prevalence of an ND or PTSD correlated with the number of mTBI exposures with LOC. The prevalence of an ND or PTSD was >90% for more than five episodes of LOC. Severity of PTSD and impairment of olfaction increased with number of LOC episodes. The prevalence of an ND for the 34 combat veterans with one episode of LOC (4/34=11.8%) was similar to that of the 21 veterans of similar age and educational background who sustained civilian mTBI with one episode of LOC (2/21=9.5%, p-NS). Conclusions Impaired olfaction was the most frequently recognised ND. Repeated episodes of combat mTBI were associated with increased likelihood of PTSD and an ND. Combat setting may not increase the likelihood of an ND. Two possible connections between mTBI and PTSD are (1) that circumstances leading to combat mTBI likely involve severe psychological trauma and (2) that altered cerebral functioning following mTBI may increase the likelihood that a traumatic event results in PTSD. PMID:22431700

  7. Unusual stab wound of the spinal cervical cord caused by a screw driver

    OpenAIRE

    Mashlehaty, Homajoun; Petridis, Athanasios K; Nabavi, Arya; Mehdorn, Hubertus Maximilian

    2009-01-01

    We present a case of dorsal cervical spinal cord injury in a 16-year-old boy caused by a screwdriver. Neurological deficits were hypaesthesia of the right body and neurovegetative functional deficits. Magnetic resonance imaging showed significant myelopathy and a subdural haematoma of the cervical spine. Surgical treatment was not necessary. Rheological infusions, lumbar puncture and rehabilitation resulted in full neurological recovery.

  8. BDNF Regains Function in Hippocampal Long-Term Potentiation Deficits Caused by Diencephalic Damage

    Science.gov (United States)

    Vedder, Lindsey C.; Savage, Lisa M.

    2017-01-01

    Thiamine deficiency (TD), commonly associated with chronic alcoholism, leads to diencephalic damage, hippocampal dysfunction, and spatial learning and memory deficits. We show a decrease in the magnitude of long-term potentiation (LTP) and paired-pulse facilitation (PPF) at CA3-CA1 synapses, independent of sex, following diencephalic damage…

  9. Single episode of mild murine malaria induces neuroinflammation, alters microglial profile, impairs adult neurogenesis, and causes deficits in social and anxiety-like behavior.

    Science.gov (United States)

    Guha, Suman K; Tillu, Rucha; Sood, Ankit; Patgaonkar, Mandar; Nanavaty, Ishira N; Sengupta, Arjun; Sharma, Shobhona; Vaidya, Vidita A; Pathak, Sulabha

    2014-11-01

    Cerebral malaria is associated with cerebrovascular damage and neurological sequelae. However, the neurological consequences of uncomplicated malaria, the most prevalent form of the disease, remain uninvestigated. Here, using a mild malaria model, we show that a single Plasmodium chabaudi adami infection in adult mice induces neuroinflammation, neurogenic, and behavioral changes in the absence of a blood-brain barrier breach. Using cytokine arrays we show that the infection induces differential serum and brain cytokine profiles, both at peak parasitemia and 15days post-parasite clearance. At the peak of infection, along with the serum, the brain also exhibited a definitive pro-inflammatory cytokine profile, and gene expression analysis revealed that pro-inflammatory cytokines were also produced locally in the hippocampus, an adult neurogenic niche. Hippocampal microglia numbers were enhanced, and we noted a shift to an activated profile at this time point, accompanied by a striking redistribution of the microglia to the subgranular zone adjacent to hippocampal neuronal progenitors. In the hippocampus, a distinct decline in progenitor turnover and survival was observed at peak parasitemia, accompanied by a shift from neuronal to glial fate specification. Studies in transgenic Nestin-GFP reporter mice demonstrated a decline in the Nestin-GFP(+)/GFAP(+) quiescent neural stem cell pool at peak parasitemia. Although these cellular changes reverted to normal 15days post-parasite clearance, specific brain cytokines continued to exhibit dysregulation. Behavioral analysis revealed selective deficits in social and anxiety-like behaviors, with no change observed in locomotor, cognitive, and depression-like behaviors, with a return to baseline at recovery. Collectively, these findings indicate that even a single episode of mild malaria results in alterations of the brain cytokine profile, causes specific behavioral dysfunction, is accompanied by hippocampal microglial

  10. Syndrome of transient headache and neurological deficits with cerebrospinal fluid lymphocytosis (HaNDL) in a patient with confusional symptoms, diffuse EEG abnormalities, and bilateral vasospasm in transcranial Doppler ultrasound: A case report and literature review.

    Science.gov (United States)

    Hidalgo de la Cruz, M; Domínguez Rubio, R; Luque Buzo, E; Díaz Otero, F; Vázquez Alén, P; Orcajo Rincón, J; Prieto Montalvo, J; Contreras Chicote, A; Grandas Pérez, F

    2017-04-17

    HaNDL syndrome (transient headache and neurological deficits with cerebrospinal fluid lymphocytosis) is characterised by one or more episodes of headache and transient neurological deficits associated with cerebrospinal fluid lymphocytosis. To date, few cases of HaNDL manifesting with confusional symptoms have been described. Likewise, very few patients with HaNDL and confusional symptoms have been evaluated with transcranial Doppler ultrasound (TCD). TCD data from patients with focal involvement reveal changes consistent with vasomotor alterations. We present the case of a 42-year-old man who experienced headache and confusional symptoms and displayed pleocytosis, diffuse slow activity on EEG, increased blood flow velocity in both middle cerebral arteries on TCD, and single-photon emission computed tomography (SPECT) findings suggestive of diffuse involvement, especially in the left hemisphere. To our knowledge, this is the first description of a patient with HaNDL, confusional symptoms, diffuse slow activity on EEG, and increased blood flow velocity in TCD. Our findings suggest a relationship between cerebral vasomotor changes and the pathophysiology of HaNDL. TCD may be a useful tool for early diagnosis of HaNDL. Copyright © 2017 Sociedad Española de Neurología. Publicado por Elsevier España, S.L.U. All rights reserved.

  11. PPARγ-induced upregulation of CD36 enhances hematoma resolution and attenuates long-term neurological deficits after germinal matrix hemorrhage in neonatal rats.

    Science.gov (United States)

    Flores, Jerry J; Klebe, Damon; Rolland, William B; Lekic, Tim; Krafft, Paul R; Zhang, John H

    2016-03-01

    Germinal matrix hemorrhage remains the leading cause of morbidity and mortality in preterm infants in the United States with little progress made in its clinical management. Survivors are often afflicted with long-term neurological sequelae, including cerebral palsy, mental retardation, hydrocephalus, and psychiatric disorders. Blood clots disrupting normal cerebrospinal fluid circulation and absorption after germinal matrix hemorrhage are thought to be important contributors towards post-hemorrhagic hydrocephalus development. We evaluated if upregulating CD36 scavenger receptor expression in microglia and macrophages through PPARγ stimulation, which was effective in experimental adult cerebral hemorrhage models and is being evaluated clinically, will enhance hematoma resolution and ameliorate long-term brain sequelae using a neonatal rat germinal matrix hemorrhage model. PPARγ stimulation (15d-PGJ2) increased short-term PPARγ and CD36 expression levels as well as enhanced hematoma resolution, which was reversed by a PPARγ antagonist (GW9662) and CD36 siRNA. PPARγ stimulation (15d-PGJ2) also reduced long-term white matter loss and post-hemorrhagic ventricular dilation as well as improved neurofunctional outcomes, which were reversed by a PPARγ antagonist (GW9662). PPARγ-induced upregulation of CD36 in macrophages and microglia is, therefore, critical for enhancing hematoma resolution and ameliorating long-term brain sequelae. Copyright © 2015 Elsevier Inc. All rights reserved.

  12. Gene-environment interaction between lead and Apolipoprotein E4 causes cognitive behavior deficits in mice.

    Science.gov (United States)

    Engstrom, Anna K; Snyder, Jessica M; Maeda, Nobuyo; Xia, Zhengui

    2017-02-07

    Alzheimer's disease (AD) is characterized by progressive cognitive decline and memory loss. Environmental factors and gene-environment interactions (GXE) may increase AD risk, accelerate cognitive decline, and impair learning and memory. However, there is currently little direct evidence supporting this hypothesis. In this study, we assessed for a GXE between lead and ApoE4 on cognitive behavior using transgenic knock-in (KI) mice that express the human Apolipoprotein E4 allele (ApoE4-KI) or Apolipoprotein E3 allele (ApoE3-KI). We exposed 8-week-old male and female ApoE3-KI and ApoE4-KI mice to 0.2% lead acetate via drinking water for 12 weeks and assessed for cognitive behavior deficits during and after the lead exposure. In addition, we exposed a second (cellular) cohort of animals to lead and assessed for changes in adult hippocampal neurogenesis as a potential underlying mechanism for lead-induced learning and memory deficits. In the behavior cohort, we found that lead reduced contextual fear memory in all animals; however, this decrease was greatest and statistically significant only in lead-treated ApoE4-KI females. Similarly, only lead-treated ApoE4-KI females exhibited a significant decrease in spontaneous alternation in the T-maze. Furthermore, all lead-treated animals developed persistent spatial working memory deficits in the novel object location test, and this deficit manifested earlier in ApoE4-KI mice, with female ApoE4-KI mice exhibiting the earliest deficit onset. In the cellular cohort, we observed that the maturation, differentiation, and dendritic development of adult-born neurons in the hippocampus was selectively impaired in lead-treated female ApoE4-KI mice. These data suggest that GXE between ApoE4 and lead exposure may contribute to cognitive impairment and that impaired adult hippocampal neurogenesis may contribute to these deficits in cognitive behavior. Together, these data suggest a role for GXE and sex differences in AD risk.

  13. Screening for inborn errors of metabolism among newborns with metabolic disturbance and/or neurological manifestations without determined cause

    Directory of Open Access Journals (Sweden)

    Allan Chiaratti de Oliveira

    2001-09-01

    observed in the tests reflects the newborn's own metabolic immaturity. The selection of 9% of the studied cases for outpatient follow-up confirms that Inborn Errors of Metabolism must be suspected whenever a patient presents metabolic disturbances or neurological manifestations without a determined cause. They should be researched in parallel with the other diagnostic possibilities and not just taken to be exceptional diagnoses.

  14. Moderate injury in motor-sensory cortex causes behavioral deficits accompanied by electrophysiological changes in mice adulthood.

    Directory of Open Access Journals (Sweden)

    Wei Ouyang

    Full Text Available Moderate traumatic brain injury (TBI in children often happen when there's a sudden blow to the frontal bone, end with long unconscious which can last for hours and progressive cognitive deficits. However, with regard to the influences of moderate TBI during children adulthood, injury-induced alterations of locomotive ability, long-term memory performance, and hippocampal electrophysiological firing changes have not yet been fully identified. In this study, lateral fluid percussion (LFP method was used to fabricate moderate TBI in motor and somatosensory cortex of the 6-weeks-old mice. The motor function, learning and memory function, extracellular CA1 neural spikes were assessed during acute and subacute phase. Moreover, histopathology was performed on day post injury (DPI 16 to evaluate the effect of TBI on tissue and cell morphological changes in cortical and hippocampal CA1 subregions. After moderate LFP injury, the 6-weeks-old mice showed severe motor deficits at the early stage in acute phase but gradually recovered later during adulthood. At the time points in acute and subacute phase after TBI, novel object recognition (NOR ability and spatial memory functions were consistently impaired in TBI mice; hippocampal firing frequency and burst probability were hampered. Analysis of the altered burst firing shows a clear hippocampal theta rhythm drop. These electrophysiological impacts were associated with substantially lowered NOR preference as compared to the sham group during adulthood. These results suggest that moderate TBI introduced at motorsenory cortex in 6-weeks-old mice causes obvious motor and cognitive deficits during their adulthood. While the locomotive ability progressively recovers, the cognitive deficits persisted while the mice mature as adult mice. The cognitive deficits may be attributed to the general suppressing of whole neural network, which could be labeled by marked reduction of excitability in hippocampal CA1

  15. The U.S. Trade Deficit: Causes, Consequences, and Policy Options

    Science.gov (United States)

    2010-07-12

    4 For further discussion of the standard model of open economy macroeconomics , see N. Gregory Mankiw , Principles of Economics...Craig K. Elwell Specialist in Macroeconomic Policy July 12, 2010 Congressional Research Service 7-5700 www.crs.gov RL31032 Report...record 6.1% in 2006. The size of the U.S. trade deficit is ultimately rooted in macroeconomic conditions at home and abroad. U.S. saving falls short

  16. Environmental Enrichment Protects against Functional Deficits caused by Traumatic Brain Injury

    Science.gov (United States)

    2012-11-01

    daily olfactory stimulation consisting of variously perfumed paper strips presented in the cage for 10 minutes (Maegele et al., 2005). The scents...to their original cages with cage mates. The EC animals were returned to their original cages, but no longer received additional enrichment, and...could not be attributed to motor deficits affecting swimming speed. On the last day of MWM testing, the platform ( originally in quadrant C) was

  17. Failure to utilize feedback causes decision-making deficits among excessive Internet gamers.

    Science.gov (United States)

    Yao, Yuan-Wei; Chen, Pin-Ru; Chen, Chang; Wang, Ling-Jiao; Zhang, Jin-Tao; Xue, Gui; Deng, Lin-Yuan; Liu, Qin-Xue; Yip, Sarah W; Fang, Xiao-Yi

    2014-11-30

    Internet gaming addiction (IGA) is an increasing mental health issue worldwide. Previous studies have revealed decision-making impairments in excessive Internet gamers (EIGs) with high symptoms of IGA. However, the role of feedback processing in decision-making deficits among EIGs remains unknown. The present study aimed to investigate the effect of feedback processing on decision-making deficits under risk among EIGs, using the Game of Dice Task (GDT) and a modified version of the GDT in which no feedback was provided. Twenty-six EIGs and 26 matched occasional Internet gamers (OIGs) were recruited. The results showed: (a) OIGs performed better on the original GDT than on the modified GDT (no feedback condition); however, EIGs performed similarly on both tasks; (b) EIGs and OIGs performed equally on the modified GDT; however, EIGs chose more disadvantageous options than OIGs on the original GDT; (c) EIGs utilized feedback less frequently on the original GDT relative to OIGs. These results suggest that EIGs are not able to utilize feedback to optimize their decisions, which could underlie their poor decision-making under risk. Copyright © 2014 Elsevier Ireland Ltd. All rights reserved.

  18. Bombesin administration impairs memory and does not reverse memory deficit caused by sleep deprivation.

    Science.gov (United States)

    Ferreira, L B T; Oliveira, S L B; Raya, J; Esumi, L A; Hipolide, D C

    2017-07-28

    Sleep deprivation impairs performance in emotional memory tasks, however this effect on memory is not completely understood. Possible mechanisms may involve an alteration in neurotransmission systems, as shown by the fact that many drugs that modulate neural pathways can prevent memory impairment by sleep loss. Gastrin releasing peptide (GRP) is a neuropeptide that emerged as a regulatory molecule of emotional memory through the modulation of other neurotransmission systems. Thus, the present study addressed the effect of intraperitoneal (IP) administration of bombesin (BB) (2.5, 5.0 and 10.0μg/kg), a GRP agonist, on the performance of Wistar rats in a multiple trail inhibitory avoidance (MTIA) task, after sleep deprivation, using the modified multiple platforms method (MMPM). Sleep deprived animals exhibited acquisition and retention impairment that was not prevented by BB injection. In addition, non-sleep deprived animals treated with BB before and after the training session, but not before the test, have shown a retention deficit. In summary, BB did not improve the memory impairment by sleep loss and, under normal conditions, produced a memory consolidation deficit. Copyright © 2017 Elsevier B.V. All rights reserved.

  19. Neurologic manifestations of hypothyroidism in dogs.

    Science.gov (United States)

    Bertalan, Abigail; Kent, Marc; Glass, Eric

    2013-03-01

    Hypothyroidism is a common endocrine disease in dogs. A variety of clinicopathologic abnormalities may be present; however, neurologic deficits are rare. In some instances, neurologic deficits may be the sole manifestation of hypothyroidism. Consequent ly, the diagnosis and management of the neurologic disorders associated with hypothyroidism can be challenging. This article describes several neurologic manifestations of primary hypothyroidism in dogs; discusses the pathophysiology of hypothyroidism-induced neurologic disorders affecting the peripheral and central nervous systems; and reviews the evidence for the neurologic effects of hypothyroidism.

  20. Is Change in Ovary Carbon Status a Cause or a Consequence of Maize Ovary Abortion in Water Deficit during Flowering?

    Science.gov (United States)

    Oury, Vincent; Caldeira, Cecilio F; Prodhomme, Duyên; Pichon, Jean-Philippe; Gibon, Yves; Tardieu, François; Turc, Olivier

    2016-06-01

    Flower or grain abortion causes large yield losses under water deficit. In maize (Zea mays), it is often attributed to a carbon limitation via the disruption of sucrose cleavage by cell wall invertases in developing ovaries. We have tested this hypothesis versus another linked to the expansive growth of ovaries and silks. We have measured, in silks and ovaries of well-watered or moderately droughted plants, the transcript abundances of genes involved in either tissue expansion or sugar metabolism, together with the concentrations and amounts of sugars, and with the activities of major enzymes of carbon metabolism. Photosynthesis and indicators of sugar export, measured during water deprivation, suggested sugar export maintained by the leaf. The first molecular changes occurred in silks rather than in ovaries and involved genes affecting expansive growth rather than sugar metabolism. Changes in the concentrations and amounts of sugars and in the activities of enzymes of sugar metabolism occurred in apical ovaries that eventually aborted, but probably after the switch to abortion of these ovaries. Hence, we propose that, under moderate water deficits corresponding to most European drought scenarios, changes in carbon metabolism during flowering time are a consequence rather than a cause of the beginning of ovary abortion. A carbon-driven ovary abortion may occur later in the cycle in the case of carbon shortage or under very severe water deficits. These findings support the view that, until the end of silking, expansive growth of reproductive organs is the primary event leading to abortion, rather than a disruption of carbon metabolism. © 2016 American Society of Plant Biologists. All Rights Reserved.

  1. Pragmatic communication deficits in children with epilepsy

    NARCIS (Netherlands)

    Broeders, Mark; Geurts, Hilde; Jennekens-Schinkel, Aag

    2010-01-01

    Background: Various psychiatric and neurological disorders including epilepsy have been associated with language deficits. Pragmatic language deficits, however, have seldom been the focus of earlier studies in children with epilepsy. Moreover, it is unknown whether these pragmatic deficits are

  2. Neurology and neurologic practice in China.

    Science.gov (United States)

    Shi, Fu-Dong; Jia, Jian-Ping

    2011-11-29

    In the wake of dramatic economic success during the past 2 decades, the specialized field of neurology has undergone a significant transformation in China. With an increase in life expectancy, the problems of aging and cognition have grown. Lifestyle alterations have been associated with an epidemiologic transition both in the incidence and etiology of stroke. These changes, together with an array of social issues and institution of health care reform, are creating challenges for practicing neurologists throughout China. Notable problems include overcrowded, decrepit facilities, overloaded physician schedules, deteriorating physician-patient relationships, and an insufficient infrastructure to accommodate patients who need specialized neurologic care. Conversely, with the creation of large and sophisticated neurology centers in many cities across the country, tremendous opportunities exist. Developments in neurologic subspecialties enable delivery of high-quality care. Clinical and translational research based on large patient populations as well as highly sophisticated technologies are emerging in many neurologic centers and pharmaceutical companies. Child neurology and neurorehabilitation will be fast-developing subdisciplines. Given China's extensive population, the growth and progress of its neurology complex, and its ever-improving quality control, it is reasonable to anticipate that Chinese neurologists will contribute notably to unraveling the pathogenic factors causing neurologic diseases and to providing new therapeutic solutions.

  3. Clinical and neurological characteristics of aortic thromboembolism in dogs.

    Science.gov (United States)

    Gonçalves, R; Penderis, J; Chang, Y P; Zoia, A; Mosley, J; Anderson, T J

    2008-04-01

    To characterise the clinical presentation and neurological abnormalities in dogs affected by aortic thromboembolism. The medical records of 13 dogs diagnosed with aortic thromboembolism as the cause of the clinical signs, and where a complete neurological examination was performed, were reviewed retrospectively. The onset was acute in only four dogs, chronic in five dogs (with all of these presenting as exercise intolerance) or chronic with acute deterioration in four dogs. Dogs with an acute onset of clinical signs were more severely affected exhibiting neurological deficits, while dogs with a chronic onset of disease predominantly presented with the exercise intolerance and minimal deficits. The locomotor deficits included exercise intolerance with pelvic limb weakness (five of 13), pelvic limb ataxia (one of 13), monoparesis (two of 13), paraparesis (two of 13), non-ambulatory paraparesis (two of 13) and paraplegia (one of 13). There was an apparent male predisposition and the cavalier King charles spaniel was overrepresented. The rate of onset of clinical signs appears to segregate dogs affected by aortic thromboembolism into two groups, with different clinical characteristics and outcomes. Dogs with an acute onset of the clinical signs tend to be more severely affected, while dogs with a chronic onset predominantly present with exercise intolerance. It is therefore important to consider aortic thromboembolism as a differential diagnosis in dogs with an acute onset of pelvic limb neurological deficits and in dogs with longer standing exercise intolerance.

  4. Stroke caused auditory attention deficits in children Acidente vascular cerebral causa défices da atenção seletiva auditiva em crianças

    Directory of Open Access Journals (Sweden)

    Karla Maria Ibraim da Freiria Elias

    2012-01-01

    Full Text Available OBJECTIVE: To verify the auditory selective attention in children with stroke. METHODS: Dichotic tests of binaural separation (non-verbal and consonant-vowel and binaural integration - digits and Staggered Spondaic Words Test (SSW - were applied in 13 children (7 boys, from 7 to 16 years, with unilateral stroke confirmed by neurological examination and neuroimaging. RESULTS: The attention performance showed significant differences in comparison to the control group in both kinds of tests. In the non-verbal test, identifications the ear opposite the lesion in the free recall stage was diminished and, in the following stages, a difficulty in directing attention was detected. In the consonant- vowel test, a modification in perceptual asymmetry and difficulty in focusing in the attended stages was found. In the digits and SSW tests, ipsilateral, contralateral and bilateral deficits were detected, depending on the characteristics of the lesions and demand of the task. CONCLUSION: Stroke caused auditory attention deficits when dealing with simultaneous sources of auditory information.OBJETIVO: Verificar a habilidade de atenção seletiva em crianças com acidente vascular cerebral (AVC. MÉTODOS: Foram aplicados testes dicóticos de separação (não verbal e consoante-vogal e integração - dígitos e Staggered Spondaic Words Test (SSW - binaural em 13 crianças (7 meninos, entre 7 e 16 anos, com AVC unilateral confirmado por neuroimagem. RESULTADOS: O desempenho atencional diferiu entre os grupos na realização de ambos os tipos de tarefa. Ao teste não verbal, houve menor quantidade de identificações com a orelha contralateral à lesão em atenção livre e dificuldade de focalizar a atenção nas etapas direcionadas. No teste consoante-vogal, houve modificação da assimetria perceptual e dificuldade de focalizar a atenção nas etapas direcionadas. Nos testes de dígitos e SSW, foram constatados défices ipsilaterais, contralaterais e

  5. Stroke caused auditory attention deficits in children Acidente vascular cerebral causa défices da atenção seletiva auditiva em crianças

    Directory of Open Access Journals (Sweden)

    Karla Maria Ibraim da Freiria Elias

    2013-01-01

    Full Text Available OBJECTIVE: To verify the auditory selective attention in children with stroke. METHODS: Dichotic tests of binaural separation (non-verbal and consonant-vowel and binaural integration - digits and Staggered Spondaic Words Test (SSW - were applied in 13 children (7 boys, from 7 to 16 years, with unilateral stroke confirmed by neurological examination and neuroimaging. RESULTS: The attention performance showed significant differences in comparison to the control group in both kinds of tests. In the non-verbal test, identifications the ear opposite the lesion in the free recall stage was diminished and, in the following stages, a difficulty in directing attention was detected. In the consonant- vowel test, a modification in perceptual asymmetry and difficulty in focusing in the attended stages was found. In the digits and SSW tests, ipsilateral, contralateral and bilateral deficits were detected, depending on the characteristics of the lesions and demand of the task. CONCLUSION: Stroke caused auditory attention deficits when dealing with simultaneous sources of auditory information.OBJETIVO: Verificar a habilidade de atenção seletiva em crianças com acidente vascular cerebral (AVC. MÉTODOS: Foram aplicados testes dicóticos de separação (não verbal e consoante-vogal e integração - dígitos e Staggered Spondaic Words Test (SSW - binaural em 13 crianças (7 meninos, entre 7 e 16 anos, com AVC unilateral confirmado por neuroimagem. RESULTADOS: O desempenho atencional diferiu entre os grupos na realização de ambos os tipos de tarefa. Ao teste não verbal, houve menor quantidade de identificações com a orelha contralateral à lesão em atenção livre e dificuldade de focalizar a atenção nas etapas direcionadas. No teste consoante-vogal, houve modificação da assimetria perceptual e dificuldade de focalizar a atenção nas etapas direcionadas. Nos testes de dígitos e SSW, foram constatados défices ipsilaterais, contralaterais e

  6. C9orf72 ablation in mice does not cause motor neuron degeneration or motor deficits

    Science.gov (United States)

    Koppers, Max; Blokhuis, Anna M.; Westeneng, Henk‐Jan; Terpstra, Margo L.; Zundel, Caroline A. C.; Vieira de Sá, Renata; Schellevis, Raymond D.; Waite, Adrian J.; Blake, Derek J.; Veldink, Jan H.; van den Berg, Leonard H.

    2015-01-01

    Objective How hexanucleotide (GGGGCC) repeat expansions in C9ORF72 cause amyotrophic lateral sclerosis (ALS) remains poorly understood. Both gain‐ and loss‐of‐function mechanisms have been proposed. Evidence supporting these mechanisms in vivo is, however, incomplete. Here we determined the effect of C9orf72 loss‐of‐function in mice. Methods We generated and analyzed a conditional C9orf72 knockout mouse model. C9orf72fl/fl mice were crossed with Nestin‐Cre mice to selectively remove C9orf72 from neurons and glial cells. Immunohistochemistry was performed to study motor neurons and neuromuscular integrity, as well as several pathological hallmarks of ALS, such as gliosis and TDP‐43 mislocalization. In addition, motor function and survival were assessed. Results Neural‐specific ablation of C9orf72 in conditional C9orf72 knockout mice resulted in significantly reduced body weight but did not induce motor neuron degeneration, defects in motor function, or altered survival. Interpretation Our data suggest that C9orf72 loss‐of‐function, by itself, is insufficient to cause motor neuron disease. These results may have important implications for the development of therapeutic strategies for C9orf72‐associated ALS. Ann Neurol 2015;78:426–438 PMID:26044557

  7. Cardiomyopathy in neurological disorders.

    Science.gov (United States)

    Finsterer, Josef; Stöllberger, Claudia; Wahbi, Karim

    2013-01-01

    According to the American Heart Association, cardiomyopathies are classified as primary (solely or predominantly confined to heart muscle), secondary (those showing pathological myocardial involvement as part of a neuromuscular disorder) and those in which cardiomyopathy is the first/predominant manifestation of a neuromuscular disorder. Cardiomyopathies may be further classified as hypertrophic cardiomyopathy, dilated cardiomyopathy, restrictive cardiomyopathy, arrhythmogenic right ventricular cardiomyopathy, or unclassified cardiomyopathy (noncompaction, Takotsubo-cardiomyopathy). This review focuses on secondary cardiomyopathies and those in which cardiomyopathy is the predominant manifestation of a myopathy. Any of them may cause neurological disease, and any of them may be a manifestation of a neurological disorder. Neurological disease most frequently caused by cardiomyopathies is ischemic stroke, followed by transitory ischemic attack, syncope, or vertigo. Neurological disease, which most frequently manifests with cardiomyopathies are the neuromuscular disorders. Most commonly associated with cardiomyopathies are muscular dystrophies, myofibrillar myopathies, congenital myopathies and metabolic myopathies. Management of neurological disease caused by cardiomyopathies is not at variance from the same neurological disorders due to other causes. Management of secondary cardiomyopathies is not different from that of cardiomyopathies due to other causes either. Patients with neuromuscular disorders require early cardiologic investigations and close follow-ups, patients with cardiomyopathies require neurological investigation and avoidance of muscle toxic medication if a neuromuscular disorder is diagnosed. Which patients with cardiomyopathy profit most from primary stroke prevention is unsolved and requires further investigations. Copyright © 2013 Elsevier Inc. All rights reserved.

  8. Severe neurological sequelae and behaviour problems after cerebral malaria in Ugandan children

    Directory of Open Access Journals (Sweden)

    Tugumisirize Joshua

    2010-04-01

    Full Text Available Abstract Background Cerebral malaria is the most severe neurological complication of falciparum malaria and a leading cause of death and neuro-disability in sub-Saharan Africa. This study aimed to describe functional deficits and behaviour problems in children who survived cerebral malaria with severe neurological sequelae and identify patterns of brain injury. Findings Records of children attending a specialist child neurology clinic in Uganda with severe neurological sequelae following cerebral malaria between January 2007 and December 2008 were examined to describe deficits in gross motor function, speech, vision and hearing, behaviour problems or epilepsy. Deficits were classified according to the time of development and whether their distribution suggested a focal or generalized injury. Any resolution during the observation period was also documented. Thirty children with probable exposure to cerebral malaria attended the clinic. Referral information was inadequate to exclude other diagnoses in 7 children and these were excluded. In the remaining 23 patients, the commonest severe deficits were spastic motor weakness (14, loss of speech (14, hearing deficit (9, behaviour problems (11, epilepsy (12, blindness (12 and severe cognitive impairment (9. Behaviour problems included hyperactivity, impulsiveness and inattentiveness as in attention deficit hyperactivity disorder (ADHD and conduct disorders with aggressive, self injurious or destructive behaviour. Two patterns were observed; a immediate onset deficits present on discharge and b late onset deficits. Some deficits e.g. blindness, resolved within 6 months while others e.g. speech, showed little improvement over the 6-months follow-up. Conclusions In addition to previously described neurological and cognitive sequelae, severe behaviour problems may follow cerebral malaria in children. The observed differences in patterns of sequelae may be due to different pathogenic mechanisms, brain

  9. Education Research: Neurology resident education

    Science.gov (United States)

    Mayans, David; Schneider, Logan; Adams, Nellie; Khawaja, Ayaz M.; Engstrom, John

    2016-01-01

    Objective: To survey US-trained graduating neurology residents who are American Academy of Neurology members, in an effort to trend perceived quality and completeness of graduate neurology education. Methods: An electronic survey was sent to all American Academy of Neurology members graduating from US neurology residency programs in the Spring of 2014. Results: Of 805 eligible respondents, 24% completed the survey. Ninety-three percent of adult neurology residents and 56% of child neurology residents reported plans to pursue fellowship training after residency. Respondents reported a desire for additional training in neurocritical care, neuro-oncology, neuromuscular diseases, botulinum toxin injection, and nerve blocks. There remains a clear deficit in business training of neurology residents, although there was notable improvement in knowledge of coding and office management compared to previous surveys. Discussion: Although there are still areas of perceived weakness in neurology training, graduating neurology residents feel generally well prepared for their chosen careers. However, most still pursue fellowship training for reasons that are little understood. In addition to certain subspecialties and procedures, practice management remains deficient in neurology training and is a point of future insecurity for most residents. Future curriculum changes should consider resident-reported gaps in knowledge, with careful consideration of improving business training. PMID:26976522

  10. CASE REPORT Extramedullary haematopoiesis causing spinal cord ...

    African Journals Online (AJOL)

    Extramedullary haematopoiesis (EMH) is a rare cause of spinal cord compression. When a patient with a haematological disorder that causes chronic anaemia (particularly thalassaemia) presents with neurological deficits referable to the spine, EMH with paraspinal masses should be considered and imaging planned ...

  11. Bystander Effect Fuels Human Induced Pluripotent Stem Cell-Derived Neural Stem Cells to Quickly Attenuate Early Stage Neurological Deficits After Stroke.

    Science.gov (United States)

    Eckert, Auston; Huang, Lei; Gonzalez, Rodolfo; Kim, Hye-Sun; Hamblin, Milton H; Lee, Jean-Pyo

    2015-07-01

    : Present therapies for stroke rest with tissue plasminogen activator (tPA), the sole licensed antithrombotic on the market; however, tPA's effectiveness is limited in that the drug not only must be administered less than 3-5 hours after stroke but often exacerbates blood-brain barrier (BBB) leakage and increases hemorrhagic incidence. A potentially promising therapy for stroke is transplantation of human induced pluripotent stem cell-derived neural stem cells (hiPSC-NSCs). To date, the effects of iPSCs on injuries that take place during early stage ischemic stroke have not been well studied. Consequently, we engrafted iPSC-NSCs into the ipsilesional hippocampus, a natural niche of NSCs, at 24 hours after stroke (prior to secondary BBB opening and when inflammatory signature is abundant). At 48 hours after stroke (24 hours after transplant), hiPSC-NSCs had migrated to the stroke lesion and quickly improved neurological function. Transplanted mice showed reduced expression of proinflammatory factors (tumor necrosis factor-α, interleukin 6 [IL-6], IL-1β, monocyte chemotactic protein 1, macrophage inflammatory protein 1α), microglial activation, and adhesion molecules (intercellular adhesion molecule 1, vascular cell adhesion molecule 1) and attenuated BBB damage. We are the first to report that engrafted hiPSC-NSCs rapidly improved neurological function (less than 24 hours after transplant). Rapid hiPSC-NSC therapeutic activity is mainly due to a bystander effect that elicits reduced inflammation and BBB damage. Clinically, cerebral vessel occlusion is rarely permanent because of spontaneous or thrombolytic therapy-mediated reperfusion. These results have clinical implications indicating a much extended therapeutic window for transplantation of human induced pluripotent stem cell-derived neural stem cells (hiPSC-NSCs; 24 hours after stroke as opposed to the 5-hour window with tissue plasminogen activator [tPA]). In addition, there is potential for a synergistic

  12. Are Social Competence Difficulties Caused by Performance or Acquisition Deficits? The Importance of Self-Regulatory Mechanisms

    Science.gov (United States)

    Gumpel, Thomas P.

    2007-01-01

    We conducted three studies which examined the performance vs. skill acquisition model of social skills deficits. In Study 1, baseline social behaviors for a random sample of 12 boys with comorbid emotional and behavioral disorders (EBD), learning disabilities (LD), language delays, and Attention Deficit Hyperactivity Disorder (ADHD) revealed that…

  13. Transiently increasing cAMP levels selectively in hippocampal excitatory neurons during sleep deprivation prevents memory deficits caused by sleep loss

    NARCIS (Netherlands)

    Havekes, Robbert; Bruinenberg, Vibeke M.; Tudor, Jennifer C.; Ferri, Sarah L.; Baumann, Arnd; Meerlo, Peter; Abel, Ted

    2014-01-01

    The hippocampus is particularly sensitive to sleep loss. Although previous work has indicated that sleep deprivation impairs hippocampal cAMP signaling, it remains to be determined whether the cognitive deficits associated with sleep deprivation are caused by attenuated cAMP signaling in the

  14. Breast Cancer Presents with a Paraneoplastic Neurologic Syndrome

    Directory of Open Access Journals (Sweden)

    Pedro Coelho Barata

    2012-11-01

    Full Text Available Background: Paraneoplastic neurologic syndromes (PNS pose quite an uncommon neurological complication, affecting less than 1% of patients with breast cancer. Nearly one third of these patients lack detectable onconeural antibodies (ONAs, and improvement in neurologic deficits with concomitant cancer treatments is achieved in less than 30% of cases. Case Presentation: A 42-year-old, premenopausal woman presented with facial paralysis on the central left side accompanied by a left tongue deviation, an upward vertical nystagmus, moderate spastic paraparesis, dystonic posturing of the left foot, lower limb hyperreflexia and bilateral extensor plantar reflex. After ruling out all other potential neurologic causes, PNS was suspected but no ONAs were found. A PET-CT scan detected increased metabolism in the right breast, as well as an ipsilateral thoracic interpectoral adenopathy. Core biopsy confirmed the presence of an infiltrating duct carcinoma. After breast surgery, the neurologic symptoms disappeared. One week later, the patient was readmitted to the hospital with a bilateral fatigable eyelid ptosis, and two weeks later, there was a noticeable improvement in eyelid ptosis, accompanied by a rapid and progressive development of lower spastic paraparesis. She started adjuvant treatment with chemotherapy with marked clinical and neurological improvement, and by the end of radiotherapy, there were no signs of neurologic impairment. Conclusion: This case study highlights the importance of a high level of vigilance for the detection of PNS, even when ONAs are not detected, as the rapid identification and treatment of the underlying tumor offers the best chance for a full recovery.

  15. Neurological damage arising from intrapartum hypoxia/acidosis.

    Science.gov (United States)

    Rei, M; Ayres-de-Campos, D; Bernardes, J

    2016-01-01

    Complications occurring at any level of foetal oxygen supply will result in hypoxaemia, and this may ultimately lead to hypoxia/acidosis and neurological damage. Hypoxic-ischaemic encephalopathy (HIE) is the short-term neurological dysfunction caused by intrapartum hypoxia/acidosis, and this diagnosis requires the presence of a number of findings, including the confirmation of newborn metabolic acidosis, low Apgar scores, early imaging evidence of cerebral oedema and the appearance of clinical signs of neurological dysfunction in the first 48 h of life. Cerebral palsy (CP) consists of a heterogeneous group of nonprogressive movement and posture disorders, frequently accompanied by cognitive and sensory impairments, epilepsy, nutritional deficiencies and secondary musculoskeletal lesions. Although CP is the most common long-term neurological complication associated with intrapartum hypoxia/acidosis, >80% of cases are caused by other phenomena. Data on minor long-term neurological deficits are scarce, but they suggest that less serious intellectual and motor impairments may result from intrapartum hypoxia/acidosis. This chapter focuses on the existing evidence of neurological damage associated with poor foetal oxygenation during labour. Copyright © 2015 Elsevier Ltd. All rights reserved.

  16. Chronic low-level exposure to the common seafood toxin domoic acid causes cognitive deficits in mice.

    Science.gov (United States)

    Lefebvre, Kathi A; Kendrick, Preston S; Ladiges, Warren; Hiolski, Emma M; Ferriss, Bridget E; Smith, Donald R; Marcinek, David J

    2017-04-01

    The consumption of one meal of seafood containing domoic acid (DA) at levels high enough to induce seizures can cause gross histopathological lesions in hippocampal regions of the brain and permanent memory loss in humans and marine mammals. Seafood regulatory limits have been set at 20mgDA/kg shellfish to protect human consumers from symptomatic acute exposure, but the effects of repetitive low-level asymptomatic exposure remain a critical knowledge gap. Recreational and Tribal-subsistence shellfish harvesters are known to regularly consume low levels of DA. The aim of this study was to determine if chronic low-level DA exposure, at doses below those that cause overt signs of neurotoxicity, has quantifiable impacts on cognitive function. To this end, female C57BL/6NJ mice were exposed to asymptomatic doses of DA (≈0.75mg/kg) or vehicle once a week for several months. Spatial learning and memory were tested in a radial water maze paradigm at one, six and 25 weeks of exposure, after a nine-week recovery period following cessation of exposure, and at three old age time points (18, 24 and 28 months old). Mice from select time points were also tested for activity levels in a novel cage environment using a photobeam activity system. Chronic low-level DA exposure caused significant spatial learning impairment and hyperactivity after 25 weeks of exposure in the absence of visible histopathological lesions in hippocampal regions of the brain. These cognitive effects were reversible after a nine-week recovery period with no toxin exposure and recovery was sustained into old age. These findings identify a new potential health risk of chronic low-level exposure in a mammalian model. Unlike the permanent cognitive impacts of acute exposure, the chronic low-level effects observed in this study were reversible suggesting that these deficits could potentially be managed through cessation of exposure if they also occur in human seafood consumers. Published by Elsevier B.V.

  17. Neurological Complications Of Chronic Myeloid Leukaemia: Any ...

    African Journals Online (AJOL)

    , of the neurological deficits complicating chronic myeloid leukaemia. Method: Using patients\\' case folders and haematological malignancy register all cases of chronic myeloid leukaemia seen in Jos University Teaching Hospital between July ...

  18. Neurological Sequelae Resulting from Encephalitic Alphavirus Infection.

    Science.gov (United States)

    Ronca, Shannon E; Dineley, Kelly T; Paessler, Slobodan

    2016-01-01

    The recent surge in viral clinical cases and associated neurological deficits have reminded us that viral infections can lead to detrimental, long-term effects, termed sequelae, in survivors. Alphaviruses are enveloped, single-stranded positive-sense RNA viruses in the Togaviridae family. Transmission of alphaviruses between and within species occurs mainly via the bite of an infected mosquito bite, giving alphaviruses a place among arboviruses, or arthropod-borne viruses. Alphaviruses are found throughout the world and typically cause arthralgic or encephalitic disease in infected humans. Originally detected in the 1930s, today the major encephalitic viruses include Venezuelan, Western, and Eastern equine encephalitis viruses (VEEV, WEEV, and EEEV, respectively). VEEV, WEEV, and EEEV are endemic to the Americas and are important human pathogens, leading to thousands of human infections each year. Despite awareness of these viruses for nearly 100 years, we possess little mechanistic understanding regarding the complications (sequelae) that emerge after resolution of acute infection. Neurological sequelae are those complications involving damage to the central nervous system that results in cognitive, sensory, or motor deficits that may also manifest as emotional instability and seizures in the most severe cases. This article serves to provide an overview of clinical cases documented in the past century as well as a summary of the reported neurological sequelae due to VEEV, WEEV, and EEEV infection. We conclude with a treatise on the utility of, and practical considerations for animal models applied to the problem of neurological sequelae of viral encephalopathies in order to decipher mechanisms and interventional strategies.

  19. Adult neurology training during child neurology residency.

    Science.gov (United States)

    Schor, Nina F

    2012-08-21

    As it is currently configured, completion of child neurology residency requires performance of 12 months of training in adult neurology. Exploration of whether or not this duration of training in adult neurology is appropriate for what child neurology is today must take into account the initial reasons for this requirement and the goals of adult neurology training during child neurology residency.

  20. High Suicide Risk after the Development of Cognitive and Working Memory Deficits Caused by Cannabis, Cocaine and Ecstasy Use

    Science.gov (United States)

    Pompili, Maurizio; Lester, David; Girardi, Paolo; Tatarelli, Roberto

    2007-01-01

    We report the case of attempted suicide by a 30-year-old man who had significant cognitive deficits that developed after at least three years of polysubstance use with cannabis, methylenedioxymethamphetamine (MDMA, "ecstasy") and cocaine. The patient reported increasing difficulties in his professional and interpersonal life which may have been…

  1. [Neurological disease and facial recognition].

    Science.gov (United States)

    Kawamura, Mitsuru; Sugimoto, Azusa; Kobayakawa, Mutsutaka; Tsuruya, Natsuko

    2012-07-01

    To discuss the neurological basis of facial recognition, we present our case reports of impaired recognition and a review of previous literature. First, we present a case of infarction and discuss prosopagnosia, which has had a large impact on face recognition research. From a study of patient symptoms, we assume that prosopagnosia may be caused by unilateral right occipitotemporal lesion and right cerebral dominance of facial recognition. Further, circumscribed lesion and degenerative disease may also cause progressive prosopagnosia. Apperceptive prosopagnosia is observed in patients with posterior cortical atrophy (PCA), pathologically considered as Alzheimer's disease, and associative prosopagnosia in frontotemporal lobar degeneration (FTLD). Second, we discuss face recognition as part of communication. Patients with Parkinson disease show social cognitive impairments, such as difficulty in facial expression recognition and deficits in theory of mind as detected by the reading the mind in the eyes test. Pathological and functional imaging studies indicate that social cognitive impairment in Parkinson disease is possibly related to damages in the amygdalae and surrounding limbic system. The social cognitive deficits can be observed in the early stages of Parkinson disease, and even in the prodromal stage, for example, patients with rapid eye movement (REM) sleep behavior disorder (RBD) show impairment in facial expression recognition. Further, patients with myotonic dystrophy type 1 (DM 1), which is a multisystem disease that mainly affects the muscles, show social cognitive impairment similar to that of Parkinson disease. Our previous study showed that facial expression recognition impairment of DM 1 patients is associated with lesion in the amygdalae and insulae. Our study results indicate that behaviors and personality traits in DM 1 patients, which are revealed by social cognitive impairment, are attributable to dysfunction of the limbic system.

  2. Transiently increasing cAMP levels selectively in hippocampal excitatory neurons during sleep deprivation prevents memory deficits caused by sleep loss.

    Science.gov (United States)

    Havekes, Robbert; Bruinenberg, Vibeke M; Tudor, Jennifer C; Ferri, Sarah L; Baumann, Arnd; Meerlo, Peter; Abel, Ted

    2014-11-19

    The hippocampus is particularly sensitive to sleep loss. Although previous work has indicated that sleep deprivation impairs hippocampal cAMP signaling, it remains to be determined whether the cognitive deficits associated with sleep deprivation are caused by attenuated cAMP signaling in the hippocampus. Further, it is unclear which cell types are responsible for the memory impairments associated with sleep deprivation. Transgenic approaches lack the spatial resolution to manipulate specific signaling pathways selectively in the hippocampus, while pharmacological strategies are limited in terms of cell-type specificity. Therefore, we used a pharmacogenetic approach based on a virus-mediated expression of a Gαs-coupled Drosophila octopamine receptor selectively in mouse hippocampal excitatory neurons in vivo. With this approach, a systemic injection with the receptor ligand octopamine leads to increased cAMP levels in this specific set of hippocampal neurons. We assessed whether transiently increasing cAMP levels during sleep deprivation prevents memory consolidation deficits associated with sleep loss in an object-location task. Five hours of total sleep deprivation directly following training impaired the formation of object-location memories. Transiently increasing cAMP levels in hippocampal neurons during the course of sleep deprivation prevented these memory consolidation deficits. These findings demonstrate that attenuated cAMP signaling in hippocampal excitatory neurons is a critical component underlying the memory deficits in hippocampus-dependent learning tasks associated with sleep deprivation. Copyright © 2014 the authors 0270-6474/14/3415715-07$15.00/0.

  3. Neurologic manifestations of achondroplasia.

    Science.gov (United States)

    Hecht, Jacqueline T; Bodensteiner, John B; Butler, Ian J

    2014-01-01

    Achondroplasia is the best described and most common form of the congenital short-limbed dwarfing conditions. Achondroplasia is apparent at birth and has a birth prevalence of 1 in 20000-30000 live-born infants. Achondroplasia is inherited as an autosomal dominant condition, although 80% of cases occur sporadically as new events in their families. Achondroplasia is caused, in virtually all of the cases, by a G380R mutation in fibroblast growth factor receptor 3 (FGFR3). Patients with achondroplasia should be evaluated by a multidisciplinary team of clinicians including geneticists, neurologists, and orthopedists, since there are numerous bony and neurological complications. The most severe complication results from craniocervical stenosis and medullary and upper spinal cord compression, which can have devastating and even lethal sequelae during early childhood. In subsequent decades, including adolescence, spinal cord and nerve compression are more prominent. The neurological complications of achondroplasia have been recognized in adults for more than a century and are attributed to bony defects, connective tissue structures, or both. Similar neurological complications are now appreciated in infants, young children, and teenagers with achondroplasia. Defective connective tissue elements in achondroplasia frequently lead to ligamentous laxity, which can aggravate the complications associated with bony stenosis. Bony abnormalities are known to cause neurological morbidity and lead to a shortened lifespan. Neurological complications associated with achondroplasia are reviewed, including recommendations for the evaluation and management of these clinical problems. © 2014 Elsevier B.V. All rights reserved.

  4. Late Proximal Pedicle Hook Migration Into Spinal Canal After Posterior Correction Surgery of Scoliosis Causing Neurologic Deficit: "Proximal Junctional Scoliosis"? Case Series and a Review of the Literature

    NARCIS (Netherlands)

    Vereijken, I.M.P.; de Kleuver, M.

    2013-01-01

    Study Design: Case series. Objectives: We describe 4 patients with proximal pedicle hook migration as a late complication (greater than 12 months postoperatively) of posterior correction surgery in adolescent idiopathic scoliosis. We studied failure mechanisms and propose strategies for revision

  5. Serum Amyloid P Component Ameliorates Neurological Damage Caused by Expressing a Lysozyme Variant in the Central Nervous System of Drosophila melanogaster.

    Directory of Open Access Journals (Sweden)

    Linda Helmfors

    Full Text Available Lysozyme amyloidosis is a hereditary disease in which mutations in the gene coding for lysozyme leads to misfolding and consequently accumulation of amyloid material. To improve understanding of the processes involved we expressed human wild type (WT lysozyme and the disease-associated variant F57I in the central nervous system (CNS of a Drosophila melanogaster model of lysozyme amyloidosis, with and without co-expression of serum amyloid p component (SAP. SAP is known to be a universal constituent of amyloid deposits and to associate with lysozyme fibrils. There are clear indications that SAP may play an important role in lysozyme amyloidosis, which requires further elucidation. We found that flies expressing the amyloidogenic variant F57I in the CNS have a shorter lifespan than flies expressing WT lysozyme. We also identified apoptotic cells in the brains of F57I flies demonstrating that the flies' neurological functions are impaired when F57I is expressed in the nerve cells. However, co-expression of SAP in the CNS prevented cell death and restored the F57I flies' lifespan. Thus, SAP has the apparent ability to protect nerve cells from damage caused by F57I. Furthermore, it was found that co-expression of SAP prevented accumulation of insoluble forms of lysozyme in both WT- and F57I-expressing flies. Our findings suggest that the F57I mutation affects the aggregation process of lysozyme resulting in the formation of cytotoxic species and that SAP is able to prevent cell death in the F57I flies by preventing accumulation of toxic F57I structures.

  6. Interleukin-1β overproduction is a common cause for neuropathic pain, memory deficit, and depression following peripheral nerve injury in rodents.

    Science.gov (United States)

    Gui, Wen-Shan; Wei, Xiao; Mai, Chun-Lin; Murugan, Madhuvika; Wu, Long-Jun; Xin, Wen-Jun; Zhou, Li-Jun; Liu, Xian-Guo

    2016-01-01

    Chronic pain is often accompanied by short-term memory deficit and depression. Currently, it is believed that short-term memory deficit and depression are consequences of chronic pain. Here, we test the hypothesis that the symptoms might be caused by overproduction of interleukin-1beta (IL-1β) in the injured nerve independent of neuropathic pain following spared nerve injury in rats and mice. Mechanical allodynia, a behavioral sign of neuropathic pain, was not correlated with short-term memory deficit and depressive behavior in spared nerve injury rats. Spared nerve injury upregulated IL-1β in the injured sciatic nerve, plasma, and the regions in central nervous system closely associated with pain, memory and emotion, including spinal dorsal horn, hippocampus, prefrontal cortex, nucleus accumbens, and amygdala. Importantly, the spared nerve injury-induced memory deficits, depressive, and pain behaviors were substantially prevented by peri-sciatic administration of IL-1β neutralizing antibody in rats or deletion of IL-1 receptor type 1 in mice. Furthermore, the behavioral abnormalities induced by spared nerve injury were mimicked in naïve rats by repetitive intravenous injection of re combinant rat IL-1β (rrIL-1β) at a pathological concentration as determined from spared nerve injury rats. In addition, microglia were activated by both spared nerve injury and intravenous injection of rrIL-1β and the effect of spared nerve injury was substantially reversed by peri-sciatic administration of anti-IL-1β. Neuropathic pain was not necessary for the development of cognitive and emotional disorders, while the overproduction of IL-1β in the injured sciatic nerve following peripheral nerve injury may be a common mechanism underlying the generation of neuropathic pain, memory deficit, and depression. © The Author(s) 2016.

  7. What drives progressive motor deficits in patients with acute pontine infarction?

    Directory of Open Access Journals (Sweden)

    Jue-bao Li

    2015-01-01

    Full Text Available Progressive motor deficits are relatively common in acute pontine infarction and frequently associated with increased functional disability. However, the factors that affect the progression of clinical motor weakness are largely unknown. Previous studies have suggested that pontine infarctions are caused mainly by basilar artery stenosis and penetrating artery disease. Recently, lower pons lesions in patients with acute pontine infarctions have been reported to be related to progressive motor deficits, and ensuing that damage to the corticospinal tracts may be responsible for the worsening of neurological symptoms. Here, we review studies on motor weakness progression in pontine infarction and discuss the mechanisms that may underlie the neurologic worsening.

  8. Neurobehavioral Deficits in Progressive Experimental ...

    African Journals Online (AJOL)

    olayemitoyin

    Departments of 1Anatomy and 2Neurological Surgery, College of Medicine, University of Ibadan, Nigeria. Summary: Hydrocephalus is usually associated with functional deficits which can be assessed by neurobehavioral tests. This study characterizes the neurobehavioral deficits occurring with increasing duration and ...

  9. Over-expression of RCAN1 causes Down syndrome-like hippocampal deficits that alter learning and memory.

    Science.gov (United States)

    Martin, Katherine R; Corlett, Alicia; Dubach, Daphne; Mustafa, Tomris; Coleman, Harold A; Parkington, Helena C; Merson, Tobias D; Bourne, James A; Porta, Sílvia; Arbonés, Maria L; Finkelstein, David I; Pritchard, Melanie A

    2012-07-01

    People with Down syndrome (DS) exhibit abnormal brain structure. Alterations affecting neurotransmission and signalling pathways that govern brain function are also evident. A large number of genes are simultaneously expressed at abnormal levels in DS; therefore, it is a challenge to determine which gene(s) contribute to specific abnormalities, and then identify the key molecular pathways involved. We generated RCAN1-TG mice to study the consequences of RCAN1 over-expression and investigate the contribution of RCAN1 to the brain phenotype of DS. RCAN1-TG mice exhibit structural brain abnormalities in those areas affected in DS. The volume and number of neurons within the hippocampus is reduced and this correlates with a defect in adult neurogenesis. The density of dendritic spines on RCAN1-TG hippocampal pyramidal neurons is also reduced. Deficits in hippocampal-dependent learning and short- and long-term memory are accompanied by a failure to maintain long-term potentiation (LTP) in hippocampal slices. In response to LTP induction, we observed diminished calcium transients and decreased phosphorylation of CaMKII and ERK1/2-proteins that are essential for the maintenance of LTP and formation of memory. Our data strongly suggest that RCAN1 plays an important role in normal brain development and function and its up-regulation likely contributes to the neural deficits associated with DS.

  10. Acute neurological signs as the predominant clinical manifestation in four dogs with Angiostrongylus vasorum infections in Denmark

    Directory of Open Access Journals (Sweden)

    Pors Susanne E

    2011-06-01

    Full Text Available Abstract Four dogs with acute neurological signs caused by haemorrhages in the central nervous system were diagnosed with Angiostrongylus vasorum infection as the underlying aetiology. Two dogs presented with brain lesions, one dog with spinal cord lesions and one with lesions in both the brain and spinal cord. Only one dog presented with concurrent signs of classical pulmonary angiostrongylosis (respiratory distress, cough, and only two dogs displayed overt clinical signs of haemorrhages. Results of coagulation assays were inconsistent. Neurological signs reflected the site of pathology and included seizures, various cranial nerve deficits, vestibular signs, proprioceptive deficits, ataxia and paraplegia. One dog died and three were euthanised due to lack of improvement despite medical treatment. This emphasises canine angiostrongylosis as a potential cause of fatal lesions of the central nervous system and the importance of including A. vasorum as a differential diagnosis in young dogs with acute neurological signs in Denmark.

  11. Acute neurological signs as the predominant clinical manifestation in four dogs with Angiostrongylus vasorum infections in Denmark.

    Science.gov (United States)

    Gredal, Hanne; Willesen, Jakob L; Jensen, Henrik E; Nielsen, Ole L; Kristensen, Annemarie T; Koch, Jørgen; Kirk, Rikke K; Pors, Susanne E; Skerritt, Geoff C; Berendt, Mette

    2011-06-28

    Four dogs with acute neurological signs caused by haemorrhages in the central nervous system were diagnosed with Angiostrongylus vasorum infection as the underlying aetiology. Two dogs presented with brain lesions, one dog with spinal cord lesions and one with lesions in both the brain and spinal cord. Only one dog presented with concurrent signs of classical pulmonary angiostrongylosis (respiratory distress, cough), and only two dogs displayed overt clinical signs of haemorrhages. Results of coagulation assays were inconsistent. Neurological signs reflected the site of pathology and included seizures, various cranial nerve deficits, vestibular signs, proprioceptive deficits, ataxia and paraplegia. One dog died and three were euthanised due to lack of improvement despite medical treatment. This emphasises canine angiostrongylosis as a potential cause of fatal lesions of the central nervous system and the importance of including A. vasorum as a differential diagnosis in young dogs with acute neurological signs in Denmark.

  12. Asiatic acid protects against cognitive deficits and reductions in cell proliferation and survival in the rat hippocampus caused by 5-fluorouracil chemotherapy.

    Directory of Open Access Journals (Sweden)

    Pornthip Chaisawang

    Full Text Available The chemotherapy drug, 5-fluorouracil (5-FU, has been reported to cause cognitive impairments in cancer patients. The drug also reduces cell proliferation and survival in the brain. Asiatic acid (AA is a triterpene compound found in Centella asiatica that can protect against reduction of neurogenesis in the hippocampus and memory deficits induced by valproic acid (VPA. In the present study, we investigated the preventive effects of AA on the deficits in spatial working memory and cell proliferation and survival caused by 5-FU chemotherapy in a rat model. Male Sprague Dawley rats received 5-FU (5 i.v. injections, 25 mg/kg on day 8, 11, 14, 17 and 20 of the study. This was co-administered with AA (30 mg/kg, oral gavage tube either 20 days before receiving 5-FU (preventive, after receiving 5-FU (recovery, or for the entire period of the experiment (throughout. Spatial working memory was determined using the novel object location (NOL test and hippocampal cell proliferation and survival of dividing cells were quantified using immunohistochemistry. Rats in the 5-FU alone and recovery groups showed memory deficits in the NOL test and reductions in cell proliferation and cell survival in the subgranular zone (SGZ of the hippocampal dentate gyrus. Rats in the control, AA alone, and both preventive and throughout co-administration groups, however, did not exhibit these characteristics. The results showed that 5-FU chemotherapy impaired memory and reduced cell proliferation and cell survival in the SGZ of the hippocampal dentate gyrus. However, these impairments in the animals receiving 5-FU chemotherapy were restored to control levels when AA was co-administered before and during 5-FU treatment. These data demonstrate that AA can prevent the spatial working memory and hippocampal neurogenesis impairments caused by 5-FU chemotherapy.

  13. RanBP9 overexpression down-regulates phospho-cofilin, causes early synaptic deficits and impaired learning, and accelerates accumulation of amyloid plaques in the mouse brain.

    Science.gov (United States)

    Palavicini, Juan Pablo; Wang, Hongjie; Minond, Dmitriy; Bianchi, Elisabetta; Xu, Shaohua; Lakshmana, Madepalli K

    2014-01-01

    Loss of synaptic proteins and functional synapses in the brains of patients with Alzheimer's disease (AD) as well as transgenic mouse models expressing amyloid-β protein precursor is now well established. However, the earliest age at which such loss of synapses occurs, and whether known markers of AD progression accelerate functional deficits is completely unknown. We previously showed that RanBP9 overexpression leads to enhanced amyloid plaque burden in a mouse model of AD. In this study, we found significant reductions in the levels of synaptophysin and spinophilin, compared with wild-type controls, in both the cortex and the hippocampus of 5- and 6-month old but not 3- or 4-month old APΔE9/RanBP9 triple transgenic mice, and not in APΔE9 double transgenic mice, nor in RanBP9 single transgenic mice. Interestingly, amyloid plaque burden was also increased in the APΔE9/RanBP9 mice at 5-6 months. Consistent with these results, we found significant deficits in learning and memory in the APΔE9/RanBP9 mice at 5 and 6 month. These data suggest that increased amyloid plaques and accelerated learning and memory deficits and loss of synaptic proteins induced by RanBP9 are correlated. Most importantly, APΔE9/RanBP9 mice also showed significantly reduced levels of the phosphorylated form of cofilin in the hippocampus. Taken together these data suggest that RanBP9 overexpression down-regulates cofilin, causes early synaptic deficits and impaired learning, and accelerates accumulation of amyloid plaques in the mouse brain.

  14. Not only the sugar, early infarct sign, hyperDense middle cerebral artery, age, neurologic deficit score but also atrial fibrillation is predictive for symptomatic intracranial hemorrhage after intravenous recombinant tissue plasminogen activator

    Directory of Open Access Journals (Sweden)

    Sombat Muengtaweepongsa

    2017-01-01

    Full Text Available Background: Symptomatic intracranial hemorrhage (sICH is the most unwanted adverse event in patients with acute ischemic stroke who received intravenous recombinant tissue plasminogen activator (i.v. rt-PA. Many tool scores are available to predict the probability of sICH. Among those scores, the Sugar, Early infarct sign, hyperDense middle cerebral artery, Age, Neurologic deficit (SEDAN gives the highest area under the curve-receiver operating characteristic value. Objective: We aimed to examine any factors other than the SEDAN score to predict the probability of sICH. Methods: Patients with acute ischemic stroke treated with i.v. rt-PA within 4.5 h time window from January 2010 to July 2012 were evaluated. Compiling demographic data, risk factors, and comorbidity (hypertension, diabetes mellitus, dyslipidemia, atrial fibrillation (AF, ischemic heart disease, valvular heart disease, previous stroke, gout, smoking cigarette, drinking alcoholic beverage, family history of stroke, and family history of ischemic heart disease, computed tomography scan of patients prior to treatment with rt-PA, and assessing the National Institutes of Health Stroke Scale (NIHSS score for the purpose of calculating SEDAN score were analyzed. Results: Of 314 patients treated with i.v. rt-PA, there were 46 ICH cases (14.6% with 14 sICH (4.4% and 32 asymptomatic intracranial hemorrhage cases (10.2%. The rate of sICH occurrence was increased in accordance with the increase in the SEDAN score and AF. Age over 75 years, early infarction, hyperdense cerebral artery, baseline blood sugar more than 12 mmol/l, NIHSS as 10 or more, and AF were the risk factors to develop sICH after treated with rt-PA at 1.535, 2.501, 1.093, 1.276, 1.253, and 2.492 times, respectively. Conclusions: Rather than the SEDAN score, AF should be a predictor of sICH in patients with acute ischemic stroke after i.v. rt-PA treatment in Thai population.

  15. Increased Coupling in the Saliency Network is the main cause/effect of Attention Deficit Hyperactivity Disorder

    CERN Document Server

    Ji, Xiaoxi; Zhang, Jie; Ge, Tian; Sun, Li; Wang, Yufeng; Feng, Jianfeng

    2011-01-01

    To uncover the underlying mechanisms of mental disorders such as attention deficit hyperactivity disorder (ADHD) for improving both early diagnosis and therapy, it is increasingly recognized that we need a better understanding of how the brain's functional connections are altered. A new brain wide association study (BWAS) has been developed and used to investigate functional connectivity changes in the brains of patients suffering from ADHD using resting state fMRI data. To reliably find out the most significantly altered functional connectivity links and associate them with ADHD, a meta-analysis on a cohort of ever reported largest population comprising 249 patients and 253 healthy controls is carried out. The greatest change in ADHD patients was the increased coupling of the saliency network involving the anterior cingulate gyrus and anterior insula. A voxel-based morphometry analysis was also carried out but this revealed no evidence in the ADHD patients for altered grey matter volumes in the regions showi...

  16. Sensory overresponsivity and anxiety in typically developing children and children with autism and attention deficit hyperactivity disorder: cause or coexistence?

    Science.gov (United States)

    Lane, Shelly J; Reynolds, Stacey; Dumenci, Levent

    2012-01-01

    OBJECTIVE. To explore the relationship between sensory overresponsivity (SOR) and anxiety in children with autism, attention deficit hyperactivity disorder, and typical development. METHOD. Path analysis was used to examine the primary SOR model (Green & Ben-Sasson, 2010) using both physiological and behavioral data. RESULTS. The magnitude of physiological responses to sensory challenge was a mediator variable between predictors (baseline arousal and attention) and outcomes (anxiety and physiological recovery). Behavioral SOR was correlated with anxiety but not with physiological variables. CONCLUSION. The intensity or magnitude of sensory responsivity mediates the relationship between baseline arousal and attention and outcome anxiety and physiologic recovery from sensory challenge. Behavioral tools used to measure SOR do not reflect physiological responsiveness; this mismatch warrants further investigation. SOR can prevent children from participating in the occupations of childhood; the greater the understanding of SOR, the more successful occupational therapy practitioners will be in developing effective interventions. Copyright © 2012 by the American Occupational Therapy Association, Inc.

  17. Pragmatic Communication Deficits in Children with Epilepsy

    Science.gov (United States)

    Broeders, Mark; Geurts, Hilde; Jennekens-Schinkel, Aag

    2010-01-01

    Background: Various psychiatric and neurological disorders including epilepsy have been associated with language deficits. Pragmatic language deficits, however, have seldom been the focus of earlier studies in children with epilepsy. Moreover, it is unknown whether these pragmatic deficits are related to general intellectual functioning. Both…

  18. Outline of restorative neurology: definition, clinical practice, assessment, intervention.

    Science.gov (United States)

    Dimitrijevic, Milan R

    2012-06-01

    Rather than focusing on the deficits and lost function caused by upper motor neuron lesions or disorders, it is more advantageous to elucidate, in each individual, the specific neural functions that remain available, and then, to build upon them by designing a treatment protocol to optimize their effectiveness and thus improve recovery. The practice of Restorative Neurology is based on detailed assessment of the individual patient, the use of neurophysiological methods to elucidate and characterize subclinical function and the application of interventions that modify neural activity to improve clinical function. Copyright © 2012 Elsevier B.V. All rights reserved.

  19. Early postnatal exposure to isoflurane causes cognitive deficits and disrupts development of newborn hippocampal neurons via activation of the mTOR pathway.

    Science.gov (United States)

    Kang, Eunchai; Jiang, Danye; Ryu, Yun Kyoung; Lim, Sanghee; Kwak, Minhye; Gray, Christy D; Xu, Michael; Choi, Jun H; Junn, Sue; Kim, Jieun; Xu, Jing; Schaefer, Michele; Johns, Roger A; Song, Hongjun; Ming, Guo-Li; Mintz, C David

    2017-07-01

    Clinical and preclinical studies indicate that early postnatal exposure to anesthetics can lead to lasting deficits in learning and other cognitive processes. The mechanism underlying this phenomenon has not been clarified and there is no treatment currently available. Recent evidence suggests that anesthetics might cause persistent deficits in cognitive function by disrupting key events in brain development. The hippocampus, a brain region that is critical for learning and memory, contains a large number of neurons that develop in the early postnatal period, which are thus vulnerable to perturbation by anesthetic exposure. Using an in vivo mouse model we demonstrate abnormal development of dendrite arbors and dendritic spines in newly generated dentate gyrus granule cell neurons of the hippocampus after a clinically relevant isoflurane anesthesia exposure conducted at an early postnatal age. Furthermore, we find that isoflurane causes a sustained increase in activity in the mechanistic target of rapamycin pathway, and that inhibition of this pathway with rapamycin not only reverses the observed changes in neuronal development, but also substantially improves performance on behavioral tasks of spatial learning and memory that are impaired by isoflurane exposure. We conclude that isoflurane disrupts the development of hippocampal neurons generated in the early postnatal period by activating a well-defined neurodevelopmental disease pathway and that this phenotype can be reversed by pharmacologic inhibition.

  20. Attention deficit hyperactivity disorder (ADHD)

    Science.gov (United States)

    ... this page: //medlineplus.gov/ency/article/001551.htm Attention deficit hyperactivity disorder To use the sharing features on this page, please enable JavaScript. Attention deficit hyperactivity disorder (ADHD) is a problem caused by the presence ...

  1. Advocacy in neurology

    National Research Council Canada - National Science Library

    Pauranik, Apoorva

    2008-01-01

    ...), launched the Neurological Alliance of Ireland, a nationwide coalition of patient advocacy groups and physicians and authored Standards of Care, the "blueprint" for the development of neurological...

  2. Alpha-tocopherol transfer protein deficiency in mice causes multi-organ deregulation of gene networks and behavioral deficits with age.

    Science.gov (United States)

    Gohil, Kishorchandra; Godzdanker, Roy; O'Roark, Erin; Schock, Bettina C; Kaini, Ramesh R; Packer, Lester; Cross, Carroll E; Traber, Maret G

    2004-12-01

    Functions of alpha-tocopherol (alpha-T) in vivo, other than those for fertility in females, are intensely debated. The discovery of alpha-T deficiency in patients with ataxia (AVED) followed by the identification of mutations in the gene encoding alpha-tocopherol transfer protein (TTP) in AVED patients demonstrates an essential role of alpha-T and TTP for normal neurological function. alpha-T molecular targets that account for alpha-T-sensitive neurological dysfunction remain to be discovered. We have used high-density oligonucleotide arrays to search for putative alpha-T-sensitive genes in the CNS and other tissues in an in vivo model of alpha-T deficiency imposed at birth by the deletion of the TTP gene in mice. Repression of genes affecting synaptic function and myelination and induction of genes for neurodegeneration in the motor cortex of alpha-T-deficient mice were identified. The expression of retinoic acid-related orphan receptor alpha (ROR-alpha) was repressed in the cortex and adrenal glands of TTP-deficient mice. Deficiency of ROR-alpha causes ataxia in mice and may account for ataxia in AVED patients. These observations suggest that some of the actions of alpha-T are mediated by the transcription factor ROR-alpha. The behavior of young TTP-null mice was essentially normal, but older mice showed inactivity, ataxia, and memory dysfunction. mRNA profiles of old alpha-T-deficient cerebral cortices are compatible with repressed activity of oligodendrocytes and astrocytes. In conclusion, gene-expression profiling studies have identified novel alpha-T-modulated genes and cells in the CNS that may be causatively linked with delayed neurodegeneration and age-related decline in behavioral repertoires.

  3. Prenatal exposure to alcohol and 3,4-methylenedioxymethamphetamine (ecstasy) alters adult hippocampal neurogenesis and causes enduring memory deficits.

    Science.gov (United States)

    Canales, Juan J; Ferrer-Donato, Agueda

    2014-01-01

    Recreational drug use among pregnant women is a source of concern due to potential harmful effects of drug exposure on prenatal and infant development. The simultaneous abuse of ecstasy [3,4-methylenedioxymethamphetamine (MDMA)] and alcohol is prevalent among young adults, including young expectant mothers. Here, we used a rat model to study the potential risks associated with exposure to alcohol and MDMA during pregnancy. Pregnant rats received alcohol, MDMA, or both alcohol and MDMA by gavage at E13 through E15 twice daily. Female offspring treated prenatally with the combination of alcohol and MDMA, but not those exposed to either drug separately, showed at 3 months of age decreased exploratory activity and impaired working memory function. Prenatal treatment with the combination of alcohol and MDMA decreased proliferation of neuronal precursors in the adult dentate gyrus of the hippocampus, as measured by 5-bromo-2-deoxyuridine labelling, and adult neurogenesis, assessed by quantifying doublecortin expression. These results provide the first evidence that the simultaneous abuse of alcohol and ecstasy during pregnancy, even for short periods of time, may cause significant abnormalities in neurocognitive development. © 2014 S. Karger AG, Basel.

  4. Neurological Respiratory Failure

    Directory of Open Access Journals (Sweden)

    Mohan Rudrappa

    2018-01-01

    Full Text Available West Nile virus infection in humans is mostly asymptomatic. Less than 1% of neuro-invasive cases show a fatality rate of around 10%. Acute flaccid paralysis of respiratory muscles leading to respiratory failure is the most common cause of death. Although the peripheral nervous system can be involved, isolated phrenic nerve palsy leading to respiratory failure is rare and described in only two cases in the English literature. We present another case of neurological respiratory failure due to West Nile virus-induced phrenic nerve palsy. Our case reiterates the rare, but lethal, consequences of West Nile virus infection, and the increase of its awareness among physicians.

  5. De novo loss-of-function mutations in WAC cause a recognizable intellectual disability syndrome and learning deficits in Drosophila.

    Science.gov (United States)

    Lugtenberg, Dorien; Reijnders, Margot R F; Fenckova, Michaela; Bijlsma, Emilia K; Bernier, Raphael; van Bon, Bregje W M; Smeets, Eric; Vulto-van Silfhout, Anneke T; Bosch, Danielle; Eichler, Evan E; Mefford, Heather C; Carvill, Gemma L; Bongers, Ernie M H F; Schuurs-Hoeijmakers, Janneke Hm; Ruivenkamp, Claudia A; Santen, Gijs W E; van den Maagdenberg, Arn M J M; Peeters-Scholte, Cacha M P C D; Kuenen, Sabine; Verstreken, Patrik; Pfundt, Rolph; Yntema, Helger G; de Vries, Petra F; Veltman, Joris A; Hoischen, Alexander; Gilissen, Christian; de Vries, Bert B A; Schenck, Annette; Kleefstra, Tjitske; Vissers, Lisenka E L M

    2016-08-01

    Recently WAC was reported as a candidate gene for intellectual disability (ID) based on the identification of a de novo mutation in an individual with severe ID. WAC regulates transcription-coupled histone H2B ubiquitination and has previously been implicated in the 10p12p11 contiguous gene deletion syndrome. In this study, we report on 10 individuals with de novo WAC mutations which we identified through routine (diagnostic) exome sequencing and targeted resequencing of WAC in 2326 individuals with unexplained ID. All but one mutation was expected to lead to a loss-of-function of WAC. Clinical evaluation of all individuals revealed phenotypic overlap for mild ID, hypotonia, behavioral problems and distinctive facial dysmorphisms, including a square-shaped face, deep set eyes, long palpebral fissures, and a broad mouth and chin. These clinical features were also previously reported in individuals with 10p12p11 microdeletion syndrome. To investigate the role of WAC in ID, we studied the importance of the Drosophila WAC orthologue (CG8949) in habituation, a non-associative learning paradigm. Neuronal knockdown of Drosophila CG8949 resulted in impaired learning, suggesting that WAC is required in neurons for normal cognitive performance. In conclusion, we defined a clinically recognizable ID syndrome, caused by de novo loss-of-function mutations in WAC. Independent functional evidence in Drosophila further supported the role of WAC in ID. On the basis of our data WAC can be added to the list of ID genes with a role in transcription regulation through histone modification.

  6. Thoracic myelocystomeningocele in a neurologically intact infant ...

    African Journals Online (AJOL)

    This case is an example of a high congenital spinal lesion with very minimal or negligible neurological deficits, with no other congenital malformations. Key Words: Thoracic spine, Myelocystomeningocele, Intact nervous system. Résumé Rapporter un cas peu commun et un cas rare d'une anomalie congenitale vertébrale ...

  7. Allan-Herndon-Dudley syndrome (AHDS) caused by a novel SLC16A2 gene mutation showing severe neurologic features and unexpectedly low TRH-stimulated serum TSH.

    Science.gov (United States)

    Boccone, Loredana; Mariotti, Stefano; Dessì, Valentina; Pruna, Dario; Meloni, Antonella; Loudianos, Georgios

    2010-01-01

    Thyroid hormones are known to be essential for growth, development and metabolism. Recently mutations in the SLC16A2 gene coding for the monocarboxylate thyroid hormone transporter 8, MCT8, have been associated with Allan-Herndon-Dudley syndrome (AHDS), an X-linked condition characterized by severe mental retardation, dysarthria, athetoid movements, muscle hypoplasia and spastic paraplegia. Here we describe in detail the clinical and biochemical features in a boy affected by AHDS with severe neurological abnormalities and a novel de novo SLC16A2 gene insertion, 1343-1344insGCCC, resulting in a truncated protein lacking the last four transmembrane domains (TMDs) as well as the carboxyl cytoplasmic end. He presents mental retardation, axial hypotonia, hypertonia of arms and legs, paroxysmal dyskinesias, seizures. The endocrine phenotype showed low serum total and free thyroxine (T4), very elevated total and free triiodothyronine (T3) and normal thyrotropin (TSH) with blunted response to thyrotropin-releasing hormone (TRH). The latter finding was unexpected and suggested that the lack of functional MCT8 was counterbalanced at the thyrotrope cell level by high serum T3 concentration and/or by increased intrapituitary type 2 deiodinase (D2) activity. Our case constitutes a relevant contribution to better characterize this disorder and to elucidate the functional consequences of SLC16A2 gene mutations. Copyright © 2010 Elsevier Masson SAS. All rights reserved.

  8. Analyzing the diagnostic accuracy of the causes of spinal pain at neurology hospital in accordance with the International Classification of Diseases

    Directory of Open Access Journals (Sweden)

    I. G. Mikhailyuk

    2014-01-01

    Full Text Available Spinal pain is of great socioeconomic significance as it is widely prevalent and a common cause of disability. However, the diagnosis of its true causes frequently leads to problems. A study has been conducted to evaluate the accuracy of a clinical diagnosis and its coding in conformity with the International Classification of Diseases. The diagnosis of vertebral osteochondrosis and the hypodiagnosis of nonspecific and nonvertebrogenic pain syndromes have been found to be unreasonably widely used. Ways to solve these problems have been proposed, by applying approaches to diagnosing the causes of spinal pain in accordance with international practice.

  9. An evidence-based approach to clinical questions in the practice of equine neurology.

    Science.gov (United States)

    Van Biervliet, Jérôme

    2007-08-01

    The practice of equine neurology has special challenges posed by the size of the animal being examined. Many diagnostic procedures routinely used in small animal practice are unsafe when applied to the equine patient or unavailable to the equine practitioner. Therefore, astute observation is the mainstay of making a neuroanatomic diagnosis, and detailed evidence on the deficits present may be difficult to obtain. Because clinical observation can sometimes be ambiguous and somewhat subjective, it is even more important to approach equine neurology from an evidence-based point of view. Here, such an approach is outlined for the diagnosis of cervical vertebral compressive myelopathy (CVCM), one of the most common noninfectious causes of equine neurologic disease. This article is an attempt to summarize all aspects of making a diagnosis of CVCM on the basis of signalment, clinical examination, ancillary diagnostic tests, and pathologic examination. Each of these considerations has inherent limitations regarding diagnostic accuracy, which are discussed.

  10. Sports neurology topics in neurologic practice

    Science.gov (United States)

    Conidi, Francis X.; Drogan, Oksana; Giza, Christopher C.; Kutcher, Jeffery S.; Alessi, Anthony G.; Crutchfield, Kevin E.

    2014-01-01

    Summary We sought to assess neurologists' interest in sports neurology and learn about their experience in treating sports-related neurologic conditions. A survey was sent to a random sample of American Academy of Neurology members. A majority of members (77%) see at least some patients with sports-related neurologic issues. Concussion is the most common sports-related condition neurologists treat. More than half of survey participants (63%) did not receive any formal or informal training in sports neurology. At least two-thirds of respondents think it is very important to address the following issues: developing evidence-based return-to-play guidelines, identifying risk factors for long-term cognitive-behavioral sequelae, and developing objective diagnostic criteria for concussion. Our findings provide an up-to-date view of the subspecialty of sports neurology and identify areas for future research. PMID:24790800

  11. β-N-methylamino-l-alanine causes neurological and pathological phenotypes mimicking Amyotrophic Lateral Sclerosis (ALS): the first step towards an experimental model for sporadic ALS.

    Science.gov (United States)

    de Munck, Estefanía; Muñoz-Sáez, Emma; Miguel, Begoña G; Solas, M Teresa; Ojeda, Irene; Martínez, Ana; Gil, Carmen; Arahuetes, Rosa Ma

    2013-09-01

    β-N-methylamino-l-alanine (L-BMAA) is a neurotoxic amino acid that has been related to various neurodegenerative diseases. The aim of this work was to analyze the biotoxicity produced by L-BMAA in vivo in rats, trying to elucidate its physiopathological mechanisms and to search for analogies between the found effects and pathologies like Amyotrophic Lateral Sclerosis (ALS). Our data demonstrated that the neurotoxic effects in vivo were dosage-dependent. For evaluating the state of the animals, a neurological evaluation scale was developed as well as a set of functional tests. Ultrastructural cell analysis of spinal motoneurons has revealed alterations both in endoplasmic reticulum and mitochondria. Since GSK3β could play a role in some neuropathological processes, we analyzed the alterations occurring in GSK3β levels in L-BMAA treated rats, we have observed an increase in the active form of GSK3β levels in lumbar spinal cord and motor cerebral cortex. On the other hand, (TAR)-DNA-binding protein 43 (TDP-43) increased in L-BMAA treated animals. Our results indicated that N-acetylaspartate (NAA) declined in animals treated with L-BMAA, and the ratio of N-acetylaspartate/choline (NAA/Cho), N-acetylaspartate/creatine (NAA/Cr) and N-acetylaspartate/choline+creatine (NAA/Cho+Cr) tended to decrease in lumbar spinal cord and motor cortex. This project offers some encouraging results that could help establishing the progress in the development of an animal model of sporadic ALS and L-BMAA could be a useful tool for this purpose. Copyright © 2013 Elsevier B.V. All rights reserved.

  12. Bridging Neuroanatomy, Neuroradiology and Neurology: Three-Dimensional Interactive Atlas of Neurological Disorders

    OpenAIRE

    Nowinski, W. L.; Chua, B.C.

    2013-01-01

    Understanding brain pathology along with the underlying neuroanatomy and the resulting neurological deficits is of vital importance in medical education and clinical practice. To facilitate and expedite this understanding, we created a three-dimensional (3D) interactive atlas of neurological disorders providing the correspondence between a brain lesion and the resulting disorder(s). The atlas contains a 3D highly parcellated atlas of normal neuroanatomy along with a brain pathology database. ...

  13. Low-Level Laser Therapy (904 nm Counteracts Motor Deficit of Mice Hind Limb following Skeletal Muscle Injury Caused by Snakebite-Mimicking Intramuscular Venom Injection.

    Directory of Open Access Journals (Sweden)

    Willians Fernando Vieira

    Full Text Available Myotoxins present in Bothrops venom disrupt the sarcolemma of muscle fibers leading to the release of sarcoplasmic proteins and loss of muscle homeostasis. Myonecrosis and tissue anoxia induced by vascularization impairment can lead to amputation or motor functional deficit. The objective of this study was to investigate the dynamic behavior of motor function in mice subjected to injection of Bothrops jararacussu venom (Bjssu and exposed to low-level laser therapy (LLLT. Male Swiss mice received Bjssu injection (830 μg/kg into the medial portion of the right gastrocnemius muscle. Three hours later the injected region was irradiated with diode semiconductor Gallium Arsenide (GaAs- 904 nm, 4 J/cm² laser following by irradiation at 24, 48 and 72 hours. Saline injection (0.9% NaCl was used as control. Gait analysis was performed 24 hours before Bjssu injection and at every period post-Bjssu using CatWalk method. Data from spatiotemporal parameters Stand, Maximum Intensity, Swing, Swing Speed, Stride Length and Step Cycle were considered. The period of 3 hours post venom-induced injury was considered critical for all parameters evaluated in the right hindlimb. Differences (p<0.05 were concentrated in venom and venom + placebo laser groups during the 3 hours post-injury period, in which the values of stand of most animals were null. After this period, the gait characteristics were re-established for all parameters. The venom + laser group kept the values at 3 hours post-Bjssu equal to that at 24 hours before Bjssu injection indicating that the GaAs laser therapy improved spatially and temporally gait parameters at the critical injury period caused by Bjssu. This is the first study to analyze with cutting edge technology the gait functional deficits caused by snake envenoming and gait gains produced by GaAs laser irradiation. In this sense, the study fills a gap on the field of motor function after laser treatment following snake envenoming.

  14. African Journal of Neurological Sciences - 2009 Vol. 28 No 1

    African Journals Online (AJOL)

    highly trained radiologists, neurology, neurosurgery and physiotherapy units. Study period: During a six months period from 1st July 2010 to 30th January 2011, 167 patients who presented to Mulago hospital's accident and emergency unit with neurologic deficits suggestive of acute stroke (29) were screened.

  15. Neurological sequelae in survivors of cerebral malaria | Oluwayemi ...

    African Journals Online (AJOL)

    Methods: This is a prospective study describing persisting neurological impairments post discharge among children treated for cerebral malaria. ... The persisting neurologic deficits among survivors at follow up were: memory impairment (1.5%), seizure disorders (0.8%), visual impairment (0.8%), speech impairment (0.8%), ...

  16. African Journal of Neurological Sciences - 2009 Vol. 28 No 1

    African Journals Online (AJOL)

    Those with symptomatic epilepsy were more likely to have neurologic deficit, simple partial seizure, secondarily generalized seizure, focal epileptiform discharges and focal slow waves. Conclusion. The most common abnormalities in LOE were cerebral infarct and brain tumor. A careful history, neurological examination and ...

  17. THE NEUROLOGICAL FACE OF CELIAC DISEASE

    Directory of Open Access Journals (Sweden)

    Sedat IŞIKAY

    2015-09-01

    Full Text Available BackgroundSeveral neurological disorders have also been widely described in celiac disease patients.ObjectiveThe aim of this study was to determine the incidence of accompanying different neurologic manifestations in children with celiac disease at the time of diagnosis and to discuss these manifestations in the light of the recent literature.MethodsThis prospective cross sectional study included 297 children diagnosed with celiac disease. The medical records of all patients were reviewed.ResultsIn neurological evaluation, totally 40 (13. 5% of the 297 celiac patients had a neurological finding including headache, epilepsy, migraine, mental retardation, breath holding spells, ataxia, cerebral palsy, attention deficit hyperactivity disorder, Down syndrome and Turner syndrome in order of frequency. There was not any significant difference between the laboratory data of the patients with and without neurological manifestations. However; type 3a biopsy was statistically significantly more common among patients without neurological manifestations, while type 3b biopsy was statistically significantly more common among patients with neurological manifestations.ConclusionIt is important to keep in mind that in clinical course of celiac disease different neurological manifestations may be reported.

  18. Neurologic Injury in Operatively Treated Acetabular Fractures.

    Science.gov (United States)

    Bogdan, Yelena; Tornetta, Paul; Jones, Clifford; Gilde, Alex K; Schemitsch, Emil; Vicente, Milena; Horwitz, Daniel; Sanders, David; Firoozabadi, Reza; Leighton, Ross; de Dios Robinson, Juan; Marcantonio, Andrew; Hamilton, Benjamin

    2015-10-01

    The purpose of this study is to evaluate a series of operatively treated acetabular fractures with neurologic injury and to track sensory and motor recovery. Operatively treated acetabular fractures with neurologic injury from 8 trauma centers were reviewed. Patients were followed for at least 6 months or to neurologic recovery. Functional outcome was documented at 3 months, 6 months, and final follow-up. Outcomes included motor and sensory recovery, brace use, development of chronic regional pain syndrome, and return to work. One hundred thirty-seven patients (101 males and 36 females), average age 42 (17-87) years, met the criteria. Mechanism of injury included MVC (67%), fall (11%), and other (22%). The most common fracture types were transverse + posterior wall (33%), posterior wall (23%), and both-column (23%). Deficits were identified as preoperative in 57%, iatrogenic in 19% (immediately after surgery), and those that developed postoperatively in 24%. A total of 187 nerve deficits associated with the following root levels were identified: 7 in L2-3, 18 in L4, 114 in L5, and 48 in S1. Full recovery occurred in 54 (29%), partial recovery in 69 (37%), and 64 (34%) had no recovery. Forty-three percent of S1 deficits and 29% of L5 deficits had no recovery. Fifty-five percent of iatrogenic injuries did not recover. Forty-eight patients wore a brace at the final follow-up, all for an L5 root level deficit. Although 60% (42/70) returned to work, chronic regional pain syndrome was seen to develop in 19% (18/94). Peripheral neurologic injury in operatively treated acetabular fractures occurs most commonly in the sciatic nerve distribution, with L5 root level deficits having only a 26% chance of full recovery. Prognostic Level IV. See Instructions for Authors for a complete description of levels of evidence.

  19. Neurologic presentation of celiac disease.

    Science.gov (United States)

    Bushara, Khalafalla O

    2005-04-01

    Celiac disease (CD) long has been associated with neurologic and psychiatric disorders including cerebellar ataxia, peripheral neuropathy, epilepsy, dementia, and depression. Earlier reports mainly have documented the involvement of the nervous system as a complication of prediagnosed CD. However, more recent studies have emphasized that a wider spectrum of neurologic syndromes may be the presenting extraintestinal manifestation of gluten sensitivity with or without intestinal pathology. These include migraine, encephalopathy, chorea, brain stem dysfunction, myelopathy, mononeuritis multiplex, Guillain-Barre-like syndrome, and neuropathy with positive antiganglioside antibodies. The association between most neurologic syndromes described and gluten sensitivity remains to be confirmed by larger epidemiologic studies. It further has been suggested that gluten sensitivity (as evidenced by high antigliadin antibodies) is a common cause of neurologic syndromes (notably cerebellar ataxia) of otherwise unknown cause. Additional studies showed high prevalence of gluten sensitivity in genetic neurodegenerative disorders such as hereditary spinocerebellar ataxia and Huntington's disease. It remains unclear whether gluten sensitivity contributes to the pathogenesis of these disorders or whether it represents an epiphenomenon. Studies of gluten-free diet in patients with gluten sensitivity and neurologic syndromes have shown variable results. Diet trials also have been inconclusive in autism and schizophrenia, 2 diseases in which sensitivity to dietary gluten has been implicated. Further studies clearly are needed to assess the efficacy of gluten-free diet and to address the underlying mechanisms of nervous system pathology in gluten sensitivity.

  20. Apolipoprotein E4 causes age- and sex-dependent impairments of hilar GABAergic interneurons and learning and memory deficits in mice.

    Directory of Open Access Journals (Sweden)

    Laura Leung

    Full Text Available Apolipoprotein (apo E4 is the major genetic risk factor for Alzheimer's disease (AD. ApoE4 has sex-dependent effects, whereby the risk of developing AD is higher in apoE4-expressing females than males. However, the mechanism underlying the sex difference, in relation to apoE4, is unknown. Previous findings indicate that apoE4 causes age-dependent impairments of hilar GABAergic interneurons in female mice, leading to learning and memory deficits. Here, we investigate whether the detrimental effects of apoE4 on hilar GABAergic interneurons are sex-dependent using apoE knock-in (KI mice across different ages. We found that in female apoE-KI mice, there was an age-dependent depletion of hilar GABAergic interneurons, whereby GAD67- or somatostatin-positive--but not NPY- or parvalbumin-positive-interneuron loss was exacerbated by apoE4. Loss of these neuronal populations was correlated with the severity of spatial learning deficits at 16 months of age in female apoE4-KI mice; however, this effect was not observed in female apoE3-KI mice. In contrast, we found an increase in the numbers of hilar GABAergic interneurons with advancing age in male apoE-KI mice, regardless of apoE genotype. Moreover, male apoE-KI mice showed a consistent ratio of hilar inhibitory GABAergic interneurons to excitatory mossy cells approximating 1.5 that is independent of apoE genotype and age, whereas female apoE-KI mice exhibited an age-dependent decrease in this ratio, which was exacerbated by apoE4. Interestingly, there are no apoE genotype effects on GABAergic interneurons in the CA1 and CA3 subregions of the hippocampus as well as the entorhinal and auditory cortexes. These findings suggest that the sex-dependent effects of apoE4 on developing AD is in part attributable to inherent sex-based differences in the numbers of hilar GABAergic interneurons, which is further modulated by apoE genotype.

  1. Attention Deficit and EEG Analysis

    OpenAIRE

    J Gordon Millichap

    1992-01-01

    Computerized power spectral analysis (PSA), permitting topographic representation and statistical analysis of EEG, of 25 right-handed males, 9-12 years of age with attention deficit hyperactivity disorder was used in studies from the Departments of Psychology, Pediatrics (Neurology) and Computing Center, University of Tennessee and East Tennessee Children’s Hospital, Knoxville, TN.

  2. Resveratrol protects against ICV collagenase-induced neurobehavioral and biochemical deficits.

    Science.gov (United States)

    Singh, Navdeep; Bansal, Yashika; Bhandari, Ranjana; Marwaha, Lovish; Singh, Raghunath; Chopra, Kanwaljit; Kuhad, Anurag

    2017-01-01

    Indeed, intracerebral hemorrhage (ICH) account for only 15% of all strokes but it is one of the most devastating subtype of stroke associated with behavioral, cognitive and neurological deficits. The primary cause of neurological deficits in ICH is the hematoma growth, generation of free radicals, inflammatory cytokines and exhausting endogenous anti-oxidant machinery. It has been found that neuroinflammation following ICH leads to exaggeration of hallmarks of ICH. With this background, the study was aimed to evaluate the protective effect of resveratrol (RSV) in intracerebroventricular (ICV) collagenase (COL) induced neurological deficits in rats. The present study was designed to explore the protective effects of resveratrol (5, 10, 20 mg/kg) against ICV-COL induced ICH. Animals were subjected to a battery of behavioral tests to access behavioral changes, including neurological scoring tests (cylinder test, spontaneous motility, righting reflex, horizontal bar test, forelimb flexion), actophotometer, rotarod, Randall Sellito and von Frey. Post stroke depression was estimated using forced swim test (FST). Memory deficit was monitored using Morris water maze (MWM). Chronic treatment with RSV (20 mg/kg) for 21 days restored various behavioral changes, including neurological scoring tests (cylinder test, spontaneous motility, righting reflex, horizontal bar test, forelimb flexion), actophotometer, rotarod, Randall Sellito and Von Frey. RSV also restores increase in immobility time forced swim test used to evaluate post stroke depression and impaired memory deficit in Morris water maze. RSV administration also attenuated increased nitro-oxidative stress and TNF-α level. RSV being a potent antioxidant also restores changes in endogenous anti-oxidant levels. In conclusion, our research demonstrates that RSV has a protective effect against ICH by virtue of its anti-inflammatory property and antioxidant and nitrosative stress restoring property.

  3. Neurological manifestations as the initial presentation of acute myelogenous leukemia.

    Science.gov (United States)

    Maynor, M L

    1989-09-01

    This case report illustrates neurological deficits as an unusual presentation of acute myelogenous leukemia. Neurological deficits are rare early in this disease. Our patient presented with anorexia, malaise, headache, and multiple cranial nerve palsies. A high WBC count and abnormal peripheral smear led to the diagnosis of leukemia. This report demonstrates that, although rare, CNS symptoms may be the initial manifestation of leukemia. Blood dyscrasias should not be overlooked in patients with the acute onset of neurological symptoms. A complete blood count and differential should be obtained under those circumstances.

  4. Proprioceptive reflexes and neurological disorders

    NARCIS (Netherlands)

    Schouten, A.C.

    2004-01-01

    Proprioceptive reflexes play an important role during the control of movement and posture. Disturbed modulation of proprioceptive reflexes is often suggested as the cause for the motoric features present in neurological disorders. In this thesis methods are developed and evaluated to quantify

  5. Can break-dance break your neck? C1/C2 luxation with a combined dens fracture without neurological deficits in an 11-year old boy after a break-dance performance

    Directory of Open Access Journals (Sweden)

    Athanasios K. Petridis

    2015-09-01

    Full Text Available Atlantoaxial dislocation in children is a very rare condition. We present the case of a dislocation happened during a break-dance maneuver. The purpose of this report is describing dangers of break-dancing and discussing the treatment we chose. The patient was followed up until 12 months after surgery. Magnetic resonance imaging and computed tomography of the cervical spine were evaluated. Translaminar fixation of C1/C2 had been performed after manual reposition under X-ray illumination. After a 12-month follow-up, the patient shows a stable condition without neurological dysfunction. He is not allowed to perform any extreme sports.

  6. Neurology and diving.

    Science.gov (United States)

    Massey, E Wayne; Moon, Richard E

    2014-01-01

    Diving exposes a person to the combined effects of increased ambient pressure and immersion. The reduction in pressure when surfacing can precipitate decompression sickness (DCS), caused by bubble formation within tissues due to inert gas supersaturation. Arterial gas embolism (AGE) can also occur due to pulmonary barotrauma as a result of breath holding during ascent or gas trapping due to disease, causing lung hyperexpansion, rupture and direct entry of alveolar gas into the blood. Bubble disease due to either DCS or AGE is collectively known as decompression illness. Tissue and intravascular bubbles can induce a cascade of events resulting in CNS injury. Manifestations of decompression illness can vary in severity, from mild (paresthesias, joint pains, fatigue) to severe (vertigo, hearing loss, paraplegia, quadriplegia). Particularly as these conditions are uncommon, early recognition is essential to provide appropriate management, consisting of first aid oxygen, targeted fluid resuscitation and hyperbaric oxygen, which is the definitive treatment. Less common neurologic conditions that do not require hyperbaric oxygen include rupture of a labyrinthine window due to inadequate equalization of middle ear pressure during descent, which can precipitate vertigo and hearing loss. Sinus and middle ear overpressurization during ascent can compress the trigeminal and facial nerves respectively, causing temporary facial hypesthesia and lower motor neuron facial weakness. Some conditions preclude safe diving, such as seizure disorders, since a convulsion underwater is likely to be fatal. Preventive measures to reduce neurologic complications of diving include exclusion of individuals with specific medical conditions and safe diving procedures, particularly related to descent and ascent. © 2014 Elsevier B.V. All rights reserved.

  7. Cell therapy: the final frontier for treatment of neurological diseases.

    Science.gov (United States)

    Dutta, Susmita; Singh, Gurbind; Sreejith, Sailaja; Mamidi, Murali Krishna; Husin, Juani Mazmin; Datta, Indrani; Pal, Rajarshi; Das, Anjan Kumar

    2013-01-01

    Neurodegenerative diseases are devastating because they cause increasing loss of cognitive and physical functions and affect an estimated 1 billion individuals worldwide. Unfortunately, no drugs are currently available to halt their progression, except a few that are largely inadequate. This mandates the search of new treatments for these progressively degenerative diseases. Neural stem cells (NSCs) have been successfully isolated, propagated, and characterized from the adult brains of mammals, including humans. The confirmation that neurogenesis occurs in the adult brain via NSCs opens up fresh avenues for treating neurological problems. The proof-of-concept studies demonstrating the neural differentiation capacity of stem cells both in vitro and in vivo have raised widespread enthusiasm toward cell-based interventions. It is anticipated that cell-based neurogenic drugs may reverse or compensate for deficits associated with neurological diseases. The increasing interest of the private sector in using human stem cells in therapeutics is evidenced by launching of several collaborative clinical research activities between Pharma giants and research institutions or small start-up companies. In this review, we discuss the major developments that have taken place in this field to position stem cells as a prospective candidate drug for the treatment of neurological disorders. © 2012 Blackwell Publishing Ltd.

  8. Neurological manifestations in Fabry's disease

    DEFF Research Database (Denmark)

    Møller, Anette Torvin; Jensen, Troels Staehelin

    2007-01-01

    . Neurological symptoms, such as burning sensations (occasionally accompanied by acroparesthesia) and stroke, are among the first to appear, and occur in both male and female patients. A delay in establishing the diagnosis of Fabry's disease can cause unnecessary problems, especially now that enzyme replacement...... treatment is available to prevent irreversible organ damage. Females with Fabry's disease who present with pain have often been ignored and misdiagnosed because of the disorder's X-linked inheritance. This Review will stress the importance of recognizing neurological symptoms for the diagnosis of Fabry...

  9. Pattern and predictors of neurological morbidities among childhood cerebral malaria survivors in central Sudan.

    Science.gov (United States)

    Mergani, Adil; Khamis, Ammar H; Fatih Hashim, E L; Gumma, Mohamed; Awadelseed, Bella; Elwali, Nasr Eldin M A; Haboor, Ali Babikir

    2015-09-01

    Cerebral malaria is considered a leading cause of neuro-disability in sub-Saharan Africa among children and about 25% of survivors have long-term neurological and cognitive deficits or epilepsy. Their development was reported to be associated with protracted seizures, deep and prolonged coma. The study was aimed to determine the discharge pattern and to identify potential and informative predictors of neurological sequelae at discharge, complicating childhood cerebral malaria in central Sudan. A cross-sectional prospective study was carried out during malaria transmission seasons from 2000 to 2004 in Wad Medani, Sinnar and Singa hospitals, central Sudan. Children suspected of having cerebral malaria were examined and diagnosed by a Pediatrician for clinical, laboratory findings and any neurological complications. Univariate and multiple regression model analysis were performed to evaluate the association of clinical and laboratory findings with occurrence of neurological complications using the SPSS. Out of 940 examined children, only 409 were diagnosed with cerebral malaria with a mean age of 6.1 ± 3.3 yr. The mortality rate associated with the study was 14.2% (58) and 18.2% (64) of survivors (351) had neurological sequelae. Abnormal posture, either decerebration or decortication, focal convulsion and coma duration of >48 h were significant predictors for surviving from cerebral malaria with a neurological sequelae in children from central Sudan by Univariate analysis. Multiple logistic regression model fitting these variables, revealed 39.6% sensitivity for prediction of childhood cerebral malaria survivors with neurological sequelae (R² = 0.396; p=0.001). Neurological sequelae are common due to childhood cerebral malaria in central Sudan. Their prediction at admission, clinical presentation and laboratory findings may guide clinical intervention and proper management that may decrease morbidity and improve CM consequences.

  10. [Neurologic presentation in haemolytic-uraemic syndrome].

    Science.gov (United States)

    Roche-Martínez, A; Póo, P; Maristany-Cucurella, M; Jiménez-Llort, A; Camacho, J A; Campistol, J

    Haemolytic-uraemic syndrome (HUS) is characterized by microangiopathic hemolytic anaemia, thrombopenia and multiorganic aggression, specially renal, gastrointestinal and central nervous system disturbances. Sporadic in Spain (2/1,500,000 inhabitants), its clinical onset includes acute renal failure, hypertension and central nervous system symptoms (irritability, drowsiness, convulsions, cortical blindness, hemiparesia or coma), due to metabolic distress, hypertension or central nervous system microangiopathy. Few long-term outcome studies have been published. A retrospective analysis of a series of 58 patients with HUS between 1981 and 2006, is reported. Clinical onset, laboratory, electrophysiology, neuroimaging tests, and prognosis factors are reviewed, together with long-term clinical outcome. 22 children presented neurologic symptoms, seven had some neurological test; one patient died; in five some neurological sequelae persisted (hemiparesia, cognitive deficit, visual-perception deficit), the other 16 remaining asymptomatic. Neurological morbility is high in HUS (27% of the children with neurological symptoms), with a 1.7% mortality. Seizure at onset was not a poor prognosis factor in our group. No positive correlation can be established between neuroimaging and long-term outcome.

  11. A Novel Closed-head Model of Mild Traumatic Brain Injury Caused by Primary Overpressure Blast to the Cranium Produces Sustained Emotional Deficits in Mice

    Directory of Open Access Journals (Sweden)

    Scott A Heldt

    2014-01-01

    Full Text Available Emotional disorders are a common outcome from mild traumatic brain injury (TBI in humans, but their pathophysiological basis is poorly understood. We have developed a mouse model of closed-head blast injury using an air pressure wave delivered to a small area on one side of the cranium, which we have used to create mild TBI. We found that 20-psi blasts in 3-month old C57BL/6 male mice yielded no obvious behavioral or histological evidence of brain injury, while 25-40 psi blasts produced transient anxiety in an open field arena but little histological evidence of brain damage. By contrast, 50-60 psi blasts resulted in anxiety-like behavior in an open field arena that became more evident with time after blast. In additional behavioral tests conducted 2-8 weeks after blast, 50-60 psi mice also demonstrated increased acoustic startle, perseverance of learned fear, and enhanced contextual fear, as well as depression-like behavior and diminished prepulse inhibition. We found no evident cerebral pathology, however, and only scattered axonal degeneration in brain sections from 50-60 psi mice 3-8 weeks after blast. Thus, the TBI caused by single 50-60 psi blasts in mice exhibits the minimal neuronal loss coupled to diffuse axonal injury characteristic of human mild TBI. A reduction in the abundance of a subpopulation of excitatory projection neurons in basolateral amygdala enriched in Thy1 was, however, observed. The reported link of this neuronal population to fear suppression suggests their damage by mild TBI may contribute to the heightened anxiety and fearfulness observed after blast in our mice. Our overpressure air blast model of concussion in mice will enable further studies of the mechanisms underlying the diverse emotional deficits seen after mild TBI.

  12. [Neurorehabilitation, neurology, rehabilitation medicine].

    Science.gov (United States)

    Urbán, Edina; Szél, István; Fáy, Veronika; Dénes, Zoltán; Lippai, Zoltán; Fazekas, Gábor

    2013-05-30

    We have read several publications of great authority on the neurological profession in the last two years in which were expressed assessments of the current situation combined with opinions about neurology and the necessity to reorganize neurological patient care. These articles took up the question of neurorehabilitation too. The authors, who on a daily basis, deal with the rehabilitation of people with disabilities as a consequence of neurological conditions, summarize some important definitions of rehabilitation medicine and the present system of neurological rehabilitation, as it is defined by the rehabilitation profession.

  13. Neurology at the bedside

    DEFF Research Database (Denmark)

    Kondziella, Daniel; Waldemar, Gunhild

    This updated and expanded new edition takes neurology trainees by the hand and guides them through the whole patient encounter - from an efficient neurological history and bedside examination through to differential diagnosis, diagnostic procedures and treatment. At each step the expert authors......, as have new chapters including neurogenetics, neurorehabilitation, neurocritical care and heuristic neurological reasoning. In addition, this second edition now includes more than 100 unique case histories. Neurology at the Bedside, Second Edition is written for neurologists in all stages of training....... Medical students, general practitioners and others with an interest in neurology will also find invaluable information here....

  14. Infantile Autism: A Syndrome of Multiple Primary Deficits?

    Science.gov (United States)

    Goodman, Robert

    1989-01-01

    Consideration of underlying neurological and psychological deficits suggests that the autistic syndrome results from the coexistence of at least two distinct constellations of functional impairments: deficits in mechanical language skills, as in the developmental dysphasias; and deficits in social relatedness, play, and nonverbal communication, as…

  15. Chapter 38: American neurology.

    Science.gov (United States)

    Freemon, Frank R

    2010-01-01

    The great formative event in the history of North America, the Civil War of 1861 to 1865, was the stimulus for the development of clinical neurology and the neurosciences. The first neurological research center on the continent was the US Army hospital at Turner's Lane, Philadelphia, PA. Silas Weir Mitchell and his colleagues described causalgia (reflex sympathetic dystrophy), phantom limb sensation, and Horner's syndrome (before Horner). The medical leader of the Northern army was William Hammond. After the conclusion of hostilities, he began a huge clinical practice in New York City. In the United States, clinical neurology began in private practice, unlike Europe, where neurology began in institutions. Hammond's textbook, which first used the term athetosis, was used by a generation of physicians who encountered patients with neurological signs and symptoms. Early in the 20th century, neurological institutions were formed around universities; probably the most famous was the Montreal Neurological Institute founded by Wilder Penfield. The US federal government sponsored extensive research into the function and dysfunction of the nervous system through the Neurological Institute of Neurological Diseases and Blindness, later called the National Institute of Neurological Diseases and Stroke. The government officially classified the final 10 years of the 20th century as the Decade of the Brain and provided an even greater level of research funding.

  16. RanBP2 modulates Cox11 and hexokinase I activities and haploinsufficiency of RanBP2 causes deficits in glucose metabolism.

    Directory of Open Access Journals (Sweden)

    Azamat Aslanukov

    2006-10-01

    Full Text Available The Ran-binding protein 2 (RanBP2 is a large multimodular and pleiotropic protein. Several molecular partners with distinct functions interacting specifically with selective modules of RanBP2 have been identified. Yet, the significance of these interactions with RanBP2 and the genetic and physiological role(s of RanBP2 in a whole-animal model remain elusive. Here, we report the identification of two novel partners of RanBP2 and a novel physiological role of RanBP2 in a mouse model. RanBP2 associates in vitro and in vivo and colocalizes with the mitochondrial metallochaperone, Cox11, and the pacemaker of glycolysis, hexokinase type I (HKI via its leucine-rich domain. The leucine-rich domain of RanBP2 also exhibits strong chaperone activity toward intermediate and mature folding species of Cox11 supporting a chaperone role of RanBP2 in the cytosol during Cox11 biogenesis. Cox11 partially colocalizes with HKI, thus supporting additional and distinct roles in cell function. Cox11 is a strong inhibitor of HKI, and RanBP2 suppresses the inhibitory activity of Cox11 over HKI. To probe the physiological role of RanBP2 and its role in HKI function, a mouse model harboring a genetically disrupted RanBP2 locus was generated. RanBP2(-/- are embryonically lethal, and haploinsufficiency of RanBP2 in an inbred strain causes a pronounced decrease of HKI and ATP levels selectively in the central nervous system. Inbred RanBP2(+/- mice also exhibit deficits in growth rates and glucose catabolism without impairment of glucose uptake and gluconeogenesis. These phenotypes are accompanied by a decrease in the electrophysiological responses of photosensory and postreceptoral neurons. Hence, RanBP2 and its partners emerge as critical modulators of neuronal HKI, glucose catabolism, energy homeostasis, and targets for metabolic, aging disorders and allied neuropathies.

  17. Genetics of neurological disorders.

    Science.gov (United States)

    Faghihi, Mohammad Ali; Mottagui-Tabar, Salim; Wahlestedt, Claes

    2004-05-01

    Neurological diseases are defined as an inappropriate function of the peripheral or central nervous system due to impaired electrical impulses throughout the brain and/or nervous system that may present with heterogeneous symptoms according to the parts of the system involved in these pathologic processes. Growing evidence on genetic components of neurological disease have been collected during recent years. Genetic studies have opened the way for understanding the underlying pathology of many neurological disorders. The outcome of current intense research into the genetics of neurological disorders will hopefully be the introduction of new diagnostic tools and the discovery of potential targets for new and more effective medications and preventive measures.

  18. Analysis of discrepancy between neurologic findings and CT findings in 60 patients with herniated nucleus pulposus

    Energy Technology Data Exchange (ETDEWEB)

    Lee, Hyun; Kim, Kab Tae; Sol, Chang Hyo; Kim, Byung Soo [College of Medicine, Pusan National University, Busan(Korea, Republic of)

    1987-06-15

    The herniated nucleus pulposus (HNP) is a major cause of low back pain and sciatica. High resolution computed tomography is the most accurate diagnostic tool to define a HNP, because it provides a complete in vivo analysis of bony framework of lumbar spine as well as the supporting soft tissue structures and neural elements. But the discrepancy between neurologic findings and CT findings is often confusing. From May 1983 to August 1986, sixty patients with HNP who had both CT and surgical intervention at Pusan National University Hospital were analyzed. The feasibility of the neurologic examination on HNP and the effect of HNP on nerve root were evaluated on the basis of CT findings. The results were as follows : 1. Thirty-four cases (56.7%) of clinical impression were matched to CT findings in determining level of HNP and affected nerve root. 2. In evaluation of affected level, there was high trend to cause discrepancy between neurologic findings and CT findings in multiple disc involvement than in single involvement. 3. There was no correlation between degree of nerve root compression determined by CT and pattern of neurologic signs (motor weakness, sensory deficit, and reflex change)

  19. Autoimmune Neurology of the Central Nervous System.

    Science.gov (United States)

    Tobin, W Oliver; Pittock, Sean J

    2017-06-01

    This article reviews the rapidly evolving spectrum of autoimmune neurologic disorders with a focus on those that involve the central nervous system, providing an understanding of how to approach the diagnostic workup of patients presenting with central nervous system symptoms or signs that could be immune mediated, either paraneoplastic or idiopathic, to guide therapeutic decision making. The past decade has seen a dramatic increase in the discovery of novel neural antibodies and their targets. Many commercial laboratories can now test for these antibodies, which serve as diagnostic markers of diverse neurologic disorders that occur on an autoimmune basis. Some are highly specific for certain cancer types, and the neural antibody profiles may help direct the physician's cancer search. The diagnosis of an autoimmune neurologic disorder is aided by the detection of an objective neurologic deficit (usually subacute in onset with a fluctuating course), the presence of a neural autoantibody, and improvement in the neurologic status after a course of immunotherapy. Neural autoantibodies should raise concern for a paraneoplastic etiology and may inform a targeted oncologic evaluation (eg, N-methyl-D-aspartate [NMDA] receptor antibodies are associated with teratoma, antineuronal nuclear antibody type 1 [ANNA-1, or anti-Hu] are associated with small cell lung cancer). MRI, EEG, functional imaging, videotaped evaluations, and neuropsychological evaluations provide objective evidence of neurologic dysfunction by which the success of immunotherapy may be measured. Most treatment information emanates from retrospective case series and expert opinion. Nonetheless, early intervention may allow reversal of deficits in many patients and prevention of future disability.

  20. Porphyromonas gingivalis causing brain abscess in patient with recurrent periodontitis.

    Science.gov (United States)

    Rae Yoo, Jeong; Taek Heo, Sang; Kim, Miyeon; Lee, Chang Sub; Kim, Young Ree

    2016-06-01

    We report an extremely rare case of Porphyromonas gingivalis causing brain abscess in a patient with recurrent periodontitis. The patient presented with right-sided homonymous hemianopsia and right hemiparesis. Emergent surgical drainage was performed and antibiotics were administered. P. gingivalis was identified from the anaerobic culture of the abscess. The clinical course of the patient improved with full recovery of the neurologic deficit. Copyright © 2016 Elsevier Ltd. All rights reserved.

  1. Morbidity and Mortality Patterns among Neurological Patients in the ...

    African Journals Online (AJOL)

    ANNALS

    Abstract. Background/Objective: The morbidity and mortality of neurological patients managed in the intensive care unit reflect the causes of neurological disorders and the effectiveness of management. Method: The morbidity and mortality patterns of neurological patients admitted into the intensive care unit of the University ...

  2. Functional neurological disorders: imaging.

    Science.gov (United States)

    Voon, V

    2014-10-01

    Functional neurological disorders, also known as conversion disorder, are unexplained neurological symptoms. These symptoms are common and can be associated with significant consequences. This review covers the neuroimaging literature focusing on functional motor symptoms including motor functioning and upstream influences including self-monitoring and internal representations, voluntariness and arousal and trauma. Copyright © 2014. Published by Elsevier SAS.

  3. Neurological Complications of AIDS

    Science.gov (United States)

    ... the National Library of Medicine’s MedlinePlus Living with HIV/AIDS × What research is being done? The National Institute of Neurological ... the National Library of Medicine’s MedlinePlus Living with HIV/AIDS See More About Research The National Institute of Neurological Disorders and Stroke ( ...

  4. Neurological and robot-controlled induction of an apparition.

    Science.gov (United States)

    Blanke, Olaf; Pozeg, Polona; Hara, Masayuki; Heydrich, Lukas; Serino, Andrea; Yamamoto, Akio; Higuchi, Toshiro; Salomon, Roy; Seeck, Margitta; Landis, Theodor; Arzy, Shahar; Herbelin, Bruno; Bleuler, Hannes; Rognini, Giulio

    2014-11-17

    Tales of ghosts, wraiths, and other apparitions have been reported in virtually all cultures. The strange sensation that somebody is nearby when no one is actually present and cannot be seen (feeling of a presence, FoP) is a fascinating feat of the human mind, and this apparition is often covered in the literature of divinity, occultism, and fiction. Although it is described by neurological and psychiatric patients and healthy individuals in different situations, it is not yet understood how the phenomenon is triggered by the brain. Here, we performed lesion analysis in neurological FoP patients, supported by an analysis of associated neurological deficits. Our data show that the FoP is an illusory own-body perception with well-defined characteristics that is associated with sensorimotor loss and caused by lesions in three distinct brain regions: temporoparietal, insular, and especially frontoparietal cortex. Based on these data and recent experimental advances of multisensory own-body illusions, we designed a master-slave robotic system that generated specific sensorimotor conflicts and enabled us to induce the FoP and related illusory own-body perceptions experimentally in normal participants. These data show that the illusion of feeling another person nearby is caused by misperceiving the source and identity of sensorimotor (tactile, proprioceptive, and motor) signals of one's own body. Our findings reveal the neural mechanisms of the FoP, highlight the subtle balance of brain mechanisms that generate the experience of "self" and "other," and advance the understanding of the brain mechanisms responsible for hallucinations in schizophrenia. Copyright © 2014 Elsevier Ltd. All rights reserved.

  5. Neurological Findings in Myeloproliferative Neoplasms

    Directory of Open Access Journals (Sweden)

    Semra Paydas

    2013-04-01

    Full Text Available Myeloproliferative neoplasms (MPN arise from genetic deficiencies at the level of pluripotent stem cells. Each of these neoplasms is a clonal stem cell disorder with specific phenotypic, genetic and clinical properties. Age is one of the most important factors in the development of symptoms and complications associated with MPNs.High white blood cell counts in chronic myelocytic leukemia also known as leukocytosis may lead to central nervous system findings. Tumors developing outside the bone marrow named as extramedullary myeloid tumors (EMMT could be detected at the initial diagnosis or during the prognosis of the disease, which may cause neurological symptoms due to pressure of leukemic cell mass on various tissues along with spinal cord. Central nervous system involvement and thrombocytopenic hemorrhage may lead to diverse neurological symptoms and findings.Transient ischemic attack and thrombotic stroke are the most common symptoms in polycythemia vera. Besides thrombosis and hemorrage, transformation to acute leukemia can cause neurological symptoms and findings. Transient ischemic attack, thrombotic stroke and specifically hemorrage can give rise to neurological symptoms similar to MPN in essential thrombocytosis.Extramedullary hematopoiesis refers to hematopoietic centers arise in organ/tissues other than bone marrow in myelofibrosis. Extramedullar hematopoietic centers may cause intracranial involvement, spinal cord compression, seizures and hydrocephalia. Though rare, extramedullary hematopoiesis can be detected in cranial/spinal meninges, paraspinal tissue and intracerebral regions. Extramedullary hematopoiesis has been reported in peripheral neurons, choroid plexus, pituitary, orbits, orbital and lacrimal fossa and in sphenoidal sinuses. [Cukurova Med J 2013; 38(2.000: 157-169

  6. Aquatic rehabilitation for the treatment of neurological disorders.

    Science.gov (United States)

    Morris, D M

    1994-01-01

    Patients with neurological disorders present therapists with complex challenges for treatment, including weakness, hypertonicity, voluntary movement deficit, limited range of motion, sensory loss, incoordination, and postural instability. The presence of one or more of these impairments negatively influences these patients by contributing to problems in walking, transferring, and reaching. Aquatic rehabilitation offers a unique, versatile approach to the treatment of these disabilities. This article examines the problems encountered by patients with neurological disorders, general principles guiding neurotreatment, and aquatic neurorehabilitation approaches.

  7. Uroflowmetry in neurologically normal children with voiding disorders

    DEFF Research Database (Denmark)

    Jensen, K M; Nielsen, K.K.; Kristensen, E S

    1985-01-01

    of neurological deficits underwent a complete diagnostic program including intravenous urography, voiding cystography and cystoscopy as well as spontaneous uroflowmetry, cystometry-emg and pressure-flow-emg study. The incidence of dyssynergia was 22%. However, neither the flow curve pattern nor single flow...... variables were able to identify children with dyssynergia. Consequently uroflowmetry seems inefficient in the screening for dyssynergia in neurological normal children with voiding disorders in the absence of anatomical bladder outlet obstruction....

  8. Neurologic complications of vaccinations.

    Science.gov (United States)

    Miravalle, Augusto A; Schreiner, Teri

    2014-01-01

    This chapter reviews the most common neurologic disorders associated with common vaccines, evaluates the data linking the disorder with the vaccine, and discusses the potential mechanism of disease. A literature search was conducted in PubMed using a combination of the following terms: vaccines, vaccination, immunization, and neurologic complications. Data were also gathered from publications of the American Academy of Pediatrics Committee on Infectious Diseases, the World Health Organization, the US Centers for Disease Control and Prevention, and the Vaccine Adverse Event Reporting System. Neurologic complications of vaccination are rare. Many associations have been asserted without objective data to support a causal relationship. Rarely, patients with a neurologic complication will have a poor outcome. However, most patients recover fully from the neurologic complication. Vaccinations have altered the landscape of infectious disease. However, perception of risk associated with vaccinations has limited the success of disease eradication measures. Neurologic complications can be severe, and can provoke fear in potential vaccines. Evaluating whether there is causal link between neurologic disorders and vaccinations, not just temporal association, is critical to addressing public misperception of risk of vaccination. Among the vaccines available today, the cost-benefit analysis of vaccinations and complications strongly argues in favor of vaccination. © 2014 Elsevier B.V. All rights reserved.

  9. Neurology in Asia.

    Science.gov (United States)

    Tan, Chong-Tin

    2015-02-10

    Asia is important as it accounts for more than half of the world population. The majority of Asian countries fall into the middle income category. As for cultural traditions, Asia is highly varied, with many languages spoken. The pattern of neurologic diseases in Asia is largely similar to the West, with some disease features being specific to Asia. Whereas Asia constitutes 60% of the world's population, it contains only 20% of the world's neurologists. This disparity is particularly evident in South and South East Asia. As for neurologic care, it is highly variable depending on whether it is an urban or rural setting, the level of economic development, and the system of health care financing. To help remedy the shortage of neurologists, most counties with larger populations have established training programs in neurology. These programs are diverse, with many areas of concern. There are regional organizations serving as a vehicle for networking in neurology and various subspecialties, as well as an official journal (Neurology Asia). The Asian Epilepsy Academy, with its emphasis on workshops in various locations, EEG certification examination, and fellowships, may provide a template of effective regional networking for improving neurology care in the region. © 2015 American Academy of Neurology.

  10. Neurology and international organizations.

    Science.gov (United States)

    Mateen, Farrah J

    2013-07-23

    A growing number of international stakeholders are engaged with neurologic diseases. This article provides a brief overview of important international stakeholders in the practice of neurology, including global disease-specific programs, United Nations agencies, governmental agencies with international influence, nongovernmental organizations, international professional organizations, large private donors, private-public partnerships, commercial interests, armed forces, and universities and colleges. The continued engagement of neurologists is essential for the growing number of international organizations that can and should incorporate neurologic disease into their global agendas.

  11. Neurological abnormalities predict disability

    DEFF Research Database (Denmark)

    Poggesi, Anna; Gouw, Alida; van der Flier, Wiesje

    2014-01-01

    To investigate the role of neurological abnormalities and magnetic resonance imaging (MRI) lesions in predicting global functional decline in a cohort of initially independent-living elderly subjects. The Leukoaraiosis And DISability (LADIS) Study, involving 11 European centres, was primarily aimed...... at evaluating age-related white matter changes (ARWMC) as an independent predictor of the transition to disability (according to Instrumental Activities of Daily Living scale) or death in independent elderly subjects that were followed up for 3 years. At baseline, a standardized neurological examination.......0 years, 45 % males), 327 (51.7 %) presented at the initial visit with ≥1 neurological abnormality and 242 (38 %) reached the main study outcome. Cox regression analyses, adjusting for MRI features and other determinants of functional decline, showed that the baseline presence of any neurological...

  12. Oculomotor Deficits after Chemotherapy in Childhood.

    Directory of Open Access Journals (Sweden)

    Einar-Jón Einarsson

    Full Text Available Advances in the diagnosis and treatment of pediatric malignancies have substantially increased the number of childhood cancer survivors. However, reports suggest that some of the chemotherapy agents used for treatment can cross the blood brain barrier which may lead to a host of neurological symptoms including oculomotor dysfunction. Whether chemotherapy at young age causes oculomotor dysfunction later in life is unknown. Oculomotor performance was assessed with traditional and novel methods in 23 adults (mean age 25.3 years, treatment age 10.2 years treated with chemotherapy for a solid malignant tumor not affecting the central nervous system. Their results were compared to those from 25 healthy, age-matched controls (mean age 25.1 years. Correlation analysis was performed between the subjective symptoms reported by the chemotherapy treated subjects (CTS and oculomotor performance. In CTS, the temporal control of the smooth pursuit velocity (velocity accuracy was markedly poorer (p<0.001 and the saccades had disproportionally shorter amplitude than normal for the associated saccade peak velocity (main sequence (p = 0.004, whereas smooth pursuit and saccade onset times were shorter (p = 0.004 in CTS compared with controls. The CTS treated before 12 years of age manifested more severe oculomotor deficits. CTS frequently reported subjective symptoms of visual disturbances (70%, unsteadiness, light-headedness and that things around them were spinning or moving (87%. Several subjective symptoms were significantly related to deficits in oculomotor performance. To conclude, chemotherapy in childhood or adolescence can result in severe oculomotor dysfunctions in adulthood. The revealed oculomotor dysfunctions were significantly related to the subjects' self-perception of visual disturbances, dizziness, light-headedness and sensing unsteadiness. Assessments of oculomotor function may, thus, offer an objective method to track and rate the level of

  13. Neurological diseases and pain

    OpenAIRE

    Borsook, David

    2011-01-01

    Chronic pain is a frequent component of many neurological disorders, affecting 20–40% of patients for many primary neurological diseases. These diseases result from a wide range of pathophysiologies including traumatic injury to the central nervous system, neurodegeneration and neuroinflammation, and exploring the aetiology of pain in these disorders is an opportunity to achieve new insight into pain processing. Whether pain originates in the central or peripheral nervous system, it frequentl...

  14. Wikipedia and neurological disorders.

    Science.gov (United States)

    Brigo, Francesco; Igwe, Stanley C; Nardone, Raffaele; Lochner, Piergiorgio; Tezzon, Frediano; Otte, Willem M

    2015-07-01

    Our aim was to evaluate Wikipedia page visits in relation to the most common neurological disorders by determining which factors are related to peaks in Wikipedia searches for these conditions. Millions of people worldwide use the internet daily as a source of health information. Wikipedia is a popular free online encyclopedia used by patients and physicians to search for health-related information. The following Wikipedia articles were considered: Alzheimer's disease; Amyotrophic lateral sclerosis; Dementia; Epilepsy; Epileptic seizure; Migraine; Multiple sclerosis; Parkinson's disease; Stroke; Traumatic brain injury. We analyzed information regarding the total article views for 90 days and the rank of these articles among all those available in Wikipedia. We determined the highest search volume peaks to identify possible relation with online news headlines. No relation between incidence or prevalence of neurological disorders and the search volume for the related articles was found. Seven out of 10 neurological conditions showed relations in search volume peaks and news headlines. Six out of these seven peaks were related to news about famous people suffering from neurological disorders, especially those from showbusiness. Identification of discrepancies between disease burden and health seeking behavior on Wikipedia is useful in the planning of public health campaigns. Celebrities who publicly announce their neurological diagnosis might effectively promote awareness programs, increase public knowledge and reduce stigma related to diagnoses of neurological disorders. Copyright © 2015 Elsevier Ltd. All rights reserved.

  15. Neuritin reverses deficits in murine novel object associative recognition memory caused by exposure to extremely low-frequency (50 Hz) electromagnetic fields

    Science.gov (United States)

    Zhao, Qian-Ru; Lu, Jun-Mei; Yao, Jin-Jing; Zhang, Zheng-Yu; Ling, Chen; Mei, Yan-Ai

    2015-01-01

    Animal studies have shown that electromagnetic field exposure may interfere with the activity of brain cells, thereby generating behavioral and cognitive disturbances. However, the underlying mechanisms and possible preventions are still unknown. In this study, we used a mouse model to examine the effects of exposure to extremely low-frequency (50 Hz) electromagnetic fields (ELF MFs) on a recognition memory task and morphological changes of hippocampal neurons. The data showed that ELF MFs exposure (1 mT, 12 h/day) induced a time-dependent deficit in novel object associative recognition memory and also decreased hippocampal dendritic spine density. This effect was observed without corresponding changes in spontaneous locomotor activity and was transient, which has only been seen after exposing mice to ELF MFs for 7-10 days. The over-expression of hippocampal neuritin, an activity-dependent neurotrophic factor, using an adeno-associated virus (AAV) vector significantly increased the neuritin level and dendritic spine density. This increase was paralleled with ELF MFs exposure-induced deficits in recognition memory and reductions of dendritic spine density. Collectively, our study provides evidence for the association between ELF MFs exposure, impairment of recognition memory, and resulting changes in hippocampal dendritic spine density. Neuritin prevented this ELF MFs-exposure-induced effect by increasing the hippocampal spine density. PMID:26138388

  16. Neurological manifestations of atypical celiac disease in childhood.

    Science.gov (United States)

    Sel, Çiğdem Genç; Aksoy, Erhan; Aksoy, Ayşe; Yüksel, Deniz; Özbay, Ferda

    2017-09-01

    Various typical and atypical neurological manifestations can be seen as the initial symptoms of celiac disease (CD). We suggest that gluten toxicity is the most suspicious triggering risk factor for probable pathophysiological pathways of neurological involvement in atypical CD. The medical charts of 117 patients diagnosed with atypical CD were retrieved from a tertiary center in Ankara, Turkey. Eight patients reported as having neurologic manifestations as initiating symptoms were evaluated in detail. The initial neurological manifestations of CD in our study included atypical absence, which was reported first in this study, generalized tonic-clonic seizures, complex partial seizures, severe axial hypotonia and down phenotype, multifocal leukoencephalopathy, mild optic neuritis, attention deficit hyperactivity disorder, and short duration headaches. Seizures mostly emphasizing atypical absence could be the initial presentation manifestation of CD, first described in this literature. Gluten toxicity could be one of the most powerful triggering factors for developing epilepsy in CD. Learning disorders such as attention deficit hyperactivity disorder, short duration headaches, mild optic neuritis, encephalopathy, and DS could also be the initial neurological manifestations of atypical CD. A gluten-restricted diet may improve neurological complaints, epileptic discharges, and neuropsychiatric symptoms. All we found may be a small part of the full range of neurological disorders of unknown origin related to CD. Clinical suspicion should be the rule for accurate diagnosis of the disease.

  17. [Gait disorders due to neurological conditions

    NARCIS (Netherlands)

    Warrenburg, B.P.C. van de; Snijders, A.H.; Munneke, M.; Bloem, B.R.

    2007-01-01

    Gait disorders are seen frequently and often have a neurological cause. The clinical management of patients presenting with a gait disorder is often complicated due to the large number of diseases that can cause a gait disorder and to the difficulties in interpreting a specific gait disorder

  18. Cardiac myxoma causing acute ischemic stroke in a pediatric patient and a review of literature.

    Science.gov (United States)

    Fuchs, Jennifer; Leszczyszyn, David; Mathew, Don

    2014-05-01

    Ischemic stroke in the pediatric population is a rare occurrence, and its possible causes span a wide differential that includes atrial myxomas. Myxomas are friable cardiac tumors that produce "showers" of emboli resulting in transient neurological deficits, cutaneous eruptions, and ophthalmologic deficits. We present an 11-year-old boy with a months-long history of an intermittent spotted "rash" who presented with acute ischemic stroke caused by a left atrial myxoma. We also review clinical features in all 16 other cases of cardiac myxoma causing pediatric stroke reported in the literature. Our case, along with the review of the literature, highlights the fact that myxomas often initially present as stroke with acute hemiplegia and transient cutaneous eruptions due to fragmentation of the tumor. Cardiac myxoma should be considered in any child presenting with ischemic stroke, and transient skin findings may provide an important diagnostic clue prior to onset of neurological symptoms. Copyright © 2014 Elsevier Inc. All rights reserved.

  19. Minor neurological dysfunction and cognition in 9-year-olds born at term

    NARCIS (Netherlands)

    Kikkert, Hedwig K; de Jong, Corina; Hadders-Algra, Mijna

    BACKGROUND: In children with developmental disorders, motor problems often co-occur with cognitive difficulties. Associations between specific cognitive deficits underlying learning problems and minor neurological dysfunction (MND) are still unknown. AIMS: To assess associations between specific

  20. Relationship of mechanical impact magnitude to neurologic dysfunction severity in a rat traumatic brain injury model.

    Directory of Open Access Journals (Sweden)

    Tsung-Hsun Hsieh

    Full Text Available Traumatic brain injury (TBI is a major brain injury type commonly caused by traffic accidents, falls, violence, or sports injuries. To obtain mechanistic insights about TBI, experimental animal models such as weight-drop-induced TBI in rats have been developed to mimic closed-head injury in humans. However, the relationship between the mechanical impact level and neurological severity following weight-drop-induced TBI remains uncertain. In this study, we comprehensively investigated the relationship between physical impact and graded severity at various weight-drop heights.The acceleration, impact force, and displacement during the impact were accurately measured using an accelerometer, a pressure sensor, and a high-speed camera, respectively. In addition, the longitudinal changes in neurological deficits and balance function were investigated at 1, 4, and 7 days post TBI lesion. The inflammatory expression markers tested by Western blot analysis, including glial fibrillary acidic protein, beta-amyloid precursor protein, and bone marrow tyrosine kinase gene in chromosome X, in the frontal cortex, hippocampus, and corpus callosum were investigated at 1 and 7 days post-lesion.Gradations in impact pressure produced progressive degrees of injury severity in the neurological score and balance function. Western blot analysis demonstrated that all inflammatory expression markers were increased at 1 and 7 days post-impact injury when compared to the sham control rats. The severity of neurologic dysfunction and induction in inflammatory markers strongly correlated with the graded mechanical impact levels.We conclude that the weight-drop-induced TBI model can produce graded brain injury and induction of neurobehavioral deficits and may have translational relevance to developing therapeutic strategies for TBI.

  1. [Neurology and literature].

    Science.gov (United States)

    Iniesta, I

    2010-10-01

    Literature complements medical literature in the academic and clinical development of neurologists. The present article explores the contributions of writers of fiction on neurology. Literary works of fiction with particular reference to neurology. A symbiosis between writers of fiction and doctors has been well recognised. From Shakespeare to Cervantes by way of Dickens and Cela to writer - physicians such as Anton Chekhov or António Lobo Antunes have contributed through their medically informed literature to the better understanding of neurology. Some writers like Dostoevsky, Machado de Assis and Margiad Evans have written about their own experiences with disease thus bringing new insights to medicine. Furthermore, some neurological disorders have been largely based on literary descriptions. For instance, Dostoevsky's epilepsy has been retrospectively analysed by famous neurologists including Freud, Alajouanine or Gastaut, whilst his writings and biography have prompted others like Waxman and Geschwind to describe typical behavioural changes in temporal lobe epilepsy, finding their source of inspiration in Dostoevsky. Likewise, Cirignotta et al have named an unusual type of seizure after the Russian novelist. Inspired by Lewis Carroll, Todd introduced the term Alice in Wonderland Syndrome to refer to visual distortions generally associated with migraine. Writers of fiction offer a humanised perception of disease by contributing new insights into the clinical history, informing about the subjective experience of the illness and helping to eradicate the stigma associated to neurological disorders.

  2. Suicide in Neurologic Illness.

    Science.gov (United States)

    Arciniegas, David B.; Anderson, C. Alan

    2002-11-01

    The risk of attempted or completed suicide is increased in patients with migraine with aura, epilepsy, stroke, multiple sclerosis, traumatic brain injury, and Huntington's disease. Contrary to the general perception that the risk of suicide among patients with Alzheimer's disease and other dementing conditions is low, several reports suggest that the risk of suicide in these patients increases relative to the general population. Some patients at risk for neurologic disorders are also at increased risk for suicide; in particular, the risk of suicide is increased among persons at risk for Huntington's disease, independent of the presence or absence of the Huntington's gene mutation. The risk of attempted or completed suicide in neurologic illness is strongly associated with depression, feelings of hopelessness or helplessness, and social isolation. Additional suicide risk factors in persons with neurologic illness include cognitive impairment, relatively younger age (under 60 years), moderate physical disability, recent onset or change in illness, a lack of future plans or perceived meaning in life, recent losses (personal, occupational, or financial), and prior history of psychiatric illness or suicidal behavior. Substance dependence, psychotic disorders, anxiety disorders, and some personality disorders (eg, borderline personality disorder) may also contribute to increased risk of suicide among persons with neurologic illnesses. Identification and aggressive treatment of psychiatric problems, especially depression, as well as reduction of modifiable suicide risk factors among patients with neurologic illness is needed to reduce the risk of attempted and completed suicide in this population.

  3. Neurological manifestations of dengue viral infection

    Directory of Open Access Journals (Sweden)

    Carod-Artal FJ

    2014-10-01

    Full Text Available Francisco Javier Carod-Artal1,21Neurology Department, Raigmore hospital, Inverness, UK; 2Universitat Internacional de Catalunya (UIC, Barcelona, Spain Abstract: Dengue is the most common mosquito-borne viral infection worldwide. There is increased evidence for dengue virus neurotropism, and neurological manifestations could make part of the clinical picture of dengue virus infection in at least 0.5%–7.4% of symptomatic cases. Neurological complications have been classified into dengue virus encephalopathy, dengue virus encephalitis, immune-mediated syndromes (acute disseminated encephalomyelitis, myelitis, Guillain–Barré syndrome, neuritis brachialis, acute cerebellitis, and others, neuromuscular complications (hypokalemic paralysis, transient benign muscle dysfunction and myositis, and dengue-associated stroke. Common neuro-ophthalmic complications are maculopathy and retinal vasculopathy. Pathogenic mechanisms include systemic complications and metabolic disturbances resulting in encephalopathy, direct effect of the virus provoking encephalitis, and postinfectious immune mechanisms causing immune-mediated syndromes. Dengue viruses should be considered as a cause of neurological disorders in endemic regions. Standardized case definitions for specific neurological complications are still needed. Keywords: encephalitis, encephalopathy, dengue fever, neurological complications

  4. Surgically acquired deficits and diffusion weighted MRI changes after glioma resection--a matched case-control study with blinded neuroradiological assessment.

    Directory of Open Access Journals (Sweden)

    Asgeir S Jakola

    Full Text Available Acquired deficits following glioma resection may not only occur due to accidental resection of normal brain tissue. The possible importance of ischemic injuries in causing neurological deficits after brain tumor surgery is not much studied. We aimed to study the volume and frequency of early postoperative circulatory changes (i.e. infarctions detected by diffusion weighted resonance imaging (DWI in patients with surgically acquired neurological deficits compared to controls.We designed a 1 ∶ 1 matched case-control study in patients with diffuse gliomas (WHO grade II-IV operated with 3D ultrasound guided resection. 42 consecutive patients with acquired postoperative dysphasia and/or new motor deficits were compared to 42 matched controls without acquired deficits. Controls were matched with respect to histopathology, preoperative tumor volumes, and eloquence of location. Two independent radiologists blinded for clinical status assessed the postoperative DWI findings.Postoperative peri-tumoral infarctions were more often seen in patients with acquired deficits (63% versus 41%, p = 0.046 and volumes of DWI abnormalities were larger in cases than in controls with median 1.08 cm3 (IQR 0-2.39 versus median 0 cm3 (IQR 0-1.67, p = 0.047. Inter-rater agreement was substantial (67/82, κ = 0.64, p<0.001 for diagnosing radiological significant DWI abnormalities.Peri-tumoral infarctions were more common and were larger in patients with acquired deficits after glioma surgery compared to glioma patients without deficits when assessed by early postoperative DWI. Infarctions may be a frequent and underestimated cause of acquired deficits after glioma resection. DWI changes may be an attractive endpoint in brain tumor surgery with both good inter-rater reliability among radiologists and clinical relevance.

  5. Surgically acquired deficits and diffusion weighted MRI changes after glioma resection--a matched case-control study with blinded neuroradiological assessment.

    Science.gov (United States)

    Jakola, Asgeir S; Berntsen, Erik M; Christensen, Pål; Gulati, Sasha; Unsgård, Geirmund; Kvistad, Kjell A; Solheim, Ole

    2014-01-01

    Acquired deficits following glioma resection may not only occur due to accidental resection of normal brain tissue. The possible importance of ischemic injuries in causing neurological deficits after brain tumor surgery is not much studied. We aimed to study the volume and frequency of early postoperative circulatory changes (i.e. infarctions) detected by diffusion weighted resonance imaging (DWI) in patients with surgically acquired neurological deficits compared to controls. We designed a 1 ∶ 1 matched case-control study in patients with diffuse gliomas (WHO grade II-IV) operated with 3D ultrasound guided resection. 42 consecutive patients with acquired postoperative dysphasia and/or new motor deficits were compared to 42 matched controls without acquired deficits. Controls were matched with respect to histopathology, preoperative tumor volumes, and eloquence of location. Two independent radiologists blinded for clinical status assessed the postoperative DWI findings. Postoperative peri-tumoral infarctions were more often seen in patients with acquired deficits (63% versus 41%, p = 0.046) and volumes of DWI abnormalities were larger in cases than in controls with median 1.08 cm3 (IQR 0-2.39) versus median 0 cm3 (IQR 0-1.67), p = 0.047. Inter-rater agreement was substantial (67/82, κ = 0.64, p<0.001) for diagnosing radiological significant DWI abnormalities. Peri-tumoral infarctions were more common and were larger in patients with acquired deficits after glioma surgery compared to glioma patients without deficits when assessed by early postoperative DWI. Infarctions may be a frequent and underestimated cause of acquired deficits after glioma resection. DWI changes may be an attractive endpoint in brain tumor surgery with both good inter-rater reliability among radiologists and clinical relevance.

  6. Surgically Acquired Deficits and Diffusion Weighted MRI Changes after Glioma Resection - A Matched Case-Control Study with Blinded Neuroradiological Assessment

    Science.gov (United States)

    Jakola, Asgeir S.; Berntsen, Erik M.; Christensen, Pål; Gulati, Sasha; Unsgård, Geirmund; Kvistad, Kjell A.; Solheim, Ole

    2014-01-01

    Background Acquired deficits following glioma resection may not only occur due to accidental resection of normal brain tissue. The possible importance of ischemic injuries in causing neurological deficits after brain tumor surgery is not much studied. We aimed to study the volume and frequency of early postoperative circulatory changes (i.e. infarctions) detected by diffusion weighted resonance imaging (DWI) in patients with surgically acquired neurological deficits compared to controls. Methods We designed a 1∶1 matched case-control study in patients with diffuse gliomas (WHO grade II–IV) operated with 3D ultrasound guided resection. 42 consecutive patients with acquired postoperative dysphasia and/or new motor deficits were compared to 42 matched controls without acquired deficits. Controls were matched with respect to histopathology, preoperative tumor volumes, and eloquence of location. Two independent radiologists blinded for clinical status assessed the postoperative DWI findings. Results Postoperative peri-tumoral infarctions were more often seen in patients with acquired deficits (63% versus 41%, p = 0.046) and volumes of DWI abnormalities were larger in cases than in controls with median 1.08 cm3 (IQR 0–2.39) versus median 0 cm3 (IQR 0–1.67), p = 0.047. Inter-rater agreement was substantial (67/82, κ = 0.64, p<0.001) for diagnosing radiological significant DWI abnormalities. Conclusion Peri-tumoral infarctions were more common and were larger in patients with acquired deficits after glioma surgery compared to glioma patients without deficits when assessed by early postoperative DWI. Infarctions may be a frequent and underestimated cause of acquired deficits after glioma resection. DWI changes may be an attractive endpoint in brain tumor surgery with both good inter-rater reliability among radiologists and clinical relevance. PMID:24992634

  7. The Clinical Spectrum Of Paediatric Neurological Disorders In ...

    African Journals Online (AJOL)

    The predominant neurologic morbidities included: cerebral palsy (42.4%), epilepsy (27.8%), febrile seizure (6.5%), mental retardation(6.2%), microcephaly (5.6%), behavioral problems (5.6%), poliomyelitis (4.5%), hydrocephalus (4.2%), visual impairment (2.8%), down syndrome (1.7%), and attention deficit hyperactivity ...

  8. [Neurological sleep disorders].

    Science.gov (United States)

    Khatami, Ramin

    2014-11-01

    Neurological sleep disorders are common in the general population and may have a strong impact on quality of life. General practitioners play a key role in recognizing and managing sleep disorders in the general population. They should therefore be familiar with the most important neurological sleep disorders. This review provides a comprehensive overview of the most prevalent and important neurological sleep disorders, including Restless legs syndrome (with and without periodic limb movements in sleep), narcolepsy, NREM- and REM-sleep parasomnias and the complex relationship between sleep and epilepsies. Although narcolepsy is considered as a rare disease, recent discoveries in narcolepsy research provided insight in the function of brain circuitries involved in sleep wake regulation. REM sleep behavioral parasomnia (RBD) is increasingly recognized to represent an early manifestation of neurodegenerative disorders, in particular evolving synucleinopathies. Early diagnosis may thus open new perspectives for developing novel treatment options by targeting neuroprotective substances.

  9. The neurological disease ontology.

    Science.gov (United States)

    Jensen, Mark; Cox, Alexander P; Chaudhry, Naveed; Ng, Marcus; Sule, Donat; Duncan, William; Ray, Patrick; Weinstock-Guttman, Bianca; Smith, Barry; Ruttenberg, Alan; Szigeti, Kinga; Diehl, Alexander D

    2013-12-06

    We are developing the Neurological Disease Ontology (ND) to provide a framework to enable representation of aspects of neurological diseases that are relevant to their treatment and study. ND is a representational tool that addresses the need for unambiguous annotation, storage, and retrieval of data associated with the treatment and study of neurological diseases. ND is being developed in compliance with the Open Biomedical Ontology Foundry principles and builds upon the paradigm established by the Ontology for General Medical Science (OGMS) for the representation of entities in the domain of disease and medical practice. Initial applications of ND will include the annotation and analysis of large data sets and patient records for Alzheimer's disease, multiple sclerosis, and stroke. ND is implemented in OWL 2 and currently has more than 450 terms that refer to and describe various aspects of neurological diseases. ND directly imports the development version of OGMS, which uses BFO 2. Term development in ND has primarily extended the OGMS terms 'disease', 'diagnosis', 'disease course', and 'disorder'. We have imported and utilize over 700 classes from related ontology efforts including the Foundational Model of Anatomy, Ontology for Biomedical Investigations, and Protein Ontology. ND terms are annotated with ontology metadata such as a label (term name), term editors, textual definition, definition source, curation status, and alternative terms (synonyms). Many terms have logical definitions in addition to these annotations. Current development has focused on the establishment of the upper-level structure of the ND hierarchy, as well as on the representation of Alzheimer's disease, multiple sclerosis, and stroke. The ontology is available as a version-controlled file at http://code.google.com/p/neurological-disease-ontology along with a discussion list and an issue tracker. ND seeks to provide a formal foundation for the representation of clinical and research data

  10. Neurologic Diseases and Sleep.

    Science.gov (United States)

    Barone, Daniel A; Chokroverty, Sudansu

    2017-03-01

    Sleep disorders and neurologic illness are common and burdensome in their own right; when combined, they can have tremendous negative impact at an individual level as well as societally. The socioeconomic burden of sleep disorders and neurologic illness can be identified, but the real cost of these conditions lies far beyond the financial realm. There is an urgent need for comprehensive care and support systems to help with the burden of disease. Further research in improving patient outcomes in those who suffer with these conditions will help patients and their families, and society in general. Copyright © 2016 Elsevier Inc. All rights reserved.

  11. Neurologic Complications in Pregnancy.

    Science.gov (United States)

    Cuero, Mauricio Ruiz; Varelas, Panayiotis N

    2016-01-01

    Pregnant women are subject to the same complications as the general population, as well to specific neurologic complications associated with pregnancy, such as preeclampsia or eclampsia. The hormonal and physiologic changes during pregnancy lead to altered incidences of these complications, which usually present during the late period of pregnancy, labor, or the puerperium. In addition, the treatment of these conditions is different from that of nonpregnant women, because special attention is paid to avoid any abnormalities or death of the fetus. This article discusses the most common of these neurologic complications. Copyright © 2016 Elsevier Inc. All rights reserved.

  12. The neurology literature 2016.

    Science.gov (United States)

    Khoujah, Danya; Chang, Wan-Tsu W; Abraham, Michael K

    2017-09-06

    Emergency neurology is a complex and rapidly changing field. Its evolution can be attributed in part to increased imaging options, debates about optimal treatment, and simply the growth of emergency medicine as a specialty. Every year, a number of articles published in emergency medicine or other specialty journals should become familiar to the emergency physician. This review summarizes neurology articles published in 2016, which the authors consider crucial to the practice of emergency medicine. The articles are categorized according to disease process, with the understanding that there can be significant overlap among articles. Copyright © 2017 Elsevier Inc. All rights reserved.

  13. Frequency of neurological deficits in Sudanese lepromatic patients ...

    African Journals Online (AJOL)

    Leprosy has been a major burden on humanity over thousands of years. Perhaps no other disease in the history of mankind has been associated with such a strong social stigma as leprosy. Failure in early detection often leads to severe disability in spite of eradication of mycobacteria at a later date. Untreated the disease is ...

  14. Low intelligence but not attention deficit hyperactivity disorder is associated with resistance to thyroid hormone caused by mutation R316H in the thyroid hormone receptor {beta} gene

    Energy Technology Data Exchange (ETDEWEB)

    Weiss, R.E.; Stein, M.A.; Chyna, B.; Phillips, W.; O`Brien, T.; Gutermuth, L.; Refetoff, S. [Univ. of Chicago, IL (United States); Duck, S.C. [Northwestern Univ. Medical School/Evanston Hospital, Evanston, IL (United States)

    1994-06-01

    Resistance to thyroid hormone (RTH) is a syndrome of reduced responsiveness of tissues to thyroid hormone. The clinical manifestations are variable and 46-50% of children with RTH have attention deficit hyperactivity disorder (ADD). The authors present a new family with RTH (F120) found to have a mutation R316H in the thyroid hormone receptor {beta} (TR{beta}) gene identical for that reported in an unrelated family. Assignment of the mutant allele and haplotyping based on CA repeat polymorphism were done on 16 family members. Semistructured diagnostic interviews and psychometric testing were used to determine the psychiatric diagnosis of 12 family members by examiners blinded to the genotype. Three subjects were identified to have the R316H allele as well as mildly elevated free T{sub 4} index (168 {+-} 12; normal range 77-135) and nonsuppressed TSH (4.1 {+-} 1.7 mU/L). Only 2 of the subjects with RTH were found to have ADD, while one family member homozygous for the wild type TR{beta} and normal thyroid function tests also had ADD. Unaffected family members had higher full scale intelligence quotients ({vert_bar}Q) (93 {+-} 7) than any of the 3 family members with RTH (77 {+-} 5, p = 0.006). These data do not support the genetic linkage of ADD and RTH, but do suggest that RTH is associated with lower IQ scores that may confer a high likelihood of exhibiting ADD symptoms. 20 refs., 2 figs., 2 tabs.

  15. Disrupted-in-schizophrenia1 (DISC1) L100P mutation alters synaptic transmission and plasticity in the hippocampus and causes recognition memory deficits.

    Science.gov (United States)

    Cui, Lin; Sun, Wei; Yu, Ming; Li, Nan; Guo, Li; Gu, Huating; Zhou, Yu

    2016-10-12

    Disrupted-in-schizophrenia 1(DISC1) is a promising candidate susceptibility gene for a spectrum of psychiatric illnesses that share cognitive impairments in common, including schizophrenia, bipolar disorder and major depression. Here we report that DISC1 L100P homozygous mutant shows normal anxiety- and depression-like behavior, but impaired object recognition which is prevented by administration of atypical antipsychotic drug clozapine. Ca2+ image analysis reveals suppression of glutamate-evoked elevation of cytoplasmic [Ca2+] in L100P hippocampal slices. L100P mutant slices exhibit decreased excitatory synaptic transmission (sEPSCs and mEPSCs) in dentate gyrus (DG) and impaired long-term potentiation in the CA1 region of the hippocampus. L100P mutation does not alter proteins expression of the excitatory synaptic markers, PSD95 and synapsin-1; neither does it changes dendrites morphology of primary cultured hippocampal neurons. Our findings suggest that the existence of abnormal synaptic transmission and plasticity in hippocampal network may disrupt declarative information processing and contribute to recognition deficits in DISC1 L100P mutant mice.

  16. PYRITINOL USAGE IN PEDIATRIC NEUROLOGY

    Directory of Open Access Journals (Sweden)

    N. N. Zavadenko

    2013-01-01

    Full Text Available Treatment of developmental disorders, correction of learning disabilities and behavioral problems in children should be prompt, complex and include pharmacotherapy with nootropic agents. The results of recent studies shown in this review proved effectiveness of pharmacotherapy with pyritinol in children with perinatal injury of central nervous system and its consequences, psychomotor and speech development delay, dyslexia, attention deficit/hyperactivity disorder, cognitive disorders and learning disabilities (including manifestations of epilepsy, chronic tic disorders and Tourette syndrome. Due to its ability to optimize metabolic processes in central nervous system, pyritinol is used in treatment of vegetative dysfunction in children and adolescents, especially associated with asthenical manifestations, as well as in complex therapy of exertion headache and migraine. The drug is effective in treatment of cognitive disorders in children and adolescents with epilepsy, pyritinol was administered without changing of the basic anticonvulsive therapy and no deterioration (increase of severity of seizures or intensity of epileptiform activity on electroencephalogramms was observed. Significant nootropic effect of pyritinol, including neurometabolic, neuroprotective, neurodynamic and other mechanisms, in association with safety and rare side effects of this drug determines its wide usage in pediatric neurology.

  17. Neurological aspects of eclampsia

    Directory of Open Access Journals (Sweden)

    Jovanović Dejana

    2003-01-01

    Full Text Available The difficult types of preeclampsia and eclampsia are presented with the neurological symptoms. The break of cerebral autoregulation mechanism plays the most important role in pathogenesis of cerebral vasospasm. Nevertheless eclampsia isn’t just an ordinary hypertensive encephalopathy because other pathogenic mechanisms are involved in its appearance. The main neuropathologic changes are multifocal vasogenic edema, perivascular multiple microinfarctions and petechial hemorrhages. Neurological clinical manifestations are convulsions, headache, visual disturbances and rarely other discrete focal neurological symptoms. Eclampsia is a high-risk factor for onset of hemorrhagic or ischemic stroke. This is a reason why neurological diagnostic tests are sometimes needed. The method of choice for evaluation of complicated eclampsia is computerized brain topography that shows multiple areas of hypodensity in occipitoparietal regions. These changes are focal vasogenic cerebral edema. For differential diagnosis of eclampsia and stroke other diagnostic methods can be used - fundoscopic exam, magnetic resonance brain imaging, cerebral angiography and cerebrospinal fluid exam. The therapy of eclampsia considers using of magnesium sulfate, antihypertensive, anticonvulsive and antiedematous drugs.

  18. Wikipedia and neurological disorders

    NARCIS (Netherlands)

    Brigo, Francesco; Igwe, Stanley C.; Nardone, Raffaele; Lochner, Piergiorgio; Tezzon, Frediano; Otte, WM

    2015-01-01

    Our aim was to evaluate Wikipedia page visits in relation to the most common neurological disorders by determining which factors are related to peaks in Wikipedia searches for these conditions. Millions of people worldwide use the internet daily as a source of health information. Wikipedia is a

  19. Astroglia in neurological diseases

    Czech Academy of Sciences Publication Activity Database

    Verkhratsky, Alexei; Rodríguez Arellano, Jose Julio; Parpura, V.

    2013-01-01

    Roč. 8, č. 2 (2013), s. 149-158 ISSN 1479-6708 R&D Projects: GA ČR(CZ) GAP304/11/0184; GA ČR GA309/09/1696 Institutional support: RVO:68378041 Keywords : amyotrophic lateral sclerosis * Alzheimer's disease * Alexander disease Subject RIV: FH - Neurology

  20. A Single Amphetamine Infusion Reverses Deficits in Dopamine Nerve-Terminal Function Caused by a History of Cocaine Self-Administration

    Science.gov (United States)

    Ferris, Mark J; Calipari, Erin S; Rose, Jamie H; Siciliano, Cody A; Sun, Haiguo; Chen, Rong; Jones, Sara R

    2015-01-01

    There are ∼1.6 million people who meet the criteria for cocaine addiction in the United States, and there are currently no FDA-approved pharmacotherapies. Amphetamine-based dopamine-releasing drugs have shown efficacy in reducing the motivation to self-administer cocaine and reducing intake in animals and humans. It is hypothesized that amphetamine acts as a replacement therapy for cocaine through elevation of extracellular dopamine levels. Using voltammetry in brain slices, we tested the ability of a single amphetamine infusion in vivo to modulate dopamine release, uptake kinetics, and cocaine potency in cocaine-naive animals and after a history of cocaine self-administration (1.5 mg/kg/infusion, fixed-ratio 1, 40 injections/day × 5 days). Dopamine kinetics were measured 1 and 24 h after amphetamine infusion (0.56 mg/kg, i.v.). Following cocaine self-administration, dopamine release, maximal rate of uptake (Vmax), and membrane-associated dopamine transporter (DAT) levels were reduced, and the DAT was less sensitive to cocaine. A single amphetamine infusion reduced Vmax and membrane DAT levels in cocaine-naive animals, but fully restored all aspects of dopamine terminal function in cocaine self-administering animals. Here, for the first time, we demonstrate pharmacologically induced, immediate rescue of deficits in dopamine nerve-terminal function in animals with a history of high-dose cocaine self-administration. This observation supports the notion that the DAT expression and function can be modulated on a rapid timescale and also suggests that the pharmacotherapeutic actions of amphetamine for cocaine addiction go beyond that of replacement therapy. PMID:25689882

  1. Neurological Effects of Acute Carbon Monoxide Poisoning in Children

    Directory of Open Access Journals (Sweden)

    Coskun YARAR

    2009-11-01

    Full Text Available Carbon monoxide poisoning (COP is one of the most common causes of mortality and morbidity due to poisoning in all over the world. Although the incidence of COP has not been known exactly in the childhood, almost one-third of CO exposures occurred in children. The data regarding COP in children are inconclusive. Children may be more vulnerable to CO exposure than adults as a result of their high respiration and metabolic rates, high oxygen metabolism, and immature central nervous system. Recent researches proposed new theories about neurological effects of CO toxicity. The clinical presentations associated acute COP may be various and nonspecific. Unrecognized CO exposure may lead to significant morbidity and mortality. CO exposed children often become symptomatic earlier, and recover more rapidly, than similarly CO exposed adults. Mild clinical signs and symptoms associated with COP are headache, dizziness, weakness, lethargy, and myalgia; however, severe signs and symptoms such as blurred vision, syncope, convulsion, coma, cardiopulmonary arrest and death can also accompany with COP. Neurologic manifestations can include altered mental status at different degrees, neck stiffness, tremor, ataxia, and positive Babinski's sign. Delayed neurologic sequels (DNS of COP might be seen in children like adults. DNS symptoms and signs in children include memory problems, mental retardation, mutism, fecal and urinary incontinence, motor deficits, facial palsy, psychosis, chronic headache, seizures, and epilepsy. After CO exposure children must be cared to detect and treat DNS. Although hyperbaric oxygen therapy (HBOT is reported to prevent development of DNS, its indications, application duration and procedures are controversial in both of the children and adults. Although their predictive values are limited, exposing to CO more than eight hours and suffering from CO-induced coma, cardiac arrest, lactic acidosis, high COHb levels, and pathologic findings

  2. Neurological manifestations of snake bite in Sri Lanka.

    OpenAIRE

    Seneviratne U; Dissanayake S

    2002-01-01

    BACKGROUND AND AIMS: Snake bite is an important cause of mortality and morbidity in certain parts of Sri Lanka. This study was designed to determine the offending snakes, neurological manifestations, disease course, and outcome in neurotoxic envenomation. METHODS AND MATERIAL: Fifty six consecutive patients admitted with neurological manifestations following snake bite were studied prospectively. Data were obtained regarding the offending snakes, neurological symptoms, time taken for onset of...

  3. Burn injury in patients with early-onset neurological impairments: 2002 ABA paper.

    Science.gov (United States)

    Alden, N E; Rabbitts, A; Rolls, J A; Bessey, P Q; Yurt, R W

    2004-01-01

    Many patients suffer from sensorimotor deficits that may contribute to burn injury. This retrospective study examines burn injuries in the subgroup of patients that suffer from the early onset neurological impairments of mental retardation, cerebral palsy, spina bifida, autism, and attention deficit-hyperactivity disorder. Fifty-one patients who suffered from the above-mentioned early-onset neurological impairments were admitted to our burn center during a 4-year period. The average TBSA burned was 8.9% yet resulted in prolonged hospitalizations. This study describes our burn center's experience in treating patients admitted with early-onset neurological impairments.

  4. The neurology of proverbs.

    Science.gov (United States)

    Van Lancker, D

    1990-01-01

    Although proverb tests are commonly used in the mental status examination surprisingly little is known about either normal comprehension or the interpretation of proverbial expressions. Current proverbs tests have conceptual and linguistic shortcomings, and few studies have been done to investigate the specific effects of neurological and psychiatric disorders on the interpretation of proverbs. Although frontal lobes have traditionally been impugned in patients who are "concrete", recent studies targeting deficient comprehension of non literal language (e.g. proverbs, idioms, speech formulas, and indirect requests) point to an important role of the right hemisphere (RH). Research describing responses of psychiatrically and neurologically classified groups to tests of proverb and idiom usage is needed to clarify details of aberrant processing of nonliteral meanings. Meanwhile, the proverb test, drawing on diverse cognitive skills, is a nonspecific but sensitive probe of mental status.

  5. The Neurology of Proverbs

    Directory of Open Access Journals (Sweden)

    Diana Van Lancker

    1990-01-01

    Full Text Available Although proverb tests are commonly used in the mental status examination surprisingly little is known about either normal comprehension or the interpretation of proverbial expressions. Current proverbs tests have conceptual and linguistic shortcomings, and few studies have been done to investigate the specific effects of neurological and psychiatric disorders on the interpretation of proverbs. Although frontal lobes have traditionally been impugned in patients who are “concrete”, recent studies targeting deficient comprehension of non literal language (e.g. proverbs, idioms, speech formulas, and indirect requests point to an important role of the right hemisphere (RH. Research describing responses of psychiatrically and neurologically classified groups to tests of proverb and idiom usage is needed to clarify details of aberrant processing of nonliteral meanings. Meanwhile, the proverb test, drawing on diverse cognitive skills, is a nonspecific but sensitive probe of mental status.

  6. Vaccination and neurological disorders

    Directory of Open Access Journals (Sweden)

    Anastasia Gkampeta

    2015-12-01

    Full Text Available Active immunization of children has been proven very effective in elimination of life threatening complications of many infectious diseases in developed countries. However, as vaccination-preventable infectious diseases and their complications have become rare, the interest focuses on immunization-related adverse reactions. Unfortunately, fear of vaccination-related adverse effects can led to decreased vaccination coverage and subsequent epidemics of infectious diseases. This review includes reports about possible side effects following vaccinations in children with neurological disorders and also published recommendations about vaccinating children with neurological disorders. From all international published data anyone can conclude that vaccines are safer than ever before, but the challenge remains to convey this message to society.

  7. [Vitamin D and neurology].

    Science.gov (United States)

    Thouvenot, Éric; Camu, William

    2013-10-01

    Vitamin D deficiency is associated with a higher risk of multiple sclerosis and also with a higher relapse rate as well as a higher number of MRI lesions. Elders with vitamin D deficiency have worse cognitive performance. Vitamin D deficiency is a risk factor for developing Alzheimer's disease. Ischemic stroke are more frequent and more severe in patients with low vitamin D levels. Carotid atherosclerosis is more frequent and more severe in patients with vitamin D deficiency. Vitamin D deficiency is associated with a higher risk and worse prognosis of Parkinson's disease. In the different neurological disorders discussed herein, gene polymorphisms that could alter vitamin D metabolism are also associated with a higher incidence or a worse disease prognosis. Despite the links between vitamin D deficiency and the risks of developing neurological disorders, there is, to date, no proof that supplementation could alter the course of these diseases. Copyright © 2013. Published by Elsevier Masson SAS.

  8. Neurological legal disability

    Directory of Open Access Journals (Sweden)

    Radhakrishna H

    2006-01-01

    Full Text Available Neurological disorders with a prolonged course, either remediable or otherwise are being seen increasingly in clinical practice and many such patients are young and are part of some organization or other wherein their services are needed if they were healthy and fit. The neurologists who are on the panel of these organizations are asked to certify whether these subjects are fit to work or how long they should be given leave. These certificates may be produced in the court of law and may be subjected to verification by another neurologist or a medical board. At present there are no standard guidelines in our country to effect such certification unlike in orthopedic specialty or in ophthalmology. The following is a beginning, based on which the neurologist can certify the neurological disability of such subjects and convey the same meaning to all neurologists across the country.

  9. Aberrant cervical vasculature anastomosis as cause of neck pain and successful treatment with embolization technique.

    Science.gov (United States)

    He, Lucy; Ladner, Travis R; Cobb, Mark; Mocco, J

    2016-01-27

    We report a patient with non-dermatomal radiating neck pain without focal neurologic deficit. Traditional workup could not identify an anatomic or biomechanical cause. Imaging showed a deep cervical vessel centered in the region of pain. Angiography later identified an aberrant anastomosis of this vessel with the occipital artery. Subsequent endovascular embolization of this arterial trunk resulted in complete pain relief. 2016 BMJ Publishing Group Ltd.

  10. Giant left atrial myxoma causing acute ischemic stroke in a child.

    Science.gov (United States)

    Ise, Hayato; Ishikawa, Natsuya; Nakanishi, Sentaro; Kamiya, Hiroyuki

    2018-01-12

    Ischemic stroke is uncommon in pediatric populations and is sometimes caused by cardiac myxoma. In such cases, neurological deficits initially present in ischemic stroke due to emboli or thrombi of the myxoma. Echocardiography is helpful to diagnose myxoma in a timely manner and allows urgent surgical resection of the myxoma. We report a successful case of myxoma in a 7-year-old boy who initially presented with left-sided hemiparesis.

  11. PSYCHIATRIC MORBIDITY IN A NIGERIAN NEUROLOGY CLINIC

    African Journals Online (AJOL)

    2013-05-28

    May 28, 2013 ... medication effects and psychological reactions to the illness. Parkinson's disease (PD) is a good example of a disabling neurological disorder and it is now apparent that the underlying neurodegenerative disorder is a major cause of psychiatric disturbances even though the psychological reactions to the ...

  12. Neurology of widely embedded free will

    NARCIS (Netherlands)

    de Jong, Bauke M.

    2011-01-01

    Free will is classically attributed to the prefrontal cortex. In clinical neurology, prefrontal lesions have consistently been shown to cause impairment of internally driven action and increased reflex-like behaviour. Recently, parietal contributions to both free selection at early stages of

  13. Distinguishing neurological from non-organic conditions

    African Journals Online (AJOL)

    Waddell's test and can easily be incorporated into any bench-side examination to identify potential non-organic back pain. Nausea and vomiting. Nausea and vomiting are common. There are, however, associated features that may indicate a neurological cause. Cerebellar lesions are probably the most commonly.

  14. Neurologic complications of alcoholism.

    Science.gov (United States)

    Noble, James M; Weimer, Louis H

    2014-06-01

    This review serves as an overview of neurologic conditions associated with alcohol abuse or withdrawal, including epidemiology, clinical symptoms, diagnostic approach, and treatment. Frequent alcohol abuse and frank alcoholism are very common among adults in the United States. Although rates decline with each decade, as many as 10% of the elderly drink excessively. Given the ubiquitous nature of alcoholism in society, its complications have been clinically recognized for generations, with recent advances focusing on improved understanding of ethanol's biochemical targets and the pathophysiology of its complications. The chronic effects of alcohol abuse are myriad and include neurologic complications through both direct and indirect effects on the central and peripheral nervous systems. These disorders include several encephalopathic states related to alcohol intoxication, withdrawal, and related nutritional deficiencies; acute and chronic toxic and nutritional peripheral neuropathies; and myopathy. Although prevention of alcoholism and its neurologic complications is the optimal strategy, this article reviews the specific treatment algorithms for alcohol withdrawal and its related nutritional deficiency states.

  15. Palliative care and neurology

    Science.gov (United States)

    Boersma, Isabel; Miyasaki, Janis; Kutner, Jean

    2014-01-01

    Palliative care is an approach to the care of patients and families facing progressive and chronic illnesses that focuses on the relief of suffering due to physical symptoms, psychosocial issues, and spiritual distress. As neurologists care for patients with chronic, progressive, life-limiting, and disabling conditions, it is important that they understand and learn to apply the principles of palliative medicine. In this article, we aim to provide a practical starting point in palliative medicine for neurologists by answering the following questions: (1) What is palliative care and what is hospice care? (2) What are the palliative care needs of neurology patients? (3) Do neurology patients have unique palliative care needs? and (4) How can palliative care be integrated into neurology practice? We cover several fundamental palliative care skills relevant to neurologists, including communication of bad news, symptom assessment and management, advance care planning, caregiver assessment, and appropriate referral to hospice and other palliative care services. We conclude by suggesting areas for future educational efforts and research. PMID:24991027

  16. Neurological complications in hyperemesis gravidarum.

    Science.gov (United States)

    Zara, Gabriella; Codemo, Valentina; Palmieri, Arianna; Schiff, Sami; Cagnin, Annachiara; Citton, Valentina; Manara, Renzo

    2012-02-01

    Hyperemesis gravidarum can impair correct absorption of an adequate amount of thiamine and can cause electrolyte imbalance. This study investigated the neurological complications in a pregnant woman with hyperemesis gravidarum. A 29-year-old pregnant woman was admitted for hyperemesis gravidarum. Besides undernutrition, a neurological examination disclosed weakness with hyporeflexia, ophthalmoparesis, multidirectional nystagmus and optic disks swelling; the patient became rapidly comatose. Brain MRI showed symmetric signal hyperintensity and swelling of periaqueductal area, hypothalamus and mammillary bodies, medial and posterior portions of the thalamus and columns of fornix, consistent with Wernicke encephalopathy (WE). Neurophysiological studies revealed an axonal sensory-motor polyneuropathy, likely due to thiamine deficiency or critical illness polyneuropathy. Sodium and potassium supplementation and parenteral thiamine were administered with improvement of consciousness state in a few days. WE evolved in Korsakoff syndrome. A repeat MRI showed a marked improvement of WE-related alterations and a new hyperintense lesion in the pons, suggestive of central pontine myelinolysis. No sign or symptom due to involvement of the pons was present.

  17. Neurological disorders in hypertensive patients

    Directory of Open Access Journals (Sweden)

    N. V. Vakhnina

    2015-01-01

    Full Text Available Hypertension is one of the most common vascular diseases. The brain as target organs in hypertension is damaged more often and earlier. Neurological complications due to hypertension are frequently hyperdiagnosed in Russian neurological practice. Thus, headache, dizziness, impaired recall of recent events, nocturnal sleep disorders, and many other complaints in a hypertensive patient are usually regarded as a manifestation of dyscirculatory encephalopathy. At the same time headaches (tension headache and migraine in hypertensive patients are predominantly primary; headache associated with dramatic marked elevations in blood pressure is encountered in only a small number of patients. The role of cerebrovascular diseases in the development of dizziness in hypertensive patients is also overestimated. The vast majority of cases, patients with this complaint are in fact identified to have benign paroxysmal postural vertigo, Mеniеre’s disease, vestibular neuronitis, or vestibular migraine. Psychogenic disorders or multisensory insufficiency are generally responsible for non-systemic vertigo in hypertensive patients. Chronic cerebral circulatory insufficiency may cause non-systemic vertigo as a subjective equivalent of postural instability.Cognitive impairments (CIs are the most common and earliest manifestation of cerebrovascular lesion in hypertension. In most cases, CIs in hypertension were vascular and associated with cerebrovascular lesion due to lacunar infarcts and leukoaraiosis. However, mixed CIs frequently occur when hypertensive patients are also found to have signs of a degenerative disease, most commonly in Alzheimer’s disease.

  18. Rare Neurological Manifestation of Celiac Disease

    Directory of Open Access Journals (Sweden)

    Uzma Rani

    2015-06-01

    Full Text Available Celiac disease (CD is an immune-mediated disease characterized by permanent gastrointestinal tract sensitivity to gluten in genetically predisposed individuals. It has varied clinical manifestations, ranging from gastrointestinal to extraintestinal, including neurological, skin, reproductive and psychiatric symptoms, which makes its diagnosis difficult and challenging. Known neurological manifestations of CD include epilepsy with or without occipital calcification, attention deficit hyperactivity disorder and ataxia, headache, neuropathies and behavior disorders. We present the case of a 14-year-old female with headaches and blurred vision for 1 year; she was noted to have papilledema on ophthalmic examination with increased cerebrospinal fluid opening pressure on lumber puncture and was diagnosed as a case of pseudotumor cerebri (PTC. Meanwhile her workup for chronic constipation revealed elevated tissue transglutaminase IgA and antiendomysial IgA antibodies. Upper gastrointestinal endoscopy with duodenal biopsy confirmed the diagnosis of CD. The patient was started on a gluten-free diet, leading to resolution of not only gastrointestinal symptoms but also to almost complete resolution of symptoms of PTC. This report describes the correlation of CD and PTC as its neurological manifestation.

  19. Neurologic Complications of Celiac Disease

    Directory of Open Access Journals (Sweden)

    J Gordon Millichap

    2004-06-01

    Full Text Available Patients with celiac disease (CD [n=l 11] and controls (n=211 were questioned regarding neurologic disorders, their charts were reviewed, and they received neurologic evaluations, including brain imaging or EEG if indicated, in a study of neurologic complications of CD at Carmel Medical Center, Technion-Israel Institute of Technology, Haifa, Israel.

  20. African Journal of Neurological Sciences

    African Journals Online (AJOL)

    African Journal of Neurological Sciences (AJNS) is owned and controlled by the Pan African Association of Neurological Sciences (PAANS). The AJNS's aim is to publish scientific papers of any aspects of Neurological Sciences. AJNS is published quarterly. Articles submitted exclusively to the AJNS are accepted if neither ...

  1. Early and Late Neurological Complications after Cardiac Transplantation

    OpenAIRE

    Mehmet Balkanay; Cengiz Köksal; Deniz Çevirme; Hasan Sunar

    2011-01-01

    The clinical use of cyclosporine as an immunosuppressant improved the recipient’s life span and revolutionized the field of cardiac transplantation. But most of the immunesuppressant drugs including cyclosporine may cause neurological and many other side effects. In this article we present three cases, from 58 patients, undergoing cardiac transplantation at our hospital from 1989 to 2008 in whom developed transient neurological complications.

  2. Early and Late Neurological Complications After Cardiac Transplantation

    OpenAIRE

    Çevirme, Deniz; Köksal, Cengiz; Balkanay, Mehmet; Sunar, Hasan

    2010-01-01

    The clinical use of cyclosporine as an immunosuppressant improved the recipient's life span and revolutionized the field of cardiac transplantation. But most of the immunesuppressant drugs including cyclosporine may cause neurological and many other side effects. In this article we present three cases, from 58 patients, undergoing cardiac transplantation at our hospital from 1989 to 2008 in whom developed transient neurological complications.

  3. Advances in genetic diagnosis of neurological disorders.

    Science.gov (United States)

    Toft, M

    2014-01-01

    Neurogenetics has developed enormously in recent years, and the genetic basis of human disorders is being unravelled rapidly. Many neurological disorders are Mendelian disorders, caused by mutations in genes involved in normal function of the brain, spinal cord, peripheral nerves or muscles. Due to high costs and time-consuming procedures, genetic tests have normally been performed late in the diagnostic process, when clinical examination and other tests have indicated a specific gene as the likely disease cause. Many neurological phenotypes are genetically very heterogeneous, and testing of all possible disease genes has been impossible. As a result, many patients with genetic neurological disorders have remained without a specific diagnosis, even when the disease is caused by mutations in known disease genes. Recent technological advances, in particular next-generation DNA sequencing techniques, have resulted in rapid identification of genes involved in Mendelian disorders and provided new possibilities for diagnostic genetic testing. The development of methods for coupling targeted capture and massively parallel DNA sequencing has made it possible to examine a large number of genes in a single reaction. Diagnostic genetic testing can today be performed by the use of gene panels and exome sequencing. This allows a more precise diagnosis of many neurological disorders, and genetic testing should now be considered earlier in the diagnostic procedure. © 2014 John Wiley & Sons A/S. Published by John Wiley & Sons Ltd.

  4. Hodgkin's Lymphoma: A Review of Neurologic Complications

    Directory of Open Access Journals (Sweden)

    Sean Grimm

    2011-01-01

    Full Text Available Hodgkin's lymphoma is a hematolymphoid neoplasm, primarily of B cell lineage, that has unique histologic, immunophenotypic, and clinical features. Neurologic complications of Hodgkin's Lymphoma can be separated into those that result directly from the disease, indirectly from the disease, or from its treatment. Direct neurologic dysfunction from Hodgkin's Lymphoma results from metastatic intracranial spinal disease, epidural metastases causing spinal cord/cauda equina compression, leptomeningeal metastases, or intradural intramedullary spinal cord metastases. Indirect neurologic dysfunction may be caused by paraneoplastic disorders (such as paraneoplastic cerebellar degeneration or limbic encephalitis and primary angiitis of the central nervous system. Hodgkin's lymphoma treatment typically includes chemotherapy or radiotherapy with potential treatment-related complications affecting the nervous system. Neurologic complications resulting from mantle-field radiotherapy include the “dropped head syndrome,” acute brachial plexopathy, and transient ischemic attacks/cerebral infarcts. Chemotherapy for Hodgkin's lymphoma may cause cerebral infarction (due to emboli from anthracycline-induced cardiomyopathy and peripheral neuropathy.

  5. Neurology and literature 2.

    Science.gov (United States)

    Iniesta, I

    2014-05-01

    Good literary fiction has the potential to move us, extend our sense of life, transform our prospective views and help us in the face of adversity. A neurological disorder is likely to be the most challenging experience a human being may have to confront in a lifetime. As such, literary recreations of illnesses have a doubly powerful effect. Study the synergies between neurology and fictional literature with particular reference to narrative based medicine (NBM). Doctors establish boundaries between the normal and the abnormal. Taking a clinical history is an act of interpretation in which the doctor integrates the science of objective signs and measurable quantities with the art of subjective clinical judgment. The more discrepancy there is between the patient's experience with the illness and the doctor's interpretation of that disease, the less likely the doctor-patient interaction is to succeed. NBM contributes to a better discernment of the meanings, thus considering disease as a biographical event rather than just a natural fact. Drawing from their own experience with disease, writers of fiction provide universal insights through their narratives, whilst neuroscientists, like Cajal, have occasionally devoted their scientific knowledge to literary narratives. Furthermore, neurologists from Alzheimer to Oliver Sacks remind us of the essential value of NBM in the clinic. Integrating NBM (the narrative of patients) and the classic holistic approach to patients with our current paradigm of evidence based medicine represents a challenge as relevant to neurologists as keeping up with technological and scientific advances. Copyright © 2011 Sociedad Española de Neurología. Published by Elsevier Espana. All rights reserved.

  6. Neurological complications of chickenpox

    Directory of Open Access Journals (Sweden)

    Girija A

    2007-01-01

    Full Text Available Aim: To assess the neurological complications of chickenpox with prognosis. Background: The neurological complications occur in 0.03% of persons who get chickenpox. There is no universal vaccination against chicken pox in India. Most patients prefer alternate modalities of treatment. Hence these complications of chickenpox are likely to continue to occur. Study Design: A prospective study was conducted for 2 years (from March 2002 on the admitted cases with neurological complications after chickenpox (with rash or scar. Patients were investigated with CT/MRI, CSF study, EEG and nerve conduction studies and hematological workup. They were followed-up for 1 year and outcome assessed using modified Rankin scale. Results: The latency for the neurological complications was 4-32 days (mean: 16.32 days. There were 18 cases: 10 adults (64% and 8 children (36%. Cerebellar ataxia (normal CT/MRI was observed in 7 cases (32% (mean age: 6.85 years. One patient (6 years had acute right hemiparesis in the fifth week due to left capsular infarct. All these cases spontaneously recovered by 4 weeks. The age range of the adult patients was 13-47 years (mean: 27 years. The manifestations included cerebellar and pyramidal signs (n-4 with features of demyelination in MRI who recovered spontaneously or with methylprednisolone by 8 weeks. Patient with encephalitis recovered in 2 weeks with acyclovir. Guillain Barre syndrome of the demyelinating type (n-2 was treated with Intravenous immunoglobulin (IVIG and they had a slow recovery by a modified Rankin scale (mRs score of 3 and 2 at 6 months and 1 year, respectively. One case died after hemorrhage into the occipital infarct. There were two cases of asymmetrical neuropathy, one each of the seventh cranial and brachial neuritis. Conclusion: Spontaneous recovery occurs in post-chickenpox cerebellar ataxia. Rarely, serious complications can occur in adults. The demyelinating disorders, either of the central or peripheral

  7. Dengue: a new challenge for neurology

    Directory of Open Access Journals (Sweden)

    Marzia Puccioni-Sohler

    2012-11-01

    Full Text Available Dengue infection is a leading cause of illness and death in tropical and subtropical regions of the world. Forty percent of the world’s population currently lives in these areas. The clinical picture resulting from dengue infection can range from relatively minor to catastrophic hemorrhagic fever. Recently, reports have increased of neurological manifestations. Neuropathogenesis seems to be related to direct nervous system viral invasion, autoimmune reaction, metabolic and hemorrhagic disturbance. Neurological manifestations include encephalitis, encephalopathy, meningitis, Guillain-Barré syndrome, myelitis, acute disseminated encephalomyelitis, polyneuropathy, mononeuropathy, and cerebromeningeal hemorrhage. The development of neurological symptoms in patients with positive Immunoglobulin M (IgM dengue serology suggests a means of diagnosing the neurological complications associated with dengue. Viral antigens, specific IgM antibodies, and the intrathecal synthesis of dengue antibodies have been successfully detected in cerebrospinal fluid. However, despite diagnostic advancements, the treatment of neurological dengue is problematic. The launch of a dengue vaccine is expected to be beneficial.

  8. Problem neurology residents: a national survey.

    Science.gov (United States)

    Tabby, David S; Majeed, Muhammed H; Schwartzman, Robert J

    2011-06-14

    Problem residents are found across most medical specialties at a prevalence of about 10%. This study was designed to explore the prevalence and causes of problem neurology residents and to compare neurology programs' responses and outcomes. Directors of 126 US neurology residency programs were sent an electronic survey. We collected data on demographics, first and all "identifiers" of problem residents, and year of training in which the problem was found. We asked about observable signs, etiology, and who performed remediation. We asked what resources were used and what outcomes occurred. Ninety-five program directors completed surveys (75% response rate). Almost all neurology programs have problem residents (81%). Age, sex, marital status, being a US native, or attending a US medical school had no effect on problem status. Being a parent carried a lower likelihood of problems (32%). Most commonly the problem is acted on during the first year of training. Faculty members without defined educational roles were the most frequent first identifiers. Program directors were the most common remediators. The most common remediation techniques were increasing supervision and assigning a faculty mentor. Graduate medical education office and psychiatric or psychological counseling services were most often used. Eleven percent of problem residents required a program for impaired physicians and 14% required a leave of absence. Sixteen percent were dismissed from their programs. The prevalence of problem residents in neurology is similar to other disciplines, and various resources are available to remediate them.

  9. Fetal Cocaine Exposure: Neurologic Effects and Sensory-Motor Delays

    Science.gov (United States)

    Arendt, Robert E.; Minnes, Sonnia; Singer, Lynn T.

    2014-01-01

    SUMMARY Research on animal models demonstrates that fetal cocaine exposure results in neurologic deficits in memory and learning. Although drug effects on human infants are difficult to separate from other environmental influences of a drug-using lifestyle, studies suggest that infants exposed to cocaine in utero have reduced growth, delays in sensory-motor development, attentional deficits, and depressed responsivity to social stimulation. Standard interventions to promote behavioral state regulation in affected infants may be helpful when parents are capable of participating. PMID:25688173

  10. Wild-type human TDP-43 expression causes TDP-43 phosphorylation, mitochondrial aggregation, motor deficits and early mortality in transgenic mice

    Science.gov (United States)

    Xu, Ya-Fei; Gendron, Tania F.; Zhang, Yong-Jie; Lin, Wen-Lang; D’Alton, Simon; Sheng, Hong; Casey, Monica Castanedes; Tong, Jimei; Knight, Joshua; Yu, Xin; Rademakers, Rosa; Boylan, Kevin; Hutton, Mike; McGowan, Eileen; Dickson, Dennis W.; Lewis, Jada; Petrucelli, Leonard

    2011-01-01

    Transactivation response DNA-binding protein 43 (TDP-43) is a principal component of ubiquitinated inclusions in frontotemporal lobar degeneration with ubiquitin-positive inclusions and in amyotrophic lateral sclerosis (ALS). Mutations in TARDBP, the gene encoding TDP-43, are associated with sporadic and familial ALS, yet multiple neurodegenerative diseases exhibit TDP-43 pathology without known TARDBP mutations. While TDP-43 has been ascribed a number of roles in normal biology, including mRNA splicing and transcription regulation, elucidating disease mechanisms associated with this protein is hindered by the lack of models to dissect such functions. We have generated transgenic (TDP-43PrP) mice expressing full-length human TDP-43 (hTDP-43) driven by the mouse prion promoter to provide a tool to analyze the role of wild-type hTDP-43 in the brain and spinal cord. Expression of hTDP-43 caused a dose dependant down regulation of mouse TDP-43 RNA and protein. Moderate overexpression of hTDP-43 resulted in TDP-43 truncation, increased cytoplasmic and nuclear ubiquitin levels, as well as intranuclear and cytoplasmic aggregates that were immunopositive for phosphorylated TDP-43. Of note, abnormal juxtanuclear aggregates of mitochondria were observed, accompanied by enhanced levels of Fis1 and phosphorylated DLP1, key components of the mitochondrial fission machinery. Conversely, a marked reduction in mitofusin 1 expression, which plays an essential role in mitochondrial fusion, was observed in TDP-43PrP mice. Finally, TDP-43PrP mice showed reactive gliosis, axonal and myelin degeneration, gait abnormalities and early lethality. This TDP-43 transgenic line provides a valuable tool for identifying potential roles of wild-type TDP-43 within the central nervous system and for studying TDP-43-associated neurotoxicity. PMID:20702714

  11. Absence of OsβCA1 causes a CO2 deficit and affects leaf photosynthesis and the stomatal response to CO2 in rice.

    Science.gov (United States)

    Chen, Taiyu; Wu, Huan; Wu, Jiemin; Fan, Xiaolei; Li, Xianghua; Lin, Yongjun

    2017-04-01

    Plants always adjust the opening of stomatal pores to adapt to the environment, for example CO2 concentration ([CO2 ]), humidity and temperature. Low [CO2 ] will trigger the opening of stomatal pores to absorb extra CO2 . However, little is known about how CO2 supply affects the carbon fixation and opening of stomatal pores in rice. Here, a chloroplast-located gene coding for β-carbonic anhydrase (βCA) was found to be involved in carbon assimilation and the CO2 -mediated stomatal pore response in rice. OsβCA1 was constitutively expressed in all tissues and its transcripts were induced by high [CO2 ] in leaves. Both T-DNA mutant and RNA interference lines showed phenotypes of lower biomass and CA activities. Knockout of OsβCA1 obviously decreased photosynthetic capacity, as demonstrated by the increased CO2 compensation point and decreased light saturation point in the mutant, while knockout increased the opening ratio of stomatal pores and the rate of water loss. Moreover, the mutant showed a delayed response to low [CO2 ], and stomatal pores could not be closed to the same degree as those of wild type even though the stomatal pores could rapidly respond to high [CO2 ]. Genome-wide gene expression analysis via RNA sequencing demonstrated that the transcript abundance of genes related to Rubisco, photosystem compounds and the opening of stomatal pores was globally upregulated in the mutant. Taken together, the inadequate CO2 supply caused by the absence of OsβCA1 reduces photosynthetic efficiency, triggers the opening of stomatal pores and finally decreases their sensitivity to CO2 fluctuation. © 2017 The Authors The Plant Journal © 2017 John Wiley & Sons Ltd.

  12. GATAD2B loss-of-function mutations cause a recognisable syndrome with intellectual disability and are associated with learning deficits and synaptic undergrowth in Drosophila.

    Science.gov (United States)

    Willemsen, Marjolein H; Nijhof, Bonnie; Fenckova, Michaela; Nillesen, Willy M; Bongers, Ernie M H F; Castells-Nobau, Anna; Asztalos, Lenke; Viragh, Erika; van Bon, Bregje W M; Tezel, Emre; Veltman, Joris A; Brunner, Han G; de Vries, Bert B A; de Ligt, Joep; Yntema, Helger G; van Bokhoven, Hans; Isidor, Bertrand; Le Caignec, Cédric; Lorino, Elsa; Asztalos, Zoltan; Koolen, David A; Vissers, Lisenka E L M; Schenck, Annette; Kleefstra, Tjitske

    2013-08-01

    GATA zinc finger domain containing 2B (GATAD2B) encodes a subunit of the MeCP1-Mi-2/nucleosome remodelling and deacetylase complex involved in chromatin modification and regulation of transcription. We recently identified two de novo loss-of-function mutations in GATAD2B by whole exome sequencing in two unrelated individuals with severe intellectual disability. To identify additional individuals with GATAD2B aberrations, we searched for microdeletions overlapping with GATAD2B in inhouse and international databases, and performed targeted Sanger sequencing of the GATAD2B locus in a selected cohort of 80 individuals based on an overlap with the clinical features in the two index cases. To address whether GATAD2B is required directly in neurones for cognition and neuronal development, we investigated the role of Drosophila GATAD2B orthologue simjang (simj) in learning and synaptic connectivity. We identified a third individual with a 240 kb microdeletion encompassing GATAD2B and a fourth unrelated individual with GATAD2B loss-of-function mutation. Detailed clinical description showed that all four individuals with a GATAD2B aberration had a distinctive phenotype with childhood hypotonia, severe intellectual disability, limited speech, tubular shaped nose with broad nasal tip, short philtrum, sparse hair and strabismus. Neuronal knockdown of Drosophila GATAD2B orthologue, simj, resulted in impaired learning and altered synapse morphology. We hereby define a novel clinically recognisable intellectual disability syndrome caused by loss-of-function of GATAD2B. Our results in Drosophila suggest that GATAD2B is required directly in neurones for normal cognitive performance and synapse development.

  13. Neurological aspects of grief.

    Science.gov (United States)

    Silva, Adriana C; de Oliveira Ribeiro, Natalia P; de Mello Schier, Alexandre R; Arias-Carrión, Oscar; Paes, Flavia; Nardi, Antonio E; Machado, Sergio; Pessoa, Tamires M

    2014-01-01

    Despite grief being a universal experience and the increased scientific attention paid to grief and bereavement in recent years, studies that seek to better understand the role of the neurological aspects of grief are still scarce. We found 5 studies that discussed the relationship between the neurological aspects of grief due to the death of a loved one. All studies showed an activation of common areas, i.e., the anterior cingulate cortex (ACC), posterior cingulate cortex (PCC), prefrontal cortex (PFC), insula and amygdala. These findings could indicate that there is a group of areas working together and responding to generate the symptomatology of grief. Because grief is a universal experience, it is essential that the necessary and effective support can be provided to those who experience the loss of someone considered important in their lives, and this requires understanding grief's manifestation, its differential diagnosis in reference to other clinical conditions, mainly psychiatric ones, and adequate forms of intervention and treatment when necessary. Proper understanding and support can help prevent the emergence of more serious health problems.

  14. Education Research: Neurology resident education: Trending skills, confidence, and professional preparation.

    Science.gov (United States)

    Jordan, Justin T; Mayans, David; Schneider, Logan; Adams, Nellie; Khawaja, Ayaz M; Engstrom, John

    2016-03-15

    To survey US-trained graduating neurology residents who are American Academy of Neurology members, in an effort to trend perceived quality and completeness of graduate neurology education. An electronic survey was sent to all American Academy of Neurology members graduating from US neurology residency programs in the Spring of 2014. Of 805 eligible respondents, 24% completed the survey. Ninety-three percent of adult neurology residents and 56% of child neurology residents reported plans to pursue fellowship training after residency. Respondents reported a desire for additional training in neurocritical care, neuro-oncology, neuromuscular diseases, botulinum toxin injection, and nerve blocks. There remains a clear deficit in business training of neurology residents, although there was notable improvement in knowledge of coding and office management compared to previous surveys. Although there are still areas of perceived weakness in neurology training, graduating neurology residents feel generally well prepared for their chosen careers. However, most still pursue fellowship training for reasons that are little understood. In addition to certain subspecialties and procedures, practice management remains deficient in neurology training and is a point of future insecurity for most residents. Future curriculum changes should consider resident-reported gaps in knowledge, with careful consideration of improving business training. © 2016 American Academy of Neurology.

  15. Children, standardization and mental health: historical figures and current chains of thought in the clinical diagnosis of attention deficit disorder and hyperactivity

    National Research Council Canada - National Science Library

    Bianchi, Eugenia

    2015-01-01

    The article describes and analyzes the behavioral and neurological aspects that bring together discussions on attention deficit disorder and hyperactivity and outlines some historical conceptual antecedents...

  16. [Neurological consequences following perinatal asphyxia in preschool age children].

    Science.gov (United States)

    Nabieva, T N

    2009-01-01

    Various groups have been addressing the question of whether perinatal asphyxia (PA) affects on newborn health and nervous system. It is widely accepted that severe PA causes motor and cognitive alterations and leads to a variety of brain disorders: cerebral palsy, epilepsy, mental retardation as well as psychiatric deficits. At the same time it was established, that large percentage of children, surviving PA didn't demonstrate apparent sequelae, but mild physical and mental delay in future. With the purpose of disclose further consequences of PA on child development, we examine 20 children (6 years old) surviving mild or moderate PA without severe neurological pathology. In most cases we revealed muscle tone disturbances, physical development and growth retardation, speech pathology in the form of dyslaliya and speech delay. Intact cognitive capacities in these children combine with limited information content. Our investigation discovered, that the presence of certain psychoneurological characteristics such as hyperexcitability, irritability, timidity, aggressiveness; reduced activity, concentration and motivation -- are the consequences of survived birth trauma. These characteristics producing undue fatiguability, inattention, restlessness and diminished working-capacity, can pose additional problems in education process. In the absence of individual approach without taking into account emotional and motivational peculiarities, this category of children could not completely realize their intact cognitive capacities and represent risk group for further mild retardation.

  17. Hypothesis-Driven Treatment of Naming Deficits.

    Science.gov (United States)

    Robinson, K M; Grossman, M

    1997-01-01

    This article proposes to use information processing models of cognition to guide behaviorally based treatments of language deficits, specifically, single-word object naming. Our approach is illustrated with a clinical case of a transcortical sensory aphasic. Clinical neuropsychological and functional imaging data demonstrate that the components comprising the information processing network that underpins naming can be mapped onto a cerebral neural network in the neurologically intact and that reorganization of function seen in transcortical sensory aphasia can demonstrate plasticity in this neural network. The observed balance of impaired and preserved clinical and physiological components in reorganizing neural networks such as this can be used to design treatment strategies to alleviate naming deficits.

  18. Neurological Complications Resulting from Non-Oral Occupational Methanol Poisoning.

    Science.gov (United States)

    Choi, Ji Hyun; Lee, Seung Keun; Gil, Young Eun; Ryu, Jia; Jung-Choi, Kyunghee; Kim, Hyunjoo; Choi, Jun Young; Park, Sun Ah; Lee, Hyang Woon; Yun, Ji Young

    2017-02-01

    Methanol poisoning results in neurological complications including visual disturbances, bilateral putaminal hemorrhagic necrosis, parkinsonism, cerebral edema, coma, or seizures. Almost all reported cases of methanol poisoning are caused by oral ingestion of methanol. However, recently there was an outbreak of methanol poisoning via non-oral exposure that resulted in severe neurological complications to a few workers at industrial sites in Korea. We present 3 patients who had severe neurological complications resulting from non-oral occupational methanol poisoning. Even though initial metabolic acidosis and mental changes were improved with hemodialysis, all of the 3 patients presented optic atrophy and ataxia or parkinsonism as neurological complications resulting from methanol poisoning. In order to manage it adequately, as well as to prevent it, physicians should recognize that methanol poisoning by non-oral exposure can cause neurologic complications.

  19. Primary care perceptions of neurology and neurology services.

    Science.gov (United States)

    Loftus, Angela M; Wade, Carrie; McCarron, Mark O

    2016-06-01

    Neurophobia (fear of neural sciences) and evaluation of independent sector contracts in neurology have seldom been examined among general practitioners (GPs). A questionnaire determined GPs' perceptions of neurology compared with other medical specialties. GP experiences of neurology services with independent sector companies and the local National Health Service (NHS) were compared. Areas of potential improvement in NHS neurology services were recorded from thematic analyses. Among 76 GPs neurology was perceived to be as interesting as other medical specialties. GPs reported less knowledge, more difficulty and less confidence in neurology compared with other medical specialties. There was a preference for a local NHS neurology service (pneurology services provided better patient satisfaction. GPs prefer local NHS neurology services to independent sector contracts. GPs' evaluations should inform commissioning of neurology services. Combating neurophobia should be an integral part of responsive commissioning. Published by the BMJ Publishing Group Limited. For permission to use (where not already granted under a licence) please go to http://www.bmj.com/company/products-services/rights-and-licensing/

  20. Deja vu in neurology.

    Science.gov (United States)

    Wild, Edward

    2005-01-01

    The significance of deja vu is widely recognised in the context of temporal lobe epilepsy, and enquiry about deja vu is frequently made in the clinical assessment of patients with possible epilepsy. Deja vu has also been associated with several psychiatric disorders. The historical context of current understanding of deja vu is discussed. The literature reveals deja vu to be a common phenomenon consistent with normality. Several authors have suggested the existence of a "pathological" form of deja vu that differs, qualitatively or quantitatively, from "non-pathological" deja vu. The features of deja vu suggesting neurological or psychiatric pathology are discussed. Several neuroanatomical and psychological models of the deja vu experience are highlighted, implicating the perceptual, mnemonic and affective regions of the lateral temporal cortex, hippocampus and amygdala in the genesis of deja vu. A possible genetic basis for a neurochemical model of deja vu is discussed. Clinical approaches to the patient presenting with possible deja vu are proposed.

  1. Consciousness: A Neurological Perspective

    Directory of Open Access Journals (Sweden)

    Andrea E. Cavanna

    2011-01-01

    Full Text Available Consciousness is a state so essentially entwined with human experience, yet so difficult to conceptually define and measure. In this article, we explore how a bidimensional model of consciousness involving both level of arousal and subjective awareness of the contents of consciousness can be used to differentiate a range of healthy and altered conscious states. These include the different sleep stages of healthy individuals and the altered states of consciousness associated with neurological conditions such as epilepsy, vegetative state and coma. In particular, we discuss how arousal and awareness are positively correlated in normal physiological states with the exception of REM sleep, while a disturbance in this relationship is characteristic of vegetative state, minimally conscious state, complex partial seizures and sleepwalking.

  2. Neurologic complications of cerebral angiography in childhood moyamoya syndrome

    Energy Technology Data Exchange (ETDEWEB)

    Robertson, R.L.; Chavali, R.V.; Robson, C.D.; Barnes, P.D.; Burrows, P.E. [Department of Radiology, Children`s Hospital Medical Center, Boston, MA (United States); Eldredge, E.A. [Department of Anesthesia, Children`s Hospital Medical Center and Harvard Medical School, Boston, MA (United States); Scott, R.M. [Department of Neurosurgery, Children`s Hospital Medical Center and Harvard Medical School, Boston, MA (United States)

    1998-11-01

    Purpose. To determine the incidence of neurologic complications of cerebral angiography in children with moyamoya syndrome (MMS) as compared to children without MMS. Materials and methods. One-hundred-ninety consecutive cerebral angiograms obtained in 152 children were evaluated. Sixty of these angiograms were obtained in 40 children with MMS. Patients underwent neurologic evaluation prior to and after the procedure. For this study, a neurologic complication was defined as any new focal neurologic deficit or alteration in mental status occurring during the procedure or within the ensuing 24 hours. Results. There were 2 neurologic complications within 24 hours of angiography, one in the MMS group and one in the non-MMS group. One patient with MMS became mute following angiography. The symptom resolved within 12 hours. One patient without MMS being examined postoperatively for residual arteriovenous malformation developed intracranial hemorrhage requiring reexploration 12 hours after the angiogram. Using a two-tail Fisher`s exact test, there was no significant statistical difference in the ischemic (P = 0.3) or hemorrhagic (P = 1.0) complication rates between the group of patients with MMS and the non-MMS groups. Conclusion. The risk of a neurologic complication from cerebral angiography in children with MMS is low and not statistically different from the risk in children with other cerebrovascular disorders. (orig.) With 8 tabs., 37 refs.

  3. History of neurologic examination books.

    Science.gov (United States)

    Boes, Christopher J

    2015-04-01

    The objective of this study was to create an annotated list of textbooks dedicated to teaching the neurologic examination. Monographs focused primarily on the complete neurologic examination published prior to 1960 were reviewed. This analysis was limited to books with the word "examination" in the title, with exceptions for the texts of Robert Wartenberg and Gordon Holmes. Ten manuals met the criteria. Works dedicated primarily to the neurologic examination without a major emphasis on disease description or treatment first appeared in the early 1900s. Georg Monrad-Krohn's "Blue Book of Neurology" ("Blue Bible") was the earliest success. These treatises served the important purpose of educating trainees on proper neurologic examination technique. They could make a reputation and be profitable for the author (Monrad-Krohn), highlight how neurology was practiced at individual institutions (McKendree, Denny-Brown, Holmes, DeJong, Mayo Clinic authors), and honor retiring mentors (Mayo Clinic authors).

  4. MRI and neurological findings in patients with spinal metastases

    Energy Technology Data Exchange (ETDEWEB)

    Switlyk, M.D.; Hole, K.H.; Knutstad, K. [Department of Radiology and Nuclear Medicine, Oslo University Hospital, Norwegian Radium Hospital, Oslo (Norway)], E-mail: marta.switlyk@radiumhospitalet.no; Skjeldal, S.; Zaikova, O. [Department of Orthopedics, Oslo University Hospital, Norwegian Radium Hospital, Oslo (Norway); Hald, J.K. [Department of Radiology and Nuclear Medicine, Oslo University Hospital, Rikshospitalet, Oslo (Norway); Seierstad, T. [Department of Radiology and Nuclear Medicine, Oslo University Hospital, Norwegian Radium Hospital, Oslo (Norway); Faculty of Health Sciences, Buskerud University College, Drammen (Norway)

    2012-12-15

    Background. Magnetic resonance imaging (MRI) is the recommended primary investigation method for metastatic spinal cord compression (MSCC). Initiating treatment before the development of motor deficits is essential to preserve neurological function. However, the relationship between MRI-assessed grades of spinal metastatic disease and neurological status has not been widely investigated. Purpose. To analyze the association between neurological function and MRI-based assessment of the extent of spinal metastases using two different grading systems. Material and Methods. A total of 284 patients admitted to our institution for initial radiotherapy or surgery for symptomatic spinal metastases were included in the study. Motor and sensory deficits were categorized according to the Frankel classification system. Pre-treatment MRI evaluations of the entire spine were scored for the extent of spinal metastases, presence and severity of spinal cord compression, and nerve root compression. Two MRI-based scales were used to evaluate the degree of cord compression and spinal canal narrowing and relate these findings to neurological function. Results. Of the patients included in the study, 28 were non-ambulatory, 49 were ambulatory with minor motor deficits, and 207 had normal motor function. Spinal cord compression was present in all patients with Frankel scores of B or C, 23 of 35 patients with a Frankel score of D (66%), and 48 of 152 patients with a Frankel score of E (32%). The percentage of patients with severe spinal canal narrowing increased with increasing Frankel grades. The grading according to the scales showed a significant association with the symptoms according to the Frankel scale (P < 0.001). Conclusion. In patients with neurological dysfunction, the presence and severity of impairment was associated with the epidural tumor burden. A significant number of patients had radiological spinal cord compression and normal motor function (occult MSCC)

  5. Perioperative Management of Neurological Conditions

    Directory of Open Access Journals (Sweden)

    Manjeet Singh Dhallu

    2017-06-01

    Full Text Available Perioperative care of the patients with neurological diseases can be challenging. Most important consideration is the management and understanding of pathophysiology of these disorders and evaluation of new neurological changes that occur perioperatively. Perioperative generally refers to 3 phases of surgery: preoperative, intraoperative, and postoperative. We have tried to address few commonly encountered neurological conditions in clinical practice, such as delirium, stroke, epilepsy, myasthenia gravis, and Parkinson disease. In this article, we emphasize on early diagnosis and management strategies of neurological disorders in the perioperative period to minimize morbidity and mortality of patients.

  6. Splicing Regulation in Neurologic Disease

    National Research Council Canada - National Science Library

    Licatalosi, Donny D; Darnell, Robert B

    2006-01-01

    .... It is becoming evident that alternative splicing plays a particularly important role in neurologic disease, which is perhaps not surprising given the important role splicing plays in generating...

  7. Cannabinoids in neurology – Brazilian Academy of Neurology

    Directory of Open Access Journals (Sweden)

    Sonia M. D. Brucki

    2015-04-01

    Full Text Available The use of cannabidiol in some neurological conditions was allowed by Conselho Regional de Medicina de São Paulo and by Agência Nacional de Vigilância Sanitária (ANVISA. Specialists on behalf of Academia Brasileira de Neurologia prepared a critical statement about use of cannabidiol and other cannabis derivatives in neurological diseases.

  8. Virtual reality in neurologic rehabilitation of spatial disorientation.

    Science.gov (United States)

    Kober, Silvia Erika; Wood, Guilherme; Hofer, Daniela; Kreuzig, Walter; Kiefer, Manfred; Neuper, Christa

    2013-02-08

    Topographical disorientation (TD) is a severe and persistent impairment of spatial orientation and navigation in familiar as well as new environments and a common consequence of brain damage. Virtual reality (VR) provides a new tool for the assessment and rehabilitation of TD. In VR training programs different degrees of active motor control over navigation may be implemented (i.e. more passive spatial navigation vs. more active). Increasing demands of active motor control may overload those visuo-spatial resources necessary for learning spatial orientation and navigation. In the present study we used a VR-based verbally-guided passive navigation training program to improve general spatial abilities in neurologic patients with spatial disorientation. Eleven neurologic patients with focal brain lesions, which showed deficits in spatial orientation, as well as 11 neurologic healthy controls performed a route finding training in a virtual environment. Participants learned and recalled different routes for navigation in a virtual city over five training sessions. Before and after VR training, general spatial abilities were assessed with standardized neuropsychological tests. Route finding ability in the VR task increased over the five training sessions. Moreover, both groups improved different aspects of spatial abilities after VR training in comparison to the spatial performance before VR training. Verbally-guided passive navigation training in VR enhances general spatial cognition in neurologic patients with spatial disorientation as well as in healthy controls and can therefore be useful in the rehabilitation of spatial deficits associated with TD.

  9. Virtual reality in neurologic rehabilitation of spatial disorientation

    Directory of Open Access Journals (Sweden)

    Kober Silvia

    2013-02-01

    Full Text Available Abstract Background Topographical disorientation (TD is a severe and persistent impairment of spatial orientation and navigation in familiar as well as new environments and a common consequence of brain damage. Virtual reality (VR provides a new tool for the assessment and rehabilitation of TD. In VR training programs different degrees of active motor control over navigation may be implemented (i.e. more passive spatial navigation vs. more active. Increasing demands of active motor control may overload those visuo-spatial resources necessary for learning spatial orientation and navigation. In the present study we used a VR-based verbally-guided passive navigation training program to improve general spatial abilities in neurologic patients with spatial disorientation. Methods Eleven neurologic patients with focal brain lesions, which showed deficits in spatial orientation, as well as 11 neurologic healthy controls performed a route finding training in a virtual environment. Participants learned and recalled different routes for navigation in a virtual city over five training sessions. Before and after VR training, general spatial abilities were assessed with standardized neuropsychological tests. Results Route finding ability in the VR task increased over the five training sessions. Moreover, both groups improved different aspects of spatial abilities after VR training in comparison to the spatial performance before VR training. Conclusions Verbally-guided passive navigation training in VR enhances general spatial cognition in neurologic patients with spatial disorientation as well as in healthy controls and can therefore be useful in the rehabilitation of spatial deficits associated with TD.

  10. Appropriate neurological evaluation and multimodality magnetic resonance imaging in eclampsia.

    Science.gov (United States)

    Hoffmann, M; Keiseb, J; Moodley, J; Corr, P

    2002-09-01

    Simultanagnosia is common in eclampsia and a visuospatial test may be the most appropriate method in assessing the degree and monitoring of neurological deficit. To determine a sensitive clinical test for the degree of neurological deficit in eclampsia and in monitoring neurological change. Thirty women with eclampsia were evaluated by clinical neurological quantitative scales including the Canadian Neurological Scale, Glasgow Coma Scale, Mini-Mental State Examination, a validated Cookie Theft Picture Test (CTPT), magnetic resonance imaging (MRI) (T1/T2), diffusion weighted imaging (DWI) and magnetic resonance angiography (MRA). The CTPT, used to measure simultanagnosia, had a sensitivity of 100% (95% CI: 84.5-100), specificity of 33.3% (95% CI: 1.8-87.5) with positive predictive value of 93.1% (95% CI: 75.8-98.8) and negative predictive value of 100% (95% CI: 5.5-100). The degree of agreement between simultanagnosia as measured by CTPT and DWI was 93.3% (Kappa=0.474; P=0.001). Standard MRI compared with DWI had a sensitivity of 77.8% (95% CI: 57.3-90.6), specificity of 100% (95% CI: 31-100), positive predictive value of 100% (95% CI: 80.8-100) and negative predictive value of 33.3% (95% CI: 9-69.1). The degree of agreement between standard MRI and DWI was 90%, this was statistically significant (Kappa=0.412: P=0.001). The validated CTPT for simultanagnosia was abnormal in the majority (n=29; 96.7%) of eclamptic patients with other neurological scales normal. Standard MRI and DWI showed excellent correlation with this simple bedside clinimetric evaluation. The oedema in eclampsia is primarily of vasogenic origin.

  11. Malaria with neurological involvement in Ugandan children: effect on cognitive ability, academic achievement and behaviour.

    Science.gov (United States)

    Bangirana, Paul; Musisi, Seggane; Boivin, Michael J; Ehnvall, Anna; John, Chandy C; Bergemann, Tracy L; Allebeck, Peter

    2011-11-03

    Malaria is a leading cause of ill health and neuro-disability in children in sub-Saharan Africa. Impaired cognition is a common outcome of malaria with neurological involvement. There is also a possibility that academic achievement may be affected by malaria with neurological involvement given the association between cognitive ability and academic achievement. This study investigated the effect of malaria with neurological involvement on cognitive ability, behaviour and academic achievement. This prospective case-control study was carried out in Kampala City, Uganda between February 2008 and October 2010. Sixty-two children with a history of malaria with neurological involvement were followed up and given assessments for cognitive ability (working memory, reasoning, learning, visual spatial skills and attention), behaviour (internalizing and externalizing problems) and academic achievement (arithmetic, spelling and reading) three months after the illness. Sixty-one community controls recruited from the homes or neighbouring families of the cases were also given the same assessments. Tests scores of the two groups were compared using analysis of covariance with age, sex, level of education, nutritional status and quality of the home environment as covariates. This study was approved by the relevant ethical bodies and informed consent sought from the caregivers. Children in the malaria group had more behavioural problems than the community controls for internalizing problems (estimated mean difference = -3.71, 95% confidence interval (CI), = -6.34 to -1.08, p = 0.007). There was marginal evidence of lower attention scores (0.40, CI = -0.05 to 0.86, p = 0.09). However, excluding one child from the analyses who was unable to perform the tests affected the attention scores to borderline significance (0.32, CI, = 0.01 to 0.62, p = 0.05). No significant differences were observed in other cognitive abilities or in academic achievement scores. Malaria with neurological

  12. Malaria with neurological involvement in Ugandan children: effect on cognitive ability, academic achievement and behaviour

    Directory of Open Access Journals (Sweden)

    Bangirana Paul

    2011-11-01

    Full Text Available Abstract Background Malaria is a leading cause of ill health and neuro-disability in children in sub-Saharan Africa. Impaired cognition is a common outcome of malaria with neurological involvement. There is also a possibility that academic achievement may be affected by malaria with neurological involvement given the association between cognitive ability and academic achievement. This study investigated the effect of malaria with neurological involvement on cognitive ability, behaviour and academic achievement. Methods This prospective case-control study was carried out in Kampala City, Uganda between February 2008 and October 2010. Sixty-two children with a history of malaria with neurological involvement were followed up and given assessments for cognitive ability (working memory, reasoning, learning, visual spatial skills and attention, behaviour (internalizing and externalizing problems and academic achievement (arithmetic, spelling and reading three months after the illness. Sixty-one community controls recruited from the homes or neighbouring families of the cases were also given the same assessments. Tests scores of the two groups were compared using analysis of covariance with age, sex, level of education, nutritional status and quality of the home environment as covariates. This study was approved by the relevant ethical bodies and informed consent sought from the caregivers. Results Children in the malaria group had more behavioural problems than the community controls for internalizing problems (estimated mean difference = -3.71, 95% confidence interval (CI, = -6.34 to -1.08, p = 0.007. There was marginal evidence of lower attention scores (0.40, CI = -0.05 to 0.86, p = 0.09. However, excluding one child from the analyses who was unable to perform the tests affected the attention scores to borderline significance (0.32, CI, = 0.01 to 0.62, p = 0.05. No significant differences were observed in other cognitive abilities or in academic

  13. [Neurologic aspects of HIV infections--follow-up of pediatric patients].

    Science.gov (United States)

    Kollár, Katalin; Jelenik, Zsuzsanna; Hegelsberger, Edit

    2003-11-20

    Before the widespread introduction of combined antiretroviral therapy (1995) complications from HIV and AIDS in the central nervous system had been reported in larger proportion in infants and children than in adults: 80-90% versus 60-70%. Particular clinical manifestations tend to occur at different stages during the evolution of HIV infection. The authors review the neurological aspects of HIV infection. First, a summary of the protocol of the neurological examinations and related experience is given. Then authors present the evaluation of neuro-psychological development, prevalence of neurological impairment and neuro-imaging of nine HIV infected children (seven boys, two girls) for the period of ten years (1991-2001). Three/ten children had vertically transmitted HIV six/nine were infected by a nosocomial route in their early childhood. Children were regularly followed up from the diagnosis of HIV. The median follow up time has been 79 month (range: 18-144 month). Four patients died during the study period. The neurological status, the motor and mental development were examined at three month intervals or monthly under one year of age. EEG was performed every six month and CT/MRI once a year. All patients received combined antiretroviral treatment and immunoglobulin therapy continuously. Three/nine children have normal development, one/nine has hyperactive and attention deficit disorder with normal IQ range, two/nine have slight, one/nine moderate and two/nine serious mental retardation. Mild neurological signs were found in two children, various moderate and serious neuro/psychological symptoms were found in four patients, one of them was treated with benign epilepsy too. There was also dose correlation between the clinical symptoms and the results of EEG examination (diffuse background slowing) and results of neuroimaging studies (cortical atrophy, calcification of the basal ganglia, toxoplasma abscesses). According to the results of different examinations

  14. Wilson's disease and other neurological copper disorders.

    Science.gov (United States)

    Bandmann, Oliver; Weiss, Karl Heinz; Kaler, Stephen G

    2015-01-01

    The copper metabolism disorder Wilson's disease was first defined in 1912. Wilson's disease can present with hepatic and neurological deficits, including dystonia and parkinsonism. Early-onset presentations in infancy and late-onset manifestations in adults older than 70 years of age are now well recognised. Direct genetic testing for ATP7B mutations are increasingly available to confirm the clinical diagnosis of Wilson's disease, and results from biochemical and genetic prevalence studies suggest that Wilson's disease might be much more common than previously estimated. Early diagnosis of Wilson's disease is crucial to ensure that patients can be started on adequate treatment, but uncertainty remains about the best possible choice of medication. Furthermore, Wilson's disease needs to be differentiated from other conditions that also present clinically with hepatolenticular degeneration or share biochemical abnormalities with Wilson's disease, such as reduced serum ceruloplasmin concentrations. Disordered copper metabolism is also associated with other neurological conditions, including a subtype of axonal neuropathy due to ATP7A mutations and the late-onset neurodegenerative disorders Alzheimer's disease and Parkinson's disease. Copyright © 2015 Elsevier Ltd. All rights reserved.

  15. Neurological complications in adult spinal deformity surgery.

    Science.gov (United States)

    Iorio, Justin A; Reid, Patrick; Kim, Han Jo

    2016-09-01

    The number of surgeries performed for adult spinal deformity (ASD) has been increasing due to an aging population, longer life expectancy, and studies supporting an improvement in health-related quality of life scores after operative intervention. However, medical and surgical complication rates remain high, and neurological complications such as spinal cord injury and motor deficits can be especially debilitating to patients. Several independent factors potentially influence the likelihood of neurological complications including surgical approach (anterior, lateral, or posterior), use of osteotomies, thoracic hyperkyphosis, spinal region, patient characteristics, and revision surgery status. The majority of ASD surgeries are performed by a posterior approach to the thoracic and/or lumbar spine, but anterior and lateral approaches are commonly performed and are associated with unique neural complications such as femoral nerve palsy and lumbar plexus injuries. Spinal morphology, such as that of hyperkyphosis, has been reported to be a risk factor for complications in addition to three-column osteotomies, which are often utilized to correct large deformities. Additionally, revision surgeries are common in ASD and these patients are at an increased risk of procedure-related complications and nervous system injury. Patient selection, surgical technique, and use of intraoperative neuromonitoring may reduce the incidence of complications and optimize outcomes.

  16. [Neurological interpretation of dreams] .

    Science.gov (United States)

    Pareja, J A; Gil-Nagel, A

    2000-10-01

    Cerebral cortical activity is constant throughout the entire human life, but substantially changes during the different phases of the sleep-wake cycle (wakefulness, non-REM sleep and REM sleep), as well as in relation to available information. In particular, perception of the environment is closely linked to the wake-state, while during sleep perception turns to the internal domain or endogenous cerebral activity. External and internal information are mutually exclusive. During wakefulness a neuronal mechanism allows attention to focus on the environment whereas endogenous cortical activity is ignored. The opposite process is provided during sleep. The function external attention-internal attention is coupled with the two modes of brain function during wakefulness and during sleep, providing two possible cortical status: thinking and dreaming. Several neurological processes may influence the declaration of the three states of being or may modify their orderly oscillation through the sleep-wake cycle. In addition, endogenous information and its perception (dreams) may be modified. Disturbances of dreaming may configurate in different general clinical scenarios: lack of dreaming, excess of dreaming (epic dreaming), paroxysmal dreaming (epileptic), nightmares, violent dreaming, daytime-dreaming (hallucinations), and lucid dreaming. Sensorial deprivation, as well as the emergence of internal perception may be the underlying mechanism of hallucinations. The probable isomorphism between hallucinations and dreaming is postulated, analyzed and discussed.

  17. Interventional neurology: a reborn subspecialty.

    Science.gov (United States)

    Edgell, Randall C; Alshekhlee, Amer; Yavagal, Dileep R; Vora, Nirav; Cruz-Flores, Salvador

    2012-10-01

    Neurologists have a long history of involvement in cerebral angiography; however, the roots of neurologist involvement in therapeutic endovascular procedures have not been previously documented. As outlined in this article, it has taken the efforts of several early pioneers to lay the ground work for interventional neurology, a specialty that has become one of the fastest growing neurological subspecialties. The ground work, along with a great clinical need, has allowed the modern interventional neurologist to tackle some of the most intractable diseases, especially those affecting the cerebral vasculature. The institutionalization of interventional neurology as a subspecialty was first advocated in 1995 in an article entitled, "Interventional Neurology, a subspecialty whose time has come." The institutions created in the wake of this article have provided the framework that has allowed interventional neurology to transition from "a subspecialty whose time has come" to a subspecialty that is here to stay and thrive. Copyright © 2010 by the American Society of Neuroimaging.

  18. Motor and Sensory Deficits in the teetering Mice Result from Mutation of the ESCRT Component HGS.

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    Jennifer A Watson

    2015-06-01

    Full Text Available Neurons are particularly vulnerable to perturbations in endo-lysosomal transport, as several neurological disorders are caused by a primary deficit in this pathway. In this report, we used positional cloning to show that the spontaneously occurring neurological mutation teetering (tn is a single nucleotide substitution in hepatocyte growth factor-regulated tyrosine kinase substrate (Hgs/Hrs, a component of the endosomal sorting complex required for transport (ESCRT. The tn mice exhibit hypokenesis, muscle weakness, reduced muscle size and early perinatal lethality by 5-weeks of age. Although HGS has been suggested to be essential for the sorting of ubiquitinated membrane proteins to the lysosome, there were no alterations in receptor tyrosine kinase levels in the central nervous system, and only a modest decrease in tropomyosin receptor kinase B (TrkB in the sciatic nerves of the tn mice. Instead, loss of HGS resulted in structural alterations at the neuromuscular junction (NMJ, including swellings and ultra-terminal sprouting at motor axon terminals and an increase in the number of endosomes and multivesicular bodies. These structural changes were accompanied by a reduction in spontaneous and evoked release of acetylcholine, indicating a deficit in neurotransmitter release at the NMJ. These deficits in synaptic transmission were associated with elevated levels of ubiquitinated proteins in the synaptosome fraction. In addition to the deficits in neuronal function, mutation of Hgs resulted in both hypermyelinated and dysmyelinated axons in the tn mice, which supports a growing body of evidence that ESCRTs are required for proper myelination of peripheral nerves. Our results indicate that HGS has multiple roles in the nervous system and demonstrate a previously unanticipated requirement for ESCRTs in the maintenance of synaptic transmission.

  19. Risk Factors and Neurologic Outcomes in Childhood Arterial Ischemic Stroke

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    Taner Sezer

    2017-09-01

    Full Text Available Objective: The aim of this study is to describe clinical characteristics, treatment modalities and outcomes of children with arterial ischemic stroke (AIS. Material and Methods: We retrospectively reviewed the charts of 102 children (62 girls and 40 boys with AIS admitted at our hospital between 2009 and 2015. Age at stroke, sex, medical history, family history, clinical findings upon admission, history of seizure, and radiological findings were recorded. Cardiac assessment, hematological and immunological tests, metabolic screening were all performed in the patients. Results: In 25 children stroke occured as a complication of cardiac disease, 12 had transient cerebral arteriopathy, 11 had Down’s syndrome, 9 had thalassemia, 7 had moyamoya disease, 6 had MTHFR mutation, 4 had homozygote for factor V Leiden, 3 had protein C deficiency, 1 had sickle cell disease, and in 24 children no underlying cause could be found. Multiple risk factors were found in 16 children and recurrent stroke was observed in 4 patients. Hemiplegia was the commonest initial clinical presentation (88.2% followed by seizure (66.6% and decreased level of consciousness (54.9%. The avarage length of follow-up was 32.1±5.4 months. The outcome in all 102 stroke patients was as follows: asymptomatic 57.8%; persistent neurologic deficit or epilepsy 40.2%; and death 2%. Conclusion: Our study showed an underlying cause for AIS in 76.5% of the patients; 42.2% of the patients either died or had motor and/or cognitive sequelae and recurrence occured despite prophylactic aspirin treatment in 4 patients. [J Contemp Med 2017; 7(3.000: 278-283

  20. Assessment of neurological clinical management reasoning in medical students.

    Science.gov (United States)

    Lukas, Rimas V; Blood, Angela; Park, Yoon Soo; Brorson, James R

    2014-06-01

    In neurology education there is evidence that trainees may have greater ability in general localization and diagnosis than they do in treatment decisions, particularly with considering longer term care and supportive care. We hypothesized that medical students completing a neurology clerkship would exhibit greater skill at considering the acute diagnostic and therapeutic management than at considering supportive management measures. Data from 720 standardized patient encounters by 360 medical students completing a neurology clerkship being evaluated via an objective structured clinical examination were analyzed for skill in three components of clinical decision making: diagnostic evaluation, therapeutic intervention, and supportive intervention. Scores for all standardized patient encounters over the 2008-2012 interval revealed a significantly higher percentage of correct responses in both the diagnostic (mean [M]=62.6%, standard deviation [SD]=20.3%) and therapeutic (M=63.0%, SD=28.8%) categories in comparison to the supportive (M=31.8%, SD=45.2%) category. However, only scores in therapeutic and supportive treatment plans were found to be significant predictors of the USA National Board of Medical Examiners (NBME) clinical neurology subject examination scores; on average, a percent increase in therapeutic and support scores led to 5 and 2 point increases in NBME scores, respectively. We demonstrate empirical evidence of deficits in a specific component of clinical reasoning in medical students at the completion of a neurology clerkship. Copyright © 2013 Elsevier Ltd. All rights reserved.

  1. Neurological examination in small animals

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    Viktor Paluš

    2014-03-01

    Full Text Available This clinical review about the neurological examination in small animals describes the basics about the first steps of investigation when dealing with neurological patients. The knowledge of how to perform the neurological examination is important however more important is how to correctly interpret these performed tests. A step-by-step approach is mandatory and examiners should master the order and the style of performing these tests. Neurological conditions can be sometimes very distressing for owners and for pets that might not be the most cooperating. The role of a veterinary surgeon, as a professional, is therefore to collect the most relevant history, to examine a patient in a professional manner and to give to owners an educated opinion about the further treatment and prognosis. However neurological examinations might look challenging for many. But it is only the clinical application of neuroanatomy and neurophysiology to an every-day situation for practicing veterinarians and it does not require any specific in-to-depth knowledge. This clinical review is aimed not only to provide the information on how to perform the neurological examination but it is also aimed to appeal on veterinarians to challenge their daily routine and to start practicing on neurologically normal patients. This is the best and only way to differentiate between the normal and abnormal in a real situation.

  2. Progress in gene therapy for neurological disorders.

    Science.gov (United States)

    Simonato, Michele; Bennett, Jean; Boulis, Nicholas M; Castro, Maria G; Fink, David J; Goins, William F; Gray, Steven J; Lowenstein, Pedro R; Vandenberghe, Luk H; Wilson, Thomas J; Wolfe, John H; Glorioso, Joseph C

    2013-05-01

    Diseases of the nervous system have devastating effects and are widely distributed among the population, being especially prevalent in the elderly. These diseases are often caused by inherited genetic mutations that result in abnormal nervous system development, neurodegeneration, or impaired neuronal function. Other causes of neurological diseases include genetic and epigenetic changes induced by environmental insults, injury, disease-related events or inflammatory processes. Standard medical and surgical practice has not proved effective in curing or treating these diseases, and appropriate pharmaceuticals do not exist or are insufficient to slow disease progression. Gene therapy is emerging as a powerful approach with potential to treat and even cure some of the most common diseases of the nervous system. Gene therapy for neurological diseases has been made possible through progress in understanding the underlying disease mechanisms, particularly those involving sensory neurons, and also by improvement of gene vector design, therapeutic gene selection, and methods of delivery. Progress in the field has renewed our optimism for gene therapy as a treatment modality that can be used by neurologists, ophthalmologists and neurosurgeons. In this Review, we describe the promising gene therapy strategies that have the potential to treat patients with neurological diseases and discuss prospects for future development of gene therapy.

  3. Technetium-99m HM-PAO SPECT in patients with delayed neurologic sequelae after carbon monoxide poisoning.

    Science.gov (United States)

    Choi, I. S.; Lee, M. S.; Lee, Y. J.; Kim, J. H.; Lee, S. S.; Kim, W. T.

    1992-01-01

    We used single photon emission computed tomography (SPECT) with technetium-99m hexamethylpropylene amine oxime (99mTc-HM-PAO) in 14 studies on 6 patients with delayed neurologic sequelae from carbon monoxide (CO) poisoning to determine whether any changes in cerebral blood flow could be correlated with clinical or computed tomographic evidence of delayed deficits. Among the six initial CT brain scans, two showed low density of both basal ganglia and two showed decreased density of the cerebral white matter. There was no correlation between the clinical outcome and the findings of the follow-up CT brain scans. Of the two SPECTS with 99mTc-HM-PAO performed during acute anoxic insult, one showed focal hypoperfusion which appeared 20 days prior to the onset of delayed neurologic sequelae after CO poisoning. Seven SPECTs in the six patients performing the delayed phase showed diffuse patched patterns of hypoperfusion which improved on follow-up images. There was good correlation between the clinical outcome and the findings of the 99mTc-HM-PAO SPECT. In preliminary conclusion, 9Tc-HM-PAO brain SPECT can be used for predicting or evaluating the outcome of delayed neurologic sequelae after CO poisoning. Cerebral vascular changes may be the possible cause of hypoperfusion in patients with CO poisoning. PMID:1418757

  4. Cocaine addiction as a neurological disorder: implications for treatment.

    Science.gov (United States)

    Majewska, M D

    1996-01-01

    Clinical and preclinical studies provide convincing evidence for persistent neurological/psychiatric impairments and possible neuronal degeneration associated with chronic cocaine/stimulant abuse. These impairments include multifocal and global cerebral ischemia, cerebral hemorrhages, infarctions, optic neuropathy, cerebral atrophy, cognitive impairments, and mood and movement disorders. These findings may encourage the placement of stimulant addiction into the category of organic brain disorders. Functional and microanatomical anomalies in the frontal and temporal cortex as well as other brain regions may be responsible for certain aspects of phenomenology and neuropsychopathology that are characteristic of stimulant polydrug addictions. These may include broad spectrum of deficits in cognition, motivation, and insight; behavioral disinhibition; attention deficits; emotional instability; impulsiveness; aggressiveness; depression; anhedonia; and persistent movement disorders. Although it is still debated whether the hypofrontality and other brain anomalies observed in stimulant abusers are a consequence or an antecedent of drug abuse, this debate seems purely academic and irrelevant with respect to the importance of compensating for these deficits in the development of treatment strategies. The neuropsychiatric impairments accompanying stimulant abuse may contribute to the very high rate of relapse in addicts that can take place after long periods (years) of abstinence. It is possible that the neurological deficits present in stimulant addicts, whether they are primary or secondary to stimulant abuse, are responsible for perpetual drug abuse which may be a form of self-medication (Weiss et al. 1991, 1992). In this context, addiction to stimulants, once fully developed, may represent a true biological dependency on drugs that temporarily compensate for existing neurological deficits. The concept of self-medication by drug addicts is supported by major theories of

  5. Neurological Manifestations of Dengue Infection

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    Guo-Hong Li

    2017-10-01

    Full Text Available Dengue counts among the most commonly encountered arboviral diseases, representing the fastest spreading tropical illness in the world. It is prevalent in 128 countries, and each year >2.5 billion people are at risk of dengue virus infection worldwide. Neurological signs of dengue infection are increasingly reported. In this review, the main neurological complications of dengue virus infection, such as central nervous system (CNS, peripheral nervous system, and ophthalmic complications were discussed according to clinical features, treatment and possible pathogenesis. In addition, neurological complications in children were assessed due to their atypical clinical features. Finally, dengue infection and Japanese encephalitis were compared for pathogenesis and main clinical manifestations.

  6. HYPONATREMIA IN CHILDREN. FOCUS — NEUROLOGICAL COMPLICATIONS

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    R.F. Tepaev

    2011-01-01

    Full Text Available Hyponatremia is the most common electrolyte disorder in patients at the hospital stage of treatment. Symptomatic hyponatremia is associated with severe neurological disorders. The degree of dysfunction varies from mild behavioral disturbances to convulsions, coma, or death, depending on the duration and depth of hyponatremia. Neurological disorders are caused, on one hand by edema and swelling of the brain on the background of hyponatremia, on the other — by the development of the osmotic demyelination syndrome in its rapid correction. Symptomatic hyponatremia is a threatening complication and is associated with a significant increase in mortality in children with a wide range of diseases. The article deals with the modern approaches to the pathophysiology, diagnosis and treatment of hyponatremia.Key words: hyponatremia, osmotic demyelination syndrome, children.

  7. Neurological abnormalities associated with CDMA exposure.

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    Hocking, B; Westerman, R

    2001-09-01

    Dysaesthesiae of the scalp and neurological abnormality after mobile phone use have been reported previously, but the roles of the phone per se or the radiations in causing these findings have been questioned. We report finding a neurological abnormality in a patient after accidental exposure of the left side of the face to mobile phone radiation [code division multiple access (CDMA)] from a down-powered mobile phone base station antenna. He had headaches, unilateral left blurred vision and pupil constriction, unilateral altered sensation on the forehead, and abnormalities of current perception thresholds on testing the left trigeminal ophthalmic nerve. His nerve function recovered during 6 months follow-up. His exposure was 0.015-0.06 mW/cm(2) over 1-2 h. The implications regarding health effects of radiofrequency radiation are discussed.

  8. An Inside Job: How Endosomal Na+/H+ Exchangers Link to Autism and Neurological Disease

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    Kalyan C. Kondapalli

    2014-06-01

    Full Text Available Autism imposes a major impediment to childhood development and a huge emotional and financial burden on society. In recent years, there has been rapidly accumulating genetic evidence that links the eNHE, a subset of Na+/H+ exchangers that localize to intracellular vesicles, to a variety of neurological conditions including autism, attention deficit hyperactivity disorder, intellectual disability and epilepsy. By providing a leak pathway for protons pumped by the V-ATPase, eNHE determine luminal pH and regulate cation (Na+, K+ content in early and recycling endosomal compartments. Loss-of-function mutations in eNHE cause hyperacidification of endosomal lumen, as a result of imbalance in pump and leak pathways. Two isoforms, NHE6 and NHE9 are highly expressed in brain, including hippocampus and cortex. Here, we summarize evidence for the importance of luminal cation content and pH on processing, delivery and fate of cargo and on the surface expression and function of membrane receptors and neurotransmitter transporters, drawing upon insights from model organisms and mammalian cells. These studies lead to cellular models of eNHE activity in pre- and post-synaptic neurons and astrocytes, where they could impact synapse development and plasticity. The study of eNHE has provided new insight on the mechanism of autism and other debilitating neurological disorders and opened up new possibilities for therapeutic intervention.

  9. Why neurology? Factors which influence career choice in neurology.

    Science.gov (United States)

    Albert, Dara V; Hoyle, Chad; Yin, Han; McCoyd, Matthew; Lukas, Rimas V

    2016-01-01

    To evaluate the factors which influence the decision to pursue a career in neurology. An anonymous survey was developed using a Likert scale to rate responses. The survey was sent to adult and child neurology faculty, residents and fellows, as well as medical students applying for neurology. Descriptive statistics were used to analyse the factors of influence. Respondents were subsequently categorized into pre-neurology trainees, neurology trainees, child neurologists and adult neurologists, and differences between the groups were analysed using Pearson's chi-square test. One hundred and thirty-three anonymous responses were received. The respondents were neurologists across all levels of training and practice. Across all respondents, the most common factor of high importance was intellectual content of specialty, challenging diagnostic problems, type of patient encountered and interest in helping people. Responses were similar across the groups; however, the earliest trainees cited interest in helping people as most important, while those in neurology training and beyond cite intellectual content of the specialty as most important. As trainees transition from their earliest levels of clinical experience into working as residents and faculty, there is a shift in the cited important factors. Lifestyle and financial factors seem to be the least motivating across all groups. Encouragement from peers, mentors, faculty and practicing physicians is considered high influences in a smaller number of neurologists. This may present an opportunity for practicing neurologists to make connections with medical students early in their education in an effort to encourage and mentor candidates.

  10. Neurologic Manifestations of Enterovirus 71 Infection in Korea.

    Science.gov (United States)

    Lee, Kyung Yeon; Lee, Myoung Sook; Kim, Dong Bin

    2016-04-01

    Enterovirus 71 frequently involves the central nervous system and may present with a variety of neurologic manifestations. Here, we aimed to describe the clinical features, magnetic resonance imaging (MRI) findings, and cerebrospinal fluid (CSF) profiles of patients presenting with neurologic complications of enterovirus 71 infection. We retrospectively reviewed the records of 31 pediatric patients hospitalized with acute neurologic manifestations accompanied by confirmed enterovirus 71 infection at Ulsan University Hospital between 2010 and 2014. The patients' mean age was 2.9 ± 5.5 years (range, 18 days to 12 years), and 80.6% of patients were less than 4 years old. Based on their clinical features, the patients were classified into 4 clinical groups: brainstem encephalitis (n = 21), meningitis (n = 7), encephalitis (n = 2), and acute flaccid paralysis (n = 1). The common neurologic symptoms included myoclonus (58.1%), lethargy (54.8%), irritability (54.8%), vomiting (48.4%), ataxia (38.7%), and tremor (35.5%). Twenty-five patients underwent an MRI scan; of these, 14 (56.0%) revealed the characteristic increased T2 signal intensity in the posterior region of the brainstem and bilateral cerebellar dentate nuclei. Twenty-six of 30 patients (86.7%) showed CSF pleocytosis. Thirty patients (96.8%) recovered completely without any neurologic deficits; one patient (3.2%) died due to pulmonary hemorrhage and shock. In the present study, brainstem encephalitis was the most common neurologic manifestation of enterovirus 71 infection. The characteristic clinical symptoms such as myoclonus, ataxia, and tremor in conjunction with CSF pleocytosis and brainstem lesions on MR images are pathognomonic for diagnosis of neurologic involvement by enterovirus 71 infection.

  11. Neurological Complications following Blood Transfusions in Sickle Cell Anemia

    Science.gov (United States)

    Khawar, Nayaab; Kulpa, Jolanta; Bellin, Anne; Proteasa, Simona; Sundaram, Revathy

    2017-01-01

    In Sickle Cell Anemia (SCA) patient blood transfusions are an important part of treatment for stroke and its prevention. However, blood transfusions can also lead to complications such as Reversible Posterior Leukoencephalopathy Syndrome (RPLS). This brief report highlights two cases of SCA who developed such neurological complications after a blood transfusion. RLPS should be considered as the cause of neurologic finding in patients with SCA and hypertension following a blood transfusion. PMID:28127478

  12. Congenital portosystemic shunts in five mature dogs with neurological signs.

    Science.gov (United States)

    Windsor, Rebecca Christine; Olby, Natasha J

    2007-01-01

    Congenital portosystemic shunts are a common cause of hepatic encephalopathy and are typically first identified when dogs are dogs with congenital portosystemic shunts; the dogs were presented for severe encephalopathic signs during middle or old age. Three dogs had portoazygos shunts, and four dogs had multifocal and lateralizing neurological abnormalities, including severe gait abnormalities and vestibular signs. All five dogs responded to medical or surgical treatment, demonstrating that older animals can respond to treatment even after exhibiting severe neurological signs.

  13. Early and Late Neurological Complications after Cardiac Transplantation

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    Mehmet Balkanay

    2011-08-01

    Full Text Available The clinical use of cyclosporine as an immunosuppressant improved the recipient’s life span and revolutionized the field of cardiac transplantation. But most of the immunesuppressant drugs including cyclosporine may cause neurological and many other side effects. In this article we present three cases, from 58 patients, undergoing cardiac transplantation at our hospital from 1989 to 2008 in whom developed transient neurological complications.

  14. Neurological Diagnostic Tests and Procedures

    Science.gov (United States)

    ... of diagnostic imaging techniques and chemical and metabolic analyses to detect, manage, and treat neurological disease. Some ... performed in a doctor’s office or at a clinic. Fluoroscopy is a type of x-ray that ...

  15. Neurological complications of underwater diving.

    Science.gov (United States)

    Rosińska, Justyna; Łukasik, Maria; Kozubski, Wojciech

    2015-01-01

    The diver's nervous system is extremely sensitive to high ambient pressure, which is the sum of atmospheric and hydrostatic pressure. Neurological complications associated with diving are a difficult diagnostic and therapeutic challenge. They occur in both commercial and recreational diving and are connected with increasing interest in the sport of diving. Hence it is very important to know the possible complications associated with this kind of sport. Complications of the nervous system may result from decompression sickness, pulmonary barotrauma associated with cerebral arterial air embolism (AGE), otic and sinus barotrauma, high pressure neurological syndrome (HPNS) and undesirable effect of gases used for breathing. The purpose of this review is to discuss the range of neurological symptoms that can occur during diving accidents and also the role of patent foramen ovale (PFO) and internal carotid artery (ICA) dissection in pathogenesis of stroke in divers. Copyright © 2014 Polish Neurological Society. Published by Elsevier Urban & Partner Sp. z o.o. All rights reserved.

  16. Neurologic Complications of Smallpox Vaccination

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    J Gordon Millichap

    2003-06-01

    Full Text Available Smallpox and smallpox vaccination is reviewed from the Departments of Neurology, Yale University School of Medicine, New Haven, CT, and University of New Mexico School of Medicine, Albuquerque.

  17. Neurological Complications of Bariatric Surgery.

    Science.gov (United States)

    Goodman, Jerry Clay

    2015-12-01

    Obesity has attained pandemic proportions, and bariatric surgery is increasingly being employed resulting in turn to more neurological complications which must be recognized and managed. Neurological complications may result from mechanical or inflammatory mechanisms but primarily result from micro-nutritional deficiencies. Vitamin B12, thiamine, and copper constitute the most frequent deficiencies. Neurological complications may occur at reasonably predictable times after bariatric surgery and are associated with the type of surgery used. During the early post-operative period, compressive or stretch peripheral nerve injury, rhabdomyolysis, Wernicke's encephalopathy, and inflammatory polyradiculoneuropathy may occur. Late complications ensue after months to years and include combined system degeneration (vitamin B12 deficiency) and hypocupric myelopathy. Bariatric surgery patients require careful nutritional follow-up with routine monitoring of micronutrients at 6 weeks and 3, 6, and 12 months post-operatively and then annually after surgery and multivitamin supplementation for life. Sustained vigilance for common and rare neurological complications is essential.

  18. Neurologic disorder and criminal responsibility.

    Science.gov (United States)

    Yaffe, Gideon

    2013-01-01

    Sufferers from neurologic and psychiatric disorders are not uncommonly defendants in criminal trials. This chapter surveys a variety of different ways in which neurologic disorder bears on criminal responsibility. It discusses the way in which a neurologic disorder might bear on the questions of whether or not the defendant acted voluntarily; whether or not he or she was in the mental state that is required for guilt for the crime; and whether or not he or she is deserving of an insanity defense. The discussion demonstrates that a just determination of whether a sufferer from a neurologic disorder is diminished in his or her criminal responsibility for harmful conduct requires equal appreciation of the nature of the relevant disorder and its impact on behavior, on the one hand, and of the legal import of facts about the psychologic mechanisms through which behavior is generated, on the other. © 2013 Elsevier B.V. All rights reserved.

  19. [The use of neurobion in neurological practice].

    Science.gov (United States)

    Kamchatnov, P R; Umarova, Kh Ya; Chugunov, A V

    2015-01-01

    Vitamins are actively involved in many metabolic processes of the nervous system. Their deficit may cause severe and, sometimes, irreversible consequences. Mechanisms of the therapeutic effects of the vitamin B complex neurobion are considered. Results of the studies on the efficacy and safety of neurobion in patients with polyneuropathies, including those caused by diabetes mellitus, pain syndromes of origin (skeletal/muscle pain, trauma etc) are presented. The necessity of using neurobion in treatment of a wide spectrum of nervous system diseases is emphasized.

  20. Historical perspective of Indian neurology

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    Shrikant Mishra

    2013-01-01

    Full Text Available Objective: To chronicle the history of medicine and neurology in India with a focus on its establishment and evolution. Background: The history of neurology in India is divided into two periods: ancient and modern. The ancient period dates back to the mid-second millennium Before Christ (B.C. during the creation of the Ayurvedic Indian system of Medicine, which detailed descriptions of neurological disorders called Vata Vyadhi. The early 20 th century witnessed the birth of modern Indian medicine with the onset of formal physician training at the nation′s first allopathic medical colleges located in Madras (1835, Calcutta (1835 and Mumbai (1848. Prior to India′s independence from Britain in 1947, only 25 medical schools existed in the entire country. Today, there are over 355. In 1951, physicians across the field of neurology and neurosurgery united to create the Neurological Society of India (NSI. Four decades later in 1991, neurologists branched out to establish a separate organization called the Indian Academy of Neurology (IAN. Design/Methods: Information was gathered through literature review using PubMed, MD Consult, OVID, primary texts and research at various academic institutions in India. Results: Neurological disorders were first described in ancient India under Ayurveda. The transition to modern medicine occurred more recently through formal training at medical schools beginning in the 1930′s. Early pioneers and founders of the NSI (1951 include Dr. Jacob Chandy, Dr. B Ramamurthi, Dr. S. T. Narasimhan and Dr. Baldev Singh. Later, Dr. J. S. Chopra, a prominent neurologist and visionary, recognized the need for primary centers of collaboration and subsequently established the IAN (1991. The future of Neurology in India is growing rapidly. Currently, there are 1100 practicing neurologists and more than 150 post-graduate trainees who join the ranks every year. As the number of neurologists rises across India, there is an increase in

  1. Historical perspective of Indian neurology

    Science.gov (United States)

    Mishra, Shrikant; Trikamji, Bhavesh; Singh, Sandeep; Singh, Parampreet; Nair, Rajasekharan

    2013-01-01

    Objective: To chronicle the history of medicine and neurology in India with a focus on its establishment and evolution. Background: The history of neurology in India is divided into two periods: ancient and modern. The ancient period dates back to the mid-second millennium Before Christ (B.C.) during the creation of the Ayurvedic Indian system of Medicine, which detailed descriptions of neurological disorders called Vata Vyadhi. The early 20th century witnessed the birth of modern Indian medicine with the onset of formal physician training at the nation's first allopathic medical colleges located in Madras (1835), Calcutta (1835) and Mumbai (1848). Prior to India's independence from Britain in 1947, only 25 medical schools existed in the entire country. Today, there are over 355. In 1951, physicians across the field of neurology and neurosurgery united to create the Neurological Society of India (NSI). Four decades later in 1991, neurologists branched out to establish a separate organization called the Indian Academy of Neurology (IAN). Design/Methods: Information was gathered through literature review using PubMed, MD Consult, OVID, primary texts and research at various academic institutions in India. Results: Neurological disorders were first described in ancient India under Ayurveda. The transition to modern medicine occurred more recently through formal training at medical schools beginning in the 1930's. Early pioneers and founders of the NSI (1951) include Dr. Jacob Chandy, Dr. B Ramamurthi, Dr. S. T. Narasimhan and Dr. Baldev Singh. Later, Dr. J. S. Chopra, a prominent neurologist and visionary, recognized the need for primary centers of collaboration and subsequently established the IAN (1991). The future of Neurology in India is growing rapidly. Currently, there are 1100 practicing neurologists and more than 150 post-graduate trainees who join the ranks every year. As the number of neurologists rises across India, there is an increase in the amount of

  2. A Neuron-Specific Gene Therapy Relieves Motor Deficits in Pompe Disease Mice.

    Science.gov (United States)

    Lee, Ni-Chung; Hwu, Wuh-Liang; Muramatsu, Shin-Ichi; Falk, Darin J; Byrne, Barry J; Cheng, Chia-Hao; Shih, Nien-Chu; Chang, Kai-Ling; Tsai, Li-Kai; Chien, Yin-Hsiu

    2017-09-11

    In Pompe disease, deficient lysosomal acid α-glucosidase (GAA) activity causes glycogen accumulation in the muscles, which leads to weakness, cardiomyopathy, and respiratory failure. Although glycogen accumulation also occurs in the nervous system, the burden of neurological deficits in Pompe disease remains obscure. In this study, a neuron-specific gene therapy was administered to Pompe mice through intracerebroventricular injection of a viral vector carrying a neuron-specific promoter. The results revealed that gene therapy increased GAA activity and decreased glycogen content in the brain and spinal cord but not in the muscles of Pompe mice. Gene therapy only slightly increased the muscle strength of Pompe mice but substantially improved their performance on the rotarod, a test measuring motor coordination. Gene therapy also decreased astrogliosis and increased myelination in the brain and spinal cord of Pompe mice. Therefore, a neuron-specific treatment improved the motor coordination of Pompe mice by lowering glycogen accumulation, decreasing astrogliosis, and increasing myelination. These findings indicate that neurological deficits are responsible for a significant burden in Pompe disease.

  3. Neurological recovery at age 92 after acute trauma and operative spinal decompression

    Directory of Open Access Journals (Sweden)

    Hazem Eltahawy, MD, PhD, FRCS, FACS

    2016-09-01

    Full Text Available People aged > 80 years are among the fastest growing segments of most Western societies. With improved lifestyles and medical care, complex surgical interventions will be increasingly offered to elderly patients. Questions will arise about the value of performing major surgery in patients near their postulated end of life. Here, we describe a near-full neurological recovery from a profound neurological deficit that occurred as a result of a spinal fracture after a fall. To our knowledge, this is the first report of neurological recovery at such an advanced age.

  4. NEUROLOGICAL DISORDERS IN PATIENTS WITH HYPERTENSION AND THEIR CORRECTION

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    N. V. Vakhnina

    2016-01-01

    Full Text Available Neurological disorders in hypertensive patients can be caused by both brain injury and concomitant diseases. The elucidation of the causes of neurological disorders and their effective treatment contribute to hypertensive patients’ better adherence to long-term antihypertensive therapy, which normalizes blood pressure (BP and reduces the risk of cerebral complications Objective: to study of the causes of neurological disorders in hypertensive patients and the efficiency of their correction using a new dispersible vinpocetine formulation (Cavinton® Comforte in combined therapy.Patients and methods. A total of 80 patients (men (20% and women (80%; mean age 63±12.3  years with neurological complaints in the presence of hypertension were examined. All the patients were diagnosed with dyscirculatory encephalopathy or chronic brain ischemia, whether they had vascular cognitive impairment. The examination of patients revealed that the neurological complaints were mainly due to concomitant diseases, such as migraine (12%, tension-type headache (66%, and the latter concurrent with migraine (4%.Results and  discussion. The  effective treatment of concomitant diseases in  combination with antihypertensive therapy contributed to normalization of BP and regression of complaints. The most pronounced effect was noted in 40 patients whose combination therapy included Vinpocetine (Cavinton® Comforte 10 mg thrice daily.Conclusion. The therapy resulted in the less severity of both the symptoms of cerebrovascular disease (vascular cognitive impairment and comorbid neurological disorders (headache, dizziness, etc..

  5. Efficacy of Urtoxazumab (TMA-15 Humanized Monoclonal Antibody Specific for Shiga Toxin 2 Against Post-Diarrheal Neurological Sequelae Caused by Escherichia coli O157:H7 Infection in the Neonatal Gnotobiotic Piglet Model

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    Rodney A. Moxley

    2017-01-01

    Full Text Available Enterohemorrhagic Escherichia coli (EHEC is the most common cause of hemorrhagic colitis and hemolytic uremic syndrome in human patients, with brain damage and dysfunction the main cause of acute death. We evaluated the efficacy of urtoxazumab (TMA-15, Teijin Pharma Limited, a humanized monoclonal antibody against Shiga toxin (Stx 2 for the prevention of brain damage, dysfunction, and death in a piglet EHEC infection model. Forty-five neonatal gnotobiotic piglets were inoculated orally with 3 × 109 colony-forming units of EHEC O157:H7 strain EDL933 (Stx1+, Stx2+ when 22–24 h old. At 24 h post-inoculation, piglets were intraperitoneally administered placebo or TMA-15 (0.3, 1.0 or 3.0 mg/kg body weight. Compared to placebo (n = 10, TMA-15 (n = 35 yielded a significantly greater probability of survival, length of survival, and weight gain (p <0.05. The efficacy of TMA-15 against brain lesions and death was 62.9% (p = 0.0004 and 71.4% (p = 0.0004, respectively. These results suggest that TMA-15 may potentially prevent or reduce vascular necrosis and infarction of the brain attributable to Stx2 in human patients acutely infected with EHEC. However, we do not infer that TMA-15 treatment will completely protect human patients infected with EHEC O157:H7 strains that produce both Stx1 and Stx2.

  6. Neurological signs in 23 dogs with suspected rostral cerebellar ischaemic stroke.

    Science.gov (United States)

    Thomsen, Barbara; Garosi, Laurent; Skerritt, Geoff; Rusbridge, Clare; Sparrow, Tim; Berendt, Mette; Gredal, Hanne

    2016-06-07

    In dogs with ischaemic stroke, a very common site of infarction is the cerebellum. The aim of this study was to characterise neurological signs in relation to infarct topography in dogs with suspected cerebellar ischaemic stroke and to report short-term outcome confined to the hospitalisation period. A retrospective multicentre study of dogs with suspected cerebellar ischaemic stroke examined from 2010-2015 at five veterinary referral hospitals was performed. Findings from clinical, neurological, and paraclinical investigations including magnetic resonance imaging were assessed. Twenty-three dogs, 13 females and 10 males with a median age of 8 years and 8 months, were included in the study. The Cavalier King Charles Spaniel (n = 9) was a commonly represented breed. All ischaemic strokes were located to the vascular territory of the rostral cerebellar artery including four extensive and 19 limited occlusions. The most prominent neurological deficits were gait abnormalities (ataxia with hypermetria n = 11, ataxia without hypermetria n = 4, non-ambulatory n = 6), head tilt (n = 13), nystagmus (n = 8), decreased menace response (n = 7), postural reaction deficits (n = 7), and proprioceptive deficits (n = 5). Neurological signs appeared irrespective of the infarct being classified as extensive or limited. All dogs survived and were discharged within 1-10 days of hospitalisation. Dogs affected by rostral cerebellar ischaemic stroke typically present with a collection of neurological deficits characterised by ataxia, head tilt, and nystagmus irrespective of the specific cerebellar infarct topography. In dogs with peracute to acute onset of these neurological deficits, cerebellar ischaemic stroke should be considered an important differential diagnosis, and neuroimaging investigations are indicated. Although dogs are often severely compromised at presentation, short-term prognosis is excellent and rapid clinical improvement may be observed within the

  7. Neurological oxygen toxicity.

    Science.gov (United States)

    Farmery, Scott; Sykes, Oliver

    2012-10-01

    SCUBA diving has several risks associated with it from breathing air under pressure--nitrogen narcosis, barotrauma and decompression sickness (the bends). Trimix SCUBA diving involves regulating mixtures of nitrogen, oxygen and helium in an attempt to overcome the risks of narcosis and decompression sickness during deep dives, but introduces other potential hazards such as hypoxia and oxygen toxicity convulsions. This study reports on a seizure during the ascent phase, its potential causes and management and discusses the hazards posed to the diver and his rescuer by an emergency ascent to the surface.

  8. Neurology in the Vietnam War.

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    Gunderson, Carl H; Daroff, Robert B

    2016-01-01

    Between December 1965 and December 1971, the United States maintained armed forces in Vietnam never less than 180,000 men and women in support of the war. At one time, this commitment exceeded half a million soldiers, sailors, and airmen from both the United States and its allies. Such forces required an extensive medical presence, including 19 neurologists. All but two of the neurologists had been drafted for a 2-year tour of duty after deferment for residency training. They were assigned to Vietnam for one of those 2 years in two Army Medical Units and one Air Force facility providing neurological care for American and allied forces, as well as many civilians. Their practice included exposure to unfamiliar disorders including cerebral malaria, Japanese B encephalitis, sleep deprivation seizures, and toxic encephalitis caused by injection or inhalation of C-4 explosive. They and neurologists at facilities in the United States published studies on all of these entities both during and after the war. These publications spawned the Defense and Veterans Head Injury Study, which was conceived during the Korean War and continues today as the Defense and Veterans Head Injury Center. It initially focused on post-traumatic epilepsy and later on all effects of brain injury. The Agent Orange controversy arose after the war; during the war, it was not perceived as a threat by medical personnel. Although soldiers in previous wars had developed serious psychological impairments, post-traumatic stress disorder was formally recognized in the servicemen returning from Vietnam. © 2016 S. Karger AG, Basel.

  9. Nanotechnology based diagnostics for neurological disorders

    Energy Technology Data Exchange (ETDEWEB)

    Kurek, Nicholas S.; Chandra, Sathees B., E-mail: schandra@roosevelt.edu [Department of Biological, Chemical and Physical Sciences, Roosevelt University, Chicago, IL (United States)

    2012-07-01

    Nanotechnology involves probing and manipulating matter at the molecular level. Nanotechnology based molecular diagnostics have the potential to alleviate the suffering caused by many diseases, including neurological disorders, due to the unique properties of nanomaterials. Most neurological illnesses are multifactorial conditions and many of these are also classified as neurobehavioral disorders. Alzheimer's disease, Parkinson's disease, Huntington disease, cerebral ischemia, epilepsy, schizophrenia and autism spectrum disorders like Rett syndrome are some examples of neurological disorders that could be better treated, diagnosed, prevented and possibly cured using nanotechnology. In order to improve the quality of life for disease afflicted people, a wide range of nanomaterials that include gold and silica nanoparticles, quantum dots and DNA along with countless other forms of nanotechnology have been investigated regarding their usefulness in advancing molecular diagnostics. Other small scaled materials like viruses and proteins also have potential for use as molecular diagnostic tools. Information obtained from nanotechnology based diagnostics can be stored and manipulated using bioinformatics software. More advanced nanotechnology based diagnostic procedures for the acquisition of even greater proteomic and genomic knowledge can then be developed along with better ways to fight various diseases. Nanotechnology also has numerous applications besides those related to biotechnology and medicine. In this article, we will discuss and analyze many novel nanotechnology based diagnostic techniques at our disposal today. (author)

  10. The neurology of acutely failing respiratory mechanics.

    Science.gov (United States)

    Wijdicks, Eelco F M

    2017-04-01

    Forces involved in breathing-which effectively pull in air-are the diaphragmatic, intercostal, spine, and neck muscles. Equally important is the bulbar musculature maintaining the architecture of a patent airway conduit and abdominal wall and internal intercostal muscles providing cough. Acute injury along a neural trajectory from brainstem to muscle will impair the coordinated interaction between these muscle groups. Acutely failing respiratory mechanics can be caused by central and peripheral lesions. In central lesions, the key lesion is in the nucleus ambiguus innervating the dilator muscles of the soft palate, pharynx, and larynx, but abnormal respiratory mechanics rarely coincide with abnormalities of the respiratory pattern generator. In peripheral lesions, diaphragmatic weakness is a main element, but in many neuromuscular disorders mechanical upper airway obstruction from oropharyngeal weakness contributes equally to an increased respiratory load. The neurology of breathing involves changes in respiratory drive, rhythm, mechanics, and dynamics. This review focuses on the fundamentals of abnormal respiratory mechanics in acute neurologic conditions, bedside judgment, interpretation of additional laboratory tests, and initial stabilization, with practical solutions provided. Many of these respiratory signs are relevant to neurologists, who in acute situations may see these patients first. Ann Neurol 2017;81:485-494. © 2017 American Neurological Association.

  11. Neurological manifestations of cardiac myxoma: experience in a referral hospital.

    Science.gov (United States)

    Pérez Andreu, J; Parrilla, G; Arribas, J M; García-Villalba, B; Lucas, J J; Garcia Navarro, M; Marín, F; Gutierrez, F; Moreno, A

    2013-01-01

    Cardiac myxoma is an important but uncommon cause of stroke in younger patients. Few published case series analyse the frequency and clinical presentation of neurological complications in patients with myxoma. To list all neurological complications from cardiac myxoma recorded in our hospital in the past 28 years. We retrospectively reviewed the neurological manifestations of cardiac myxoma in patients treated in our hospital between December 1983 and March 2012. Of the 36 patients with cardiac myxoma, 8 (22%) presented neurological manifestations. Half were women and mean age of patients was 52.4 ± 11.6 years. Sudden-onset hemiparesis was the most frequent neurological symptom (63%). Established ischaemic stroke was the most common clinical manifestation (75%), followed by transient ischemic attack. The most commonly affected territory corresponded to the middle cerebral artery. Myxoma was diagnosed by echocardiography in all cases. Mean myxoma size was 4.1cm and most of the tumours (63%) had a polypoid surface. All tumours were successfully removed by surgery. There were no in-hospital deaths. Cardiac myxomas frequently present with neurological symptoms, especially ischaemic events (established stroke or transient ischaemic attack), in younger patients with no cardiovascular risk factors. The anterior circulation is more frequently affected, especially the middle cerebral artery. Echocardiography can facilitate prompt diagnosis and early treatment of the lesion. Copyright © 2012 Sociedad Española de Neurología. Published by Elsevier Espana. All rights reserved.

  12. [Paraneoplastic neurological syndrome--definition and history].

    Science.gov (United States)

    Inuzuka, Takashi

    2010-04-01

    Paraneoplastic neurological syndrome (PNS) may affect any part of the nervous system and muscles. PNS is a rare disorder caused by the remote effects of cancer and is considered to be immune-mediated. Since the 1980s, several specific onco-neural antibodies and T-cell responses against onco-neural molecules have been reported, as shown in the historical review in this article. Immunoresponses to cancer are considered to cross-react with self-antigens in the nervous system or muscle. The presence of such onco-neural antibodies is a useful diagnostic marker for PNS and occult cancer. Despite sustained efforts to elucidate the effects of such antibodies on neuron, only a few onco-neural antibodies have been identified as primary effectors of neurological symptoms. However the absence of these antibodies does not exclude a PNS. In some instances, these antibodies can be detected in cancer patients without PNS. PNS diagnosis requires excluding many other complications of cancer and mimics of other neurological diseases as differential diagnoses. Recently, an international panel of experts provided useful diagnostic criteria for PNS. These criteria are based on well-characterized onco-neural antibodies and specific neurological syndromes. Probable cases of PNS are strongly advised to undergo early antitumor therapy and immunotherapy to prevent progressive neuronal death. As the symptoms of PNS often appear before the diagnosis of malignant cancer, repeated searches for occult cancer are recommended, if the tumor has not yet been found. Further studies are required to clarify the exact mechanisms underlying neuronal damage in PNS, which may lead to the development of more rational therapies and greater understanding of immunology in the nervous system.

  13. The natural history and management of patients with congenital deficits associated with lumbosacral lipomas.

    Science.gov (United States)

    Tu, Albert; Hengel, Ross; Cochrane, D Douglas

    2016-04-01

    Many patients with lumbosacral lipoma are asymptomatic; however, a significant proportion will have neurological deficits present at birth. Implication of these deficits with respect to natural history and management are not well understood. A retrospective review of all infants with lumbosacral lipoma seen at BCCH between 1997 and 2013 was carried out. The study population was stratified on the presence of a congenital, non-progressive deficit and subdivided on treatment approach. The subsequent developments of deficits resulting in untethering procedures were recorded. Of the 44 infants in this study, 24 patients had no neurologic deficit while 20 patients had a fixed, non-progressive deficit evident at birth. Ten of 24 patients without a neurological deficit at birth underwent a prophylactic untethering with 3 eventually requiring repeat untethering after, on average, 62.7 months. Eleven of 14 asymptomatic, monitored patients required untethering for clinical deterioration. Two required a second untethering procedure after 48.7 months. Ten of 20 infants with congenital deficits present at birth underwent prophylactic untethering, and 4 required further surgery after 124 months. Ten patients underwent observation with 8 eventually requiring surgery. Two required repeat untethered after 154 months. The complication rates and operative burden for patients are similar whether prophylactic or delayed surgery is performed. The presence of congenital neurologic deficit does not affect the likelihood of deterioration in patients managed expectantly; prophylactic detethering of these patients did not prevent delayed neurologic deterioration. Comparing the need for repeat surgery in prophylactically untethered patients with initial untethering of patients operated upon at the time of deterioration, prophylactic untethering may confer a benefit with respect to subsequent symptomatic tethering if complication rates are low. However, in a setting with multidisciplinary

  14. MULTIPLE MYELOMA OF THE SPINE: SURVIVAL, COMPLICATIONS, AND NEUROLOGICAL STATUS AFTER SURGICAL TREATMENT

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    N. S. Zaborovskii

    2016-01-01

    Full Text Available Purpose – to evaluate the survival, neurological status, and complications after surgical management of patients with multiple myeloma of the spine. Materials and methods. A retrospective study of 44 patients with multiple myeloma of the spine operated in Vreden Institute of Traumatology and Orthopedics was held in the period between 2000 and 2015. Patients underwent decompressive surgery with additional spinal instrumentation. following parameters were evaluated: demographic data, pain intensity, neurological deficit, survival, and complications after surgery. Results. Overall results showed efficiency of surgical management of spinal instability and neurological compromise due to multiple myeloma of the spine. The mean postoperative survival time was 63 months. A significant improvement in VAS scale and neurological function was observed in the study population after surgery. Postoperative VAS was 7.1 scores compared with 3.6 scores preoperatively (p = 0.021. Twenty nine of 31 patients improved their neurological status. Poor life expectancy was associated with neurological deficit both before and after surgery (p<0.0001. There were 28 postoperative complications. Most frequent complications were deep wound infection and adjacent degenerative disease. There was no survival difference in cohorts with and without complications (p = 0.942.> <0.0001. There were 28 postoperative complications. Most frequent complications were deep wound infection and adjacent degenerative disease. There was no survival difference in cohorts with and without complications (p = 0.942. Conclusion. Decompression surgery with additional instrumentation significantly decrease pain intensity and improve neurological function in selected patients affected by spinal myeloma with spinal instability. Severe neurological deficit influence on survival both before and after surgery. Survival did not depend on complications.

  15. Neurological aspects of vibroacoustic disease.

    Science.gov (United States)

    Martinho Pimenta, A J; Castelo Branco, N A

    1999-03-01

    Mood and behavioral abnormalities are the most common early findings related to vibroacoustic disease (VAD). Other signs and symptoms have been observed in VAD patients. Brain MRI discloses small multifocal lesions in about 50% of subjects with more than 10 yr of occupational exposure to large pressure amplitude (> or = 90 dB SPL) and low frequency (< or = 500 Hz) (LPALF) noise. However, to date, there have been no studies globally integrating all the neurological, imaging and neurophysiological data of VAD patients. This is the main goal of this study. The 60 male Caucasians diagnosed with VAD were neurologically evaluated in extreme detail in order to systematically identify the most common and significant neurological disturbances in VAD. This population demonstrates cognitive changes (identified through psychological and neurophysiological studies (ERP P300)), vertigo and auditory changes, visual impairment, epilepsy, and cerebrovascular diseases. Neurological examination reveals pathological signs and reflexes, most commonly the palmo-mental reflex. A vascular pattern underlying the multifocal hyperintensities in T2 MR imaging, with predominant involvement of the small arteries of the white matter, is probably the visible organic substratum of the neurological picture. However, other pathophyisological mechanisms are involved in epileptic symptomatology.

  16. Neurological manifestations in HIV positive patients in Tehran, Iran

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    Minoo Mohraz

    2014-02-01

    Full Text Available Objective: To evaluate the neurological complications among Iranian HIV-positive patients. Methods: This cross-sectional study was conducted among 428 patients diagnosed with HIV infection between 2006 and 2009 at Imam Khomeini hospital, Tehran, Iran. Demographic and clinical variables as well as laboratory tests were extracted and analyzed. Also, another 100 patients refereed to Voluntary Counseling and Testing center of the hospital were visited and evaluated for neurological complications. Results: Among the patients, neurologic manifestations were observed in 34 (7.94% patients. Twenty three percent of the patients received antiretroviral therapy. Identified causes included brain toxoplasmosis (14.7%, progressive multi-focal leuko encephalopathy (5.9%, HIV encephalopathy (5.9%, TB meningitis (5% and unknown etiologies (11.8%. Also, among 100 patients who were admitted and visited at the Voluntary Counseling and Testing center, no one was diagnosed for any neurological manifestations. Conclusions: According to our results, toxoplasmosis is the most frequent cause of neurological conditions among Iranian HIV infected patients and should be considered in any HIV/AIDS patient with neurological manifestations.

  17. Neurological complications of kernicterus.

    Science.gov (United States)

    AlOtaibi, Suad F; Blaser, Susan; MacGregor, Daune L

    2005-08-01

    Prevention of bilirubin encephalopathy relies on the detection of newborns who are at risk of developing serious hyperbilirubinemia. The objective of this study was to reassess the clinical syndrome of kernicterus as neurodiagnostic studies have become more readily available and can be used to evaluate these infants. The study population was neonates born at term or near term admitted to The Hospital for Sick Children in Toronto, Ontario, Canada, between January 1990 and May 2000. During the study period, there were 9776 admissions (average number of admissions per year--888 infants). The inclusion criteria were that patients had total serum bilirubin levels of >400 micromol/L at the time of diagnosis and no evidence of hypoxic ischemic encephalopathy. Records were reviewed to establish neurodevelopment outcomes. Twelve neonates (nine males) were identified. Bilirubin levels at the time of diagnosis ranged from 405 to 825 micromol/L. Causes of these elevated levels included glucose-6-phosphate dehydrogenase deficiency (seven patients), dehydration (three patients), sepsis (one patient), and was undetermined in one patient. Abnormal visual evoked potentials were found in three of nine patients and abnormal brainstem auditory evoked potentials in seven of ten patients. Abnormal electroencephalograms were documented in five patients studied. Brain magnetic resonance imaging results were abnormal in three of four patients. Magnetic resonance imaging typically showed an increased signal in the posteromedial aspect of the globus pallidus and was, therefore, useful in the assessment of the structural changes of chronic bilirubin encephalopathy after kernicterus.

  18. Neurological abnormalities in the `cri-du-chat' syndrome 1

    Science.gov (United States)

    Colover, Jack; Lucas, Mary; Comley, J. A.; Roe, A. M.

    1972-01-01

    An unusual case of the cri-du-chat syndrome is described in a 6½ year old boy, who, as well as attacks of stridor and choking, showed disorders of spatial perception and cerebellar signs in the form of nystagmus, clumsiness of the hands, and ataxia. Pyramidal signs were also present. He was only mildly retarded mentally. Psychological testing showed that he had a severe deficit for number processing, and also constructional apraxia. Surprisingly, his vocabulary was quite good, as was his reading capacity. Chromosome analysis showed a very small deletion of the short arm of the group B chromosome. In infancy this diagnosis may be suspected because of the high-pitched cry and attacks of stridor and choking. In late childhood, when the signs may be only of a neurological disorder, its recognition may be difficult without confirmation from chromosome studies. The neurological features of this disease are reviewed. Images PMID:5084140

  19. Neurobehavioral, neurologic, and neuroimaging characteristics of fetal alcohol spectrum disorders.

    Science.gov (United States)

    Glass, Leila; Ware, Ashley L; Mattson, Sarah N

    2014-01-01

    Alcohol consumption during pregnancy can have deleterious consequences for the fetus, including changes in central nervous system development leading to permanent neurologic alterations and cognitive and behavioral deficits. Individuals affected by prenatal alcohol exposure, including those with and without fetal alcohol syndrome, are identified under the umbrella of fetal alcohol spectrum disorders (FASD). While studies of humans and animal models confirm that even low to moderate levels of exposure can have detrimental effects, critical doses of such exposure have yet to be specified and the most clinically significant and consistent consequences occur following heavy exposure. These consequences are pervasive, devastating, and can result in long-term dysfunction. This chapter summarizes the neurobehavioral, neurologic, and neuroimaging characteristics of FASD, focusing primarily on clinical research of individuals with histories of heavy prenatal alcohol exposure, although studies of lower levels of exposure, particularly prospective, longitudinal studies, will be discussed where relevant. © 2014 Elsevier B.V. All rights reserved.

  20. Specific Language Impairment, Nonverbal IQ, Attention-Deficit/Hyperactivity Disorder, Autism Spectrum Disorder, Cochlear Implants, Bilingualism, and Dialectal Variants: Defining the Boundaries, Clarifying Clinical Conditions, and Sorting out Causes

    Science.gov (United States)

    Rice, Mabel L.

    2016-01-01

    Purpose: The purpose of this research forum article is to provide an overview of a collection of invited articles on the topic "specific language impairment (SLI) in children with concomitant health conditions or nonmainstream language backgrounds." Topics include SLI, attention-deficit/hyperactivity disorder, autism spectrum disorder,…

  1. Neurologic long term outcome after drowning in children

    Directory of Open Access Journals (Sweden)

    Suominen Pertti K

    2012-08-01

    Full Text Available Abstract Drowning is a major source of mortality and morbidity in children worldwide. Neurocognitive outcome of children after drowning incidents cannot be accurately predicted in the early course of treatment. Therefore, aggressive out-of-hospital and in-hospital treatment is emphasized. There are "miracle" cases after long submersion times that have been reported in the medical literature, which mostly concern small children. However, many of the survivors will remain severely neurologically compromised after remarkably shorter submersion times and will consequently be a great burden to their family and society for the rest of their lives. The duration of submersion, the need of advanced life support at the site of the accident, the duration of cardiopulmonary resuscitation, whether spontaneous breathing and circulation are present on arrival at the emergency room are important factors related to survival with mild neurological deficits or intact function in drowned children. Data on long-term outcome are scarce. The used outcome measurement methods and the duration of follow-up have not been optimal in most of the existing studies. Proper neurological and neurophysiological examinations for drowned children are superior to outcome scales based chart reviews. There is evidence that gross neurological examination at the time of discharge from the hospital in young children does not reveal all the possible sequelae related to hypoxic brain injury and thus long-term follow-up of drowned resuscitated children is strongly recommended.

  2. Neurologic considerations in propionic acidemia.

    Science.gov (United States)

    Schreiber, John; Chapman, Kimberly A; Summar, Marshall L; Ah Mew, Nicholas; Sutton, V Reid; MacLeod, Erin; Stagni, Kathy; Ueda, Keiko; Franks, Jill; Island, Eddie; Matern, Dietrich; Peña, Loren; Smith, Brittany; Urv, Tiina; Venditti, Charles; Chakarapani, Anupam; Gropman, Andrea L

    2012-01-01

    Propionic acidemia (PA) is an organic acidemia which has a broad range of neurological complications, including developmental delay, intellectual disability, structural abnormalities, metabolic stroke-like episodes, seizures, optic neuropathy, and cranial nerve abnormalities. As the PA consensus conference hosted by Children's National Medical Center progressed from January 28 to 30, 2011, it became evident that neurological complications were common and a major component of morbidity, but the role of imaging and the basis for brain pathophysiology were unclear. This paper reviews the hypothesized pathophysiology, presentation and uses the best available evidence to suggest programs for treatment, imaging, and monitoring the neurological complications of PA. Copyright © 2011. Published by Elsevier Inc. All rights reserved.

  3. Acupuncture application for neurological disorders.

    Science.gov (United States)

    Lee, Hyangsook; Park, Hi-Joon; Park, Jongbae; Kim, Mi-Ja; Hong, Meesuk; Yang, Jongsoo; Choi, Sunmi; Lee, Hyejung

    2007-01-01

    Acupuncture has been widely used for a range of neurological disorders. Despite its popularity, the evidence to support the use of acupuncture is contradictory. This review was designed to summarize and to evaluate the available evidence of acupuncture for neurological disorders. Most of the reviewed studies suffer from lack of methodological rigor. Owing to paucity and poor quality of the primary studies, no firm conclusion could be drawn on the use of acupuncture for epilepsy, Alzheimer's disease, Parkinson's disease, ataxic disorders, multiple sclerosis, amyotrophic lateral sclerosis and spinal cord injury. For stroke rehabilitation, the evidence from recent high-quality trials and previous systematic reviews is not convincing. More rigorous trials are warranted to establish acupuncture's role in neurological disorders.

  4. Quality Metrics in Inpatient Neurology.

    Science.gov (United States)

    Dhand, Amar

    2015-12-01

    Quality of care in the context of inpatient neurology is the standard of performance by neurologists and the hospital system as measured against ideal models of care. There are growing regulatory pressures to define health care value through concrete quantifiable metrics linked to reimbursement. Theoretical models of quality acknowledge its multimodal character with quantitative and qualitative dimensions. For example, the Donabedian model distils quality as a phenomenon of three interconnected domains, structure-process-outcome, with each domain mutually influential. The actual measurement of quality may be implicit, as in peer review in morbidity and mortality rounds, or explicit, in which criteria are prespecified and systemized before assessment. As a practical contribution, in this article a set of candidate quality indicators for inpatient neurology based on an updated review of treatment guidelines is proposed. These quality indicators may serve as an initial blueprint for explicit quality metrics long overdue for inpatient neurology. Thieme Medical Publishers 333 Seventh Avenue, New York, NY 10001, USA.

  5. [Child neurology and multimedia technology].

    Science.gov (United States)

    Nihei, Kenji

    2002-01-01

    Methods of computer technology (intelligent technology, IT), such as multimedia and virtual reality, are utilized more and more in all medical fields including child neurology. Advances in the digitalization of individual medical data and multi-media technology have enabled patients to be able to obtain their own medical data by small media and to receive medical treatment at any hospitals even if they are located in distance place. Changes from a doctor oriented to patients oriented medicine is anticipated. It is necessary to store medical data from birth to adulthood and to accumulate epidemiological data of rare diseases such as metabolic diseases or degenerative diseases especially in child neurology, which highly require tele medicine and telecare at home. Moreover, IT may improve in the QOL of patients with neurological diseases and of their families. Cooperation of medicine and engineering is therefore necessary. Results of our experiments on telemedicine, telecare and virtual reality are described.

  6. Neurological manifestation of colonic adenocarcinoma

    Directory of Open Access Journals (Sweden)

    Uzair Chaudhary

    2012-04-01

    Full Text Available Paraneoplastic neurologic disorders are extremely rare in cancer patients and are most commonly associated with certain tumors, such as ovarian cancer, small cell lung cancer, and breast cancer. We report here a paraneoplastic neurological syndrome in a 53-year-old man with colonic adenocarcinoma with a solitary liver metastasis. His paraneoplastic syndrome was successfully treated by methylprednisolone and primary oncologic therapies including neoadjuvant chemotherapy and definitive surgery. This is also the first documented case of simultaneous manifestation of a sensory neuropathy and limbic encephalitis with colon cancer.

  7. Sleep disorders in neurological practice

    Directory of Open Access Journals (Sweden)

    Mikhail Guryevich Poluektov

    2012-01-01

    Full Text Available Sleep disorders are closely associated with both nervous system diseases and mental disorders; however, such patients prefer to seek just neurological advice. Insomnia is the most common complaint in routine clinical practice. It is characterized by different impairments in sleep and daytime awakening. Obstructive sleep apnea syndrome is less common, but more clinically important because of its negative impact on the cardiovascular and nervous systems. The common neurological disorders are restless legs syndrome and REM sleep behavior disorder, as well as narcolepsy, the major manifestations of which are impaired nocturnal sleep and daytime awakening.

  8. Good neurological outcome after accidental hyopthermia presenting with asytole.

    Science.gov (United States)

    Eckert, I; Imboden, P; Paal, P; Koppenberg, J

    2017-03-01

    A 43-year-old woman became exhausted and fainted on descent at 1127 MAMSL altitude and snowfall. A rescue team diagnosed asystole. With manual cardiopulmonary resuscitation (CPR) she was transported to the next extracorporeal life support (ECLS) center. Admission temperature was 20.7 °C. CPR continued until ECLS was initiated. Two days later she was awake, orientated, and with no neurological deficits. With hypothermic cardiac arrest, a favorable outcome depends on early continuous CPR, triage, and ECLS rewarming. It holds true that "nobody is dead until they are warmed and dead" if one cools first and arrests thereafter.

  9. Adhesive arachnoiditis in mixed connective tissue disease: a rare neurological manifestation.

    Science.gov (United States)

    Khan, Maria Usman; Devlin, James Anthony Joseph; Fraser, Alexander

    2016-12-16

    The overall incidence of neurological manifestations is relatively low among patients with mixed connective tissue disease (MCTD). We recently encountered a case of autoimmune adhesive arachnoiditis in a young woman with 7 years history of MCTD who presented with severe back pain and myeloradiculopathic symptoms of lower limbs. To the best of our knowledge, adhesive arachnoiditis in an MCTD patient has never been previously reported. We report here this rare case, with the clinical picture and supportive ancillary data, including serology, cerebral spinal fluid analysis, electrophysiological evaluation and spinal neuroimaging, that is, MRI and CT (CT scan) of thoracic and lumbar spine. Her neurological deficit improved after augmenting her immunosuppressant therapy. Our case suggests that adhesive arachnoiditis can contribute to significant neurological deficits in MCTD and therefore requires ongoing surveillance. 2016 BMJ Publishing Group Ltd.

  10. Expanding the neurological examination using functional neurologic assessment: part II neurologic basis of applied kinesiology.

    Science.gov (United States)

    Schmitt, W H; Yanuck, S F

    1999-03-01

    Functional Neurologic Assessment and treatment methods common to the practice of applied kinesiology are presented. These methods are proposed to enhance neurological examination and treatment procedures toward more effective assessment and care of functional impairment. A neurologic model for these procedures is proposed. Manual assessment of muscular function is used to identify changes associated with facilitation and inhibition, in response to the introduction of sensory receptor-based stimuli. Muscle testing responses to sensory stimulation of known value are compared with usually predictable patterns based on known neuroanatomy and neurophysiology, guiding the clinician to an understanding of the functional status of the patient's nervous system. These assessment procedures are used in addition to other standard diagnostic measures to augment rather than replace the existing diagnostic armamentarium. The proper understanding of the neurophysiologic basis of muscle testing procedures will assist in the design of further investigations into applied kinesiology. Accordingly, the neurophysiologic basis and proposed mechanisms of these methods are reviewed.

  11. Auditory Temporal Processing as a Specific Deficit among Dyslexic Readers

    Science.gov (United States)

    Fostick, Leah; Bar-El, Sharona; Ram-Tsur, Ronit

    2012-01-01

    The present study focuses on examining the hypothesis that auditory temporal perception deficit is a basic cause for reading disabilities among dyslexics. This hypothesis maintains that reading impairment is caused by a fundamental perceptual deficit in processing rapid auditory or visual stimuli. Since the auditory perception involves a number of…

  12. Edgar Allan Poe and neurology

    Directory of Open Access Journals (Sweden)

    Hélio Afonso Ghizoni Teive

    2014-06-01

    Full Text Available Edgar Allan Poe was one of the most celebrated writers of all time. He published several masterpieces, some of which include references to neurological diseases. Poe suffered from recurrent depression, suggesting a bipolar disorder, as well as alcohol and drug abuse, which in fact led to his death from complications related to alcoholism. Various hypotheses were put forward, including Wernicke's encephalopathy.

  13. Edgar Allan Poe and neurology.

    Science.gov (United States)

    Teive, Hélio Afonso Ghizoni; Paola, Luciano de; Munhoz, Renato Puppi

    2014-06-01

    Edgar Allan Poe was one of the most celebrated writers of all time. He published several masterpieces, some of which include references to neurological diseases. Poe suffered from recurrent depression, suggesting a bipolar disorder, as well as alcohol and drug abuse, which in fact led to his death from complications related to alcoholism. Various hypotheses were put forward, including Wernicke's encephalopathy.

  14. [Neurology in medieval regimina sanitatis].

    Science.gov (United States)

    de Frutos González, V; Guerrero Peral, A L

    2011-09-01

    In medical medieval literature some works about dietetics stand out. Dietetics, as a separate branch of medicine, includes not only food or drinks, but other environmental factors influencing on health. They are known as regimina sanitatis or salutis, and specially developed in the Christian west. They generally consisted of a balance between the Galenic "six non-natural things"; factors regulating health and its protection: environment, exercise, food, sleep, bowel movements and emotions. After reviewing the sources and defining the different stages of this genre, we have considered three of the most out-standing medieval regimina, the anonymous Regimen sanitatis salernitanum, Arnaldo de Vilanova's Regimen sanitatis ad regem aragonum and Bernardo de Gordon's Tractatus of conservatione vite humane. In them we review references to neurological disease. Though not independently considered, there is a significant presence of neurological diseases in the regimina. Dietetics measures are proposed to preserve memory, nerves, or hearing, as well as for the treatment of migraine, epilepsy, stroke or dizziness. Regimina are quiet representative among medical medieval literature, and they show medieval physicians vision of neurological diseases. Dietetics was considered useful to preserve health, and therapeutics was based on natural remedies. 2010 Sociedad Española de Neurología. Published by Elsevier Espana. All rights reserved.

  15. Education Research: Neurology training reassessed

    Science.gov (United States)

    Maas, Matthew B.; Coleman, Mary; Jozefowicz, Ralph; Engstrom, John

    2012-01-01

    Objective: To assess the strengths and weaknesses of neurology resident education using survey methodology. Methods: A 27-question survey was sent to all neurology residents completing residency training in the United States in 2011. Results: Of eligible respondents, 49.8% of residents returned the survey. Most residents believed previously instituted duty hour restrictions had a positive impact on resident quality of life without impacting patient care. Most residents rated their faculty and clinical didactics favorably. However, many residents reported suboptimal preparation in basic neuroscience and practice management issues. Most residents (71%) noted that the Residency In-service Training Examination (RITE) assisted in self-study. A minority of residents (14%) reported that the RITE scores were used for reasons other than self-study. The vast majority (86%) of residents will enter fellowship training following residency and were satisfied with the fellowship offers they received. Conclusions: Graduating residents had largely favorable neurology training experiences. Several common deficiencies include education in basic neuroscience and clinical practice management. Importantly, prior changes to duty hours did not negatively affect the resident perception of neurology residency training. PMID:23091077

  16. International electives in neurology training

    Science.gov (United States)

    Lyons, Jennifer L.; Coleman, Mary E.; Engstrom, John W.

    2014-01-01

    Objective: To ascertain the current status of global health training and humanitarian relief opportunities in US and Canadian postgraduate neurology programs. Background: There is a growing interest among North American trainees to pursue medical electives in low- and middle-income countries. Such training opportunities provide many educational and humanitarian benefits but also pose several challenges related to organization, human resources, funding, and trainee and patient safety. The current support and engagement of neurology postgraduate training programs for trainees to pursue international rotations is unknown. Methods: A survey was distributed to all program directors in the United States and Canada (December 2012–February 2013) through the American Academy of Neurology to assess the training opportunities, institutional partnerships, and support available for international neurology electives. Results: Approximately half of responding programs (53%) allow residents to pursue global health–related electives, and 11% reported that at least 1 trainee participated in humanitarian relief during training (survey response rate 61%, 143/234 program directors). Canadian programs were more likely to allow residents to pursue international electives than US programs (10/11, 91% vs 65/129, 50%, p = 0.023). The number of trainees participating in international electives was low: 0%–9% of residents (55% of programs) and 10%–19% of residents (21% of programs). Lack of funding was the most commonly cited reason for residents not participating in global health electives. If funding was available, 93% of program directors stated there would be time for residents to participate. Most program directors (75%) were interested in further information on global health electives. Conclusions: In spite of high perceived interest, only half of US neurology training programs include international electives, mostly due to a reported lack of funding. By contrast, the majority

  17. Neurological and cardiac complications in a cohort of children with end-stage renal disease

    Directory of Open Access Journals (Sweden)

    Jumana H Albaramki

    2016-01-01

    Full Text Available Adult patients with chronic kidney disease are at risk of major neurologic and cardiac complications. The purpose of this study is to review the neurological and cardiac complications in children with end-stage renal disease (ESRD. A retrospective review of medical records of children with ESRD at Jordan University Hospital was performed. All neurological and cardiac events were recorded and analyzed. Data of a total of 68 children with ESRD presenting between 2002 and 2013 were reviewed. Neurological complications occurred in 32.4%; seizures were the most common event. Uncontrolled hypertension was the leading cause of neurological events. Cardiac complications occurred in 39.7%, the most common being pericardial effusion. Mortality from neurological complications was 45%. Neurological and cardiac complications occurred in around a third of children with ESRD with a high mortality rate. More effective control of hypertension, anemia, and intensive and gentle dialysis are needed.

  18. Neurological manifestations of snake bite in Sri Lanka.

    Directory of Open Access Journals (Sweden)

    Seneviratne U

    2002-10-01

    Full Text Available BACKGROUND AND AIMS: Snake bite is an important cause of mortality and morbidity in certain parts of Sri Lanka. This study was designed to determine the offending snakes, neurological manifestations, disease course, and outcome in neurotoxic envenomation. METHODS AND MATERIAL: Fifty six consecutive patients admitted with neurological manifestations following snake bite were studied prospectively. Data were obtained regarding the offending snakes, neurological symptoms, time taken for onset of symptoms, neurological signs, and time taken for recovery. RESULTS: The offending snake was Russell′s viper in 27(48.2%, common and Sri Lankan krait in 19(33.9%, cobra in 3(5.4%, and unidentified in 7(12.5%. Ptosis was the commonest neurological manifestation seen in 48(85.7% followed by ophthalmoplegia (75%, limb weakness (26.8%, respiratory failure (17.9%, palatal weakness (10.7%, neck muscle weakness (7.1%, and delayed sensory neuropathy (1.8%. Neurological symptoms were experienced usually within 6 hours after the bite. Following administration of antivenom, the signs of recovery became evident within a few hours to several days. The duration for complete recovery ranged from four hours to two weeks. CONCLUSIONS: Complete recovery of neuromuscular weakness was observed in all patients except for one who died with intracerebral haemorrhage shortly after admission.

  19. Apollo's curse: neurological causes of motor impairments in musicians.

    Science.gov (United States)

    Altenmüller, Eckart; Ioannou, Christos I; Lee, Andre

    2015-01-01

    Performing music at a professional level is probably one of the most complex human accomplishments. Extremely fast and complex, temporo-spatially predefined movement patterns have to be learned, memorized, and retrieved with high reliability in order to meet the expectations of listeners. Performing music requires not only the integration of multimodal sensory and motor information, and its precise monitoring via auditory and kinesthetic feedback, but also emotional communicative skills, which provide a "speaking" rendition of a musical masterpiece. To acquire these specialized auditory-sensory-motor and emotional skills, musicians must undergo extensive training periods over many years, which start in early childhood and continue on through stages of increasing physical and strategic complexities. Performance anxiety, linked to high societal pressures such as the fear of failure and heightened self-demands, frequently accompanies these learning processes. Motor disturbances in musicians are common and include mild forms, such as temporary motor fatigue with short-term reduction of motor skills, painful overuse injuries following prolonged practice, anxiety-related motor failures during performances (choking under pressure), as well as more persistent losses of motor control, here termed "dynamic stereotypes" (DSs). Musician's dystonia (MD), which is characterized by the permanent loss of control of highly skilled movements when playing a musical instrument, is the gravest manifestation of dysfunctional motor programs, frequently linked to a genetic susceptibility to develop such motor disturbances. In this review chapter, we focus on different types of motor failures in musicians. We argue that motor failures in musicians develop along a continuum, starting with subtle transient degradations due to fatigue, overuse, or performance stress, which transform by and by into more permanent, still fluctuating motor degradations, the DSs, until a more irreversible condition, MD manifests. We will review the epidemiology and the principles of medical treatment of MD and discuss prevention strategies. © 2015 Elsevier B.V. All rights reserved.

  20. Phenobarbital use and neurological problems in FMR1 premutation carriers.

    Science.gov (United States)

    Saldarriaga, Wilmar; Lein, Pamela; González Teshima, Laura Yuriko; Isaza, Carolina; Rosa, Lina; Polyak, Andrew; Hagerman, Randi; Girirajan, Santhosh; Silva, Marisol; Tassone, Flora

    2016-03-01

    Fragile X Syndrome (FXS) is a neurodevelopmental disorder caused by a CGG expansion in the FMR1 gene located at Xq27.3. Patients with the premutation in FMR1 present specific clinical problems associated with the number of CGG repeats (55-200 CGG repeats). Premutation carriers have elevated FMR1 mRNA expression levels, which have been associated with neurotoxicity potentially causing neurodevelopmental problems or neurological problems associated with aging. However, cognitive impairments or neurological problems may also be related to increased vulnerability of premutation carriers to neurotoxicants, including phenobarbital. Here we present a study of three sisters with the premutation who were exposed differentially to phenobarbital therapy throughout their lives, allowing us to compare the neurological effects of this drug in these patients. Copyright © 2016 Elsevier Inc. All rights reserved.

  1. [Neurological soft signs in pervasive developmental disorders].

    Science.gov (United States)

    Halayem, S; Bouden, A; Halayem, M B; Tabbane, K; Amado, I; Krebs, M O

    2010-09-01

    Many studies have focused on specific motor signs in autism and Asperger's syndrome, but few has been published on the complete range of neurological soft signs (NSS) in children with pervasive developmental disorder (PDD). Scarce are the studies evaluating NSS in children suffering from PDD not otherwise specified (PDDNOS). This study compared performance of 11 autistic children (AD) and 10 children with PDDNOS, with controls matched on age, sex and cognitive performance on Krebs et al.'s NSS scale. Because of the duration of the assessments and specific difficulties encountered in managing some items, an adaptation of the scale had to be made during a pilot study with the agreement of the author. To be eligible, patients had to meet the following inclusion criteria: an age range of 6-16 years, a diagnosis of autistic disorder or PDDNOS based on the DSM IV criteria (American Psychiatric Association 1994). The autism diagnostic interview-revised (ADI-R) was used in order to confirm the diagnosis and to evaluate the association of the symptoms to the severity of the NSS. The childhood autism rating scale (CARS) was completed for the patients in order to evaluate symptoms at the time of the NSS examination. Cognitive ability was assessed with Raven's progressive matrices. Were excluded patients with: history of cerebral palsy, congenital anomaly of the central nervous system, epilepsy, known genetic syndrome, tuberous sclerosis, neurofibromatosis, antecedent of severe head trauma, Asperger's syndrome, obvious physical deformities or sensory deficits that would interfere with neurological assessment, deep mental retardation and recent or chronic substance use or abuse. Healthy controls shared the same exclusion criteria, with no personal history of neurological, psychiatric disorder or substance abuse, no family history of psychiatric disorder and normal or retardation in schooling. All study procedures were approved by the local Ethics Committee (Comité d

  2. “Dazed and diffused”: making sense of diffusion abnormalities in neurologic pathologies

    OpenAIRE

    O'Connor, K M; Barest, G; Moritani, T; Sakai, O.; Mian, A

    2013-01-01

    To review diffusion abnormalities seen in diffusion-weighted MRI in neurological pathologies. We examine the clinical significance of the abnormalities in a broad spectrum of neurological diseases and highlight our current understanding of their causes. Diffusion abnormalities seen on diffusion-weighted MRI can play an important role in the diagnosis and follow-up of a broad spectrum of neurological diseases. A thorough understanding of the appearance and significance of these abnormalities i...

  3. Quality of Life Following Permanent Neurological Damage after Subarachnoid Block

    Directory of Open Access Journals (Sweden)

    Yvonne Dabota Buowari

    2011-01-01

    Full Text Available Introduction. Caesarean section is the commonest operation carried out in females of the reproductive age group. Spinal anaesthesia is commonly used for caesarean section with its risk. Permanent paralysis of the lower limbs following subarachnoid block is a rare complication but can occur even in the best of hands. Case Summary. This is a 29-year-old final-year university student now 34 years old who had emergency caesarean section for cephalopelvic disproportion in 2005 under spinal anaesthesia in a low-resource setting in a developing country. She developed permanent neurological deficit thereafter. She had urinary and faecal incontinence for one year. She lost one academic session at her school because of long hospital stay and is now confined to a wheel chair. She celebrated her daughter's fifth birthday in October, 2010. Although there is ability in inability, she is now disabled. Conclusion. It is important for clinicians to recognise the complications of subarachnoid block promptly to avoid delay in treatment and severe neurological deficits.

  4. [Application of psychophysics to neurology].

    Science.gov (United States)

    Koyama, Shinichi

    2008-04-01

    Although psychophysics has already been used in many neurological evaluations including the visual and hearing tests, the use of psychophysics has been limited to the evaluation of sensory disorders. In this review paper, however, the author introduced recent attempts to apply psychophysics to the evaluation of higher cognitive functions such as perception of scenes and facial expressions. Psychophysics was also used to measure visual hypersensitivity in a patient with migraine. The benefits of the use of psychophysics in neurological and neuropsychological settings would be as follows. (1) We can evaluate higher cognitive functions quantitatively. (2) We can measure performance both above and below the normal range by the same method. (3) We can use the same stimulus and task as other research areas such as neuroscience and neuroimaging, and compare results between research areas.

  5. Neurological diseases in famous painters.

    Science.gov (United States)

    Piechowski-Jozwiak, Bartlomiej; Bogousslavsky, Julien

    2013-01-01

    Visual art production involves multiple processes including basic motor skills, such as coordination of movements, visual-spatial processing, emotional output, sociocultural context, and creativity. Thus, the relationship between artistic output and brain diseases is particularly complex, and brain disorders may lead to impairment of artistic production in multiple domains. Neurological conditions may also occasionally modify artistic style and lead to surprisingly innovative features in people with an initial loss of creativity. This chapter focuses on anecdotal reports of various neurological disorders and their potential consequences on works produced by famous or well-established artists, including Carl Frederik Reutersward, Giorgio de Chirico, Krystyna Habura, Leo Schnug, Ignatius Brennan, and many others. © 2013 Elsevier B.V. All rights reserved.

  6. PET and SPECT in neurology

    Energy Technology Data Exchange (ETDEWEB)

    Dierckx, Rudi A.J.O. [Groningen University Medical Center (Netherlands). Dept. of Nuclear Medicine and Molecular Imaging; Ghent Univ. (Belgium). Dept. of Radiology and Nuclear Medicine; Vries, Erik F.J. de; Waarde, Aren van [Groningen University Medical Center (Netherlands). Dept. of Nuclear Medicine and Molecular Imaging; Otte, Andreas (ed.) [Univ. of Applied Sciences Offenburg (Germany). Faculty of Electrical Engineering and Information Technology

    2014-07-01

    PET and SPECT in Neurology highlights the combined expertise of renowned authors whose dedication to the investigation of neurological disorders through nuclear medicine technology has achieved international recognition. Classical neurodegenerative disorders are discussed as well as cerebrovascular disorders, brain tumors, epilepsy, head trauma, coma, sleeping disorders, and inflammatory and infectious diseases of the CNS. The latest results in nuclear brain imaging are detailed. Most chapters are written jointly by a clinical neurologist and a nuclear medicine specialist to ensure a multidisciplinary approach. This state-of-the-art compendium will be valuable to anybody in the field of neuroscience, from the neurologist and the radiologist/nuclear medicine specialist to the interested general practitioner and geriatrician. It is the second volume of a trilogy on PET and SPECT imaging in the neurosciences, the other volumes covering PET and SPECT in psychiatry and in neurobiological systems.

  7. Proust, neurology and Stendhal's syndrome.

    Science.gov (United States)

    Teive, Hélio A G; Munhoz, Renato P; Cardoso, Francisco

    2014-01-01

    Marcel Proust is one of the most important French writers of the 20th century. His relationship with medicine and with neurology is possibly linked to the fact that his asthma was considered to be a psychosomatic disease classified as neurasthenia. Stendhal's syndrome is a rare psychiatric syndrome characterized by anxiety and affective and thought disturbances when a person is exposed to a work of art. Here, the authors describe neurological aspects of Proust's work, particularly the occurrence of Stendhal's syndrome and syncope when he as well as one of the characters of In Search of Lost Time see Vermeer's View of Delft during a visit to a museum. © 2014 S. Karger AG, Basel.

  8. Correlation between neurological recovery and magnetic resonance imaging in Pott's paraplegia.

    Science.gov (United States)

    Gupta, Anil Kumar; Kumar, Chandan; Kumar, Praveen; Verma, Ashok Kumar; Nath, Rohit; Kulkarni, Chaitanya D

    2014-07-01

    Spinal cord/nerve root compression secondary to a tubercular epidural abscess leads to neurological deficit. Depending on the extent and duration of compression, the end result after treatment may vary from complete recovery to permanent deficit. ASIA has been used extensively to correlate between MRI and neurological status due to traumatic spine injuries. MRI has stood as an invaluable diagnostic tool out of the entire range of current imaging modalities. However, inspite of considerable literature on the applications of MRI in spinal tuberculosis, there have been few studies to assess the relationship between the MRI findings and the neurological deficit as assessed by clinical examination. The objective of this study was to ascertain whether the findings of magnetic resonance imaging (MRI) correlate well with the actual neurological recovery status using the American Spinal Injury Association impairment scale (ASIA) in patients with spinal compression secondary to tuberculous spondylitis. 60 patients (mean age 43.6 years) diagnosed as spinal tuberculosis by MRI/cytology/histopathology were examined and classified into ASIA impairment scale A-E based on the ASIA and again reclassified after 6 months of therapy to assess functional recovery. Similarly, they underwent MR imaging at the start and at the completion of 6 months of therapy to assess the structural recovery. The MRI features of recovery were correlated with the actual neurological recovery as ascertained by the ASIA. Before starting treatment 1 patient (2.08%) was in ASIA A, 2 (4.16%) were in ASIA B, 9 (18.75%) were in ASIA C, 36 (75%) were in ASIA D and 12 (20%) were in ASIA E. There was a significant difference in the epidural abscess thickness, thecal compression and cord compression between ambulatory (ASIA D and ASIA E) and non ambulatory patients (ASIA A, ASIA B and ASIA C). After 6 months of therapy 30 (90%) patients in ASIA D and 5 (55.5%) in ASIA C had complete neurological recovery. Both

  9. [Deficiency, disability, neurology and cinema].

    Science.gov (United States)

    Collado-Vázquez, Susana; Cano de la Cuerda, Roberto; Jiménez-Antona, Carmen

    2010-12-16

    Cinema has been defined in many different ways, but most of them agree that it should be considered both a technique and an art. Although films often depict fantasy stories, in many cases they also reflect day-to-day realities. In its earliest days cinema was already attracted to the world of health and sickness, and frequently addressed topics like medical practice, how patients lived with their illnesses, bioethical issues, the relationship between physician and patient or research. To review the presence of neurological pathologies in the cinema with a view to identifying the main neurological disorders that have been portrayed in films. Likewise it also intends to describe the medical praxis that is employed, the relationship between physician and patient, how the experiences of the patient and the family are represented, the adaptation to social and occupational situations, and the intervention of other health care professionals related with neurological patients. Some of the most significant films that have addressed these topics were reviewed and it was seen that in some of them the illness is dealt with in a very true-to-life manner, whereas others tend to include a greater number of inaccuracies and a larger degree of fiction. Cinema has helped to shape certain ways of thinking about the health care professionals who work with neurological patients, the importance of support from the family and the social role, among other things. This confirms that resorting to cinematographic productions is a fruitful tool for stimulating a critical interest in the past and present of medical practice.

  10. Neurological manifestation of phenytoin toxicity, resulting from drug ...

    African Journals Online (AJOL)

    Phenytoin toxicity masquerading as deterioration of neurological symptoms caused by interaction with chloramphenicol is a very rare but real risk. To the authors' knowledge only one such case occurring in humans has been reported in the English literature. No case of clinical phenytoin toxicity occurring at less than ...

  11. Primary Epstein-Barr virus infection with neurological complications

    NARCIS (Netherlands)

    Bathoorn, E.; Vlaminckx, B.J.; Schoondermark-Stolk, S.; Donders, R.; Meulen, M. van der; Thijsen, S.F.

    2011-01-01

    Several case studies have reported on neurological complications caused by a primary Epstein-Barr virus (EBV) infection. We aimed to investigate the viral loads and the clinical and inflammatory characteristics of this disease entity. We evaluated all 84 cases in which the EBV polymerase chain

  12. The Pattern Of Neurological Admissions At The Lagos University ...

    African Journals Online (AJOL)

    Cerebrovascular diseases were the most common cause, accounting for 11.65% of medical admissions; followed by infection of the nervous system which made up 6.07%. Cerebral malaria, pyogenic meningitis and tetanus were the most common infections All the other neurological diseases constituted less than 2% of ...

  13. Distinct neurological disorders with ATP1A3 mutations

    NARCIS (Netherlands)

    Heinzen, E.L.; Arzimanoglou, A.; Brashear, A.; Clapcote, S.J.; Gurrieri, F.; Goldstein, D.B; Johannesson, S.H.; Mikati, M.A.; Neville, B.; Nicole, S.; Ozelius, L.J.; Poulsen, H.; Schyns, T.; Sweadner, K.J.; Maagdenberg, A. van den; Vilsen, B.; Koenderink, J.B.

    2014-01-01

    Genetic research has shown that mutations that modify the protein-coding sequence of ATP1A3, the gene encoding the alpha3 subunit of Na(+)/K(+)-ATPase, cause both rapid-onset dystonia parkinsonism and alternating hemiplegia of childhood. These discoveries link two clinically distinct neurological

  14. Neurological Manifestations Hiv-Infected Patients Around Varanasi ...

    African Journals Online (AJOL)

    Opportunistic infections were the leading cause of neurological disorders in our study population. Apart from Central nervous ... There were equal responses to Amphoterecin B Cholesterol Dispersion (ABCD) and conventional Amphoterecin B therapies, and no significant differences in their side effect profiles. Keywords: ...

  15. Neurological complications of HIV/AIDS in childhood

    African Journals Online (AJOL)

    2011-04-02

    Apr 2, 2011 ... Other causes of neurological and developmental disorders (e.g. hypothyroidism .... Phenytoin, phenobarbitone and carbamaze- pine increase ... antiretrovirals in children. Lamotrigine is a useful second-line agent, but children have an increased risk of developing Stevens-. Johnson syndrome. It should be ...

  16. Prospects for neurology and psychiatry.

    Science.gov (United States)

    Cowan, W M; Kandel, E R

    2001-02-07

    Neurological and psychiatric illnesses are among the most common and most serious health problems in developed societies. The most promising advances in neurological and psychiatric diseases will require advances in neuroscience for their elucidation, prevention, and treatment. Technical advances have improved methods for identifying brain regions involved during various types of cognitive activity, for tracing connections between parts of the brain, for visualizing individual neurons in living brain preparations, for recording the activities of neurons, and for studying the activity of single-ion channels and the receptors for various neurotransmitters. The most significant advances in the past 20 years have come from the application to the nervous system of molecular genetics and molecular cell biology. Discovery of the monogenic disorder responsible for Huntington disease and understanding its pathogenesis can serve as a paradigm for unraveling the much more complex, polygenic disorders responsible for such psychiatric diseases as schizophrenia, manic depressive illness, and borderline personality disorder. Thus, a new degree of cooperation between neurology and psychiatry is likely to result, especially for the treatment of patients with illnesses such as autism, mental retardation, cognitive disorders associated with Alzheimer and Parkinson disease that overlap between the 2 disciplines.

  17. A reversal learning task detects cognitive deficits in a Dachshund model of late-infantile neuronal ceroid lipofuscinosis

    Science.gov (United States)

    Sanders, Douglas N.; Kanazono, Shinichi; Wininger, Fred A.; Whiting, Rebecca E.H.; Flournoy, Camille A.; Coates, Joan R.; Castaner, Lani J.; O’Brien, Dennis P.; Katz, Martin L.

    2011-01-01

    The neuronal ceroid lipofuscinoses (NCLs) are autosomal recessive lysosomal storage diseases characterized by progressive neurodegeneration and by accumulation of autofluorescent storage material in the central nervous system and other tissues. One of the most prominent clinical signs of NCL is progressive decline in cognitive function. We previously described a frame shift mutation of TPP1 in miniature long-haired Dachshunds which causes an early-onset form of NCL analogous to classical late-infantile onset NCL (CLN2) in children. Dogs homozygous for the TPP1 mutation exhibit progressive neurological signs similar to those exhibited by human patients. In order to establish biomarkers for evaluating the efficacy of ongoing therapeutic studies in this canine model, we characterized phenotypic changes in 13 dogs through 9 months of age. Cognitive function was assessed using a T-maze reversal learning task. Cognitive dysfunction was detected in affected dogs as early as 6 months of age and worsened as the disease progressed. Physical and neurological examination, funduscopy, and electroretinography (ERG) were performed at regular intervals. Only changes in ERG responses revealed signs of disease progression earlier than the reversal learning task. In the later stages of the disease clinical signs of visual and motor deficits became evident. The visual and motor deficits were not severe enough to affect the performance of dogs in the T-maze. Declining performance on the reversal learning task is a sensitive measure of higher order cognitive dysfunction which can serve as a useful biomarker of disease progression. PMID:21745338

  18. MENTALIZÁCIÓS DEFICIT NEUROLÓGIAI BETEGSÉGEKBEN: ÖSSZEFOGLALÓ KÖZLEMÉNY

    DEFF Research Database (Denmark)

    Herold, Róbert; Varga, Eszter; Mike, Andrea

    2015-01-01

    disorders (e.g. epilepsy, Parkinson's disease, multiple sclerosis, dementias, traumatic brain injury). DISCUSSION: The results indicate that a number of neurological disorders associate with mentalizing deficit. This deficit is often present in the early stages of the diseases and has a prognostic value...

  19. Functional Disorders in Neurology : Case Studies

    NARCIS (Netherlands)

    Stone, Jon; Hoeritzauer, Ingrid; Gelauff, Jeannette; Lehn, Alex; Gardiner, Paula; van Gils, Anne; Carson, Alan

    Functional, often called psychogenic, disorders are common in neurological practice. We illustrate clinical issues and highlight some recent research findings using six case studies of functional neurological disorders. We discuss dizziness as a functional disorder, describing the relatively new

  20. Clinical trials in neurology: design, conduct, analysis

    National Research Council Canada - National Science Library

    Ravina, Bernard

    2012-01-01

    .... Clinical Trials in Neurology aims to improve the efficiency of clinical trials and the development of interventions in order to enhance the development of new treatments for neurologic diseases...

  1. Cervical spinal canal narrowing and cervical neurologi-cal injuries

    Directory of Open Access Journals (Sweden)

    ZHANG Ling

    2012-04-01

    Full Text Available 【Abstract】Cervical spinal canal narrowing can lead to injury of the spinal cord and neurological symptoms in-cluding neck pain, headache, weakness and parasthesisas. According to previous and recent clinical researches, we investigated the geometric parameters of normal cervical spinal canal including the sagittal and transverse diameters as well as Torg ratio. The mean sagittal diameter of cervical spinal canal at C 1 to C 7 ranges from 15.33 mm to 20.46 mm, the mean transverse diameter at the same levels ranges from 24.45 mm to 27.00 mm and the mean value of Torg ratio is 0.96. With respect to narrow cervical spinal canal, the following charaterstics are found: firstly, extension of the cervical spine results in statistically significant stenosis as compared with the flexed or neutral positions; secondly, females sustain cervical spinal canal narrowing more easily than males; finally, the consistent narrowest cervical canal level is at C 4 for all ethnicity, but there is a slight variation in the sagittal diameter of cervical spinal stenosis (≤14 mm in Whites, ≤ 12 mm in Japanese, ≤13.7 mm in Chinese. Narrow sagittal cervical canal diameter brings about an increased risk of neurological injuries in traumatic, degenerative and inflam-matory conditions and is related with extension of cervical spine, gender, as well as ethnicity. It is hoped that this re-view will be helpful in diagnosing spinal cord and neuro-logical injuries with the geometric parameters of cervical spine in the future. Key words: Spinal cord injuries; Spinal stenosis; Trauma, nervous system

  2. Comorbidities in Neurology: Is Adenosine the Common Link?

    Science.gov (United States)

    Boison, Detlev; Aronica, Eleonora

    2015-01-01

    Comorbidities in Neurology represent a major conceptual and therapeutic challenge. For example, temporal lobe epilepsy (TLE) is a syndrome comprised of epileptic seizures and comorbid symptoms including memory and psychiatric impairment, depression, and sleep dysfunction. Similarly, Alzheimer’s disease (AD), Parkinson’s disease (PD), and Amyotrophic Lateral Sclerosis (ALS) are accompanied by various degrees of memory dysfunction. Patients with AD have an increased likelihood for seizures, whereas all four conditions share certain aspects of psychosis, depression, and sleep dysfunction. This remarkable overlap suggests common pathophysiological mechanisms, which include synaptic dysfunction and synaptotoxicity, as well as glial activation and astrogliosis. Astrogliosis is linked to synapse function via the tripartite synapse, but astrocytes also control the availability of gliotransmitters and adenosine. Here we will specifically focus on the ‘adenosine hypothesis of comorbidities’ implying that astrocyte activation, via overexpression of adenosine kinase (ADK), induces a deficiency in the homeostatic tone of adenosine. We present evidence from patient-derived samples showing astrogliosis and overexpression of ADK as common pathological hallmark of epilepsy, AD, PD, and ALS. We discuss a transgenic ‘comorbidity model’, in which brain-wide overexpression of ADK and resulting adenosine deficiency produces a comorbid spectrum of seizures, altered dopaminergic function, attentional impairment, and deficits in cognitive domains and sleep regulation. We conclude that dysfunction of adenosine signaling is common in neurological conditions, that adenosine dysfunction can explain comorbid phenotypes, and that therapeutic adenosine augmentation might be effective for the treatment of comorbid symptoms in multiple neurological conditions. PMID:25979489

  3. Transient global amnesia and neurological events: the Framingham Heart Study

    Directory of Open Access Journals (Sweden)

    Jose Rafael Romero

    2013-05-01

    Full Text Available Background/ objective: Transient global amnesia (TGA is a temporary amnestic syndrome characterized by lack of other focal neurological deficits. Cerebrovascular disease, migraine and seizures have been suggested as underlying mechanisms. TGA may be a risk factor for cerebrovascular or other neurological events. We studied the relation of TGA, vascular risk factors, brain magnetic resonance imaging (MRI indices of subclinical ischemia and neurological events in a community-based sample. Design/setting: A total of 12 TGA cases were ascertained using standard criteria by experienced neurologists, and matched to 41 stroke- and seizure-free controls. Vascular risk factors, brain MRI findings, and subsequent cerebrovascular or seizure events were compared in cases and controls. Participants: Framingham Heart Study (FHS original and offspring cohort participants were included.Results: No significant differences between the groups were observed in the prevalence of vascular risk factors, or brain MRI measures. Few incident stroke/transient ischemic attacks (TIA (1 event among the cases and 4 in controls or subsequent seizures occurred in either group. Head CT during the acute event (n=11 and brain MRI (n=7 were negative for acute abnormalities. Electroencephalograms (EEG (n=5 were negative for epileptiform activity. Extracranial vascular studies were negative for significant stenosis in all cases.Conclusions: In our community-based study TGA was not related to traditional vascular risk factors, or cerebrovascular disease. However, our study is limited by small sample size and power, and larger studies are required to exclude an association.

  4. Herbal Medicines In The Treatment of Psychiatric and Neurological Disorders

    Directory of Open Access Journals (Sweden)

    Shahin Akhondzadeh

    2006-04-01

    Full Text Available Objective: This review will indicate the quality of the evidence supporting the clinical effects of a number of commonly used types of herbal medicines for psychiatric and neurological disorders. Method: We conducted a review of literature to understand the biochemical and evidential bases for the use of herbs in psychiatric and neurological disorders as follow: 1 Alzheimer’s disease, 2 Depression, 3 Anxiety, 4 Insomnia, 5 Substance use disorders, 6 Attention deficit/hyperactivity disorder (ADHD, 7 Migraine. Results: Evidences support use of Ginkgo biloba, Huperzine A, Galantamine, Melissa officinalis,and Salvia officinalis for Alzheimer’s disease; St. John’s wort, Lavender, and Saffron for depression; Passionflower, and Kava, for anxiety disorders; Valerian, and English Lavender for sleep disorders; Hypericum for substance related disorders; Ginkgo biloba, and Passionflower for ADHD; and feverfew, and Butterbur root for migraine. The highest level of confidence derives from well-designed, randomized, double blind controlled studies. Conclusion: Herbs may have beneficial effects in variety of psychiatric and neurological disorder; however we must consider their potential side effects and drug-drug interactions.

  5. Neurologic disorders associated with weight lifting and bodybuilding.

    Science.gov (United States)

    Busche, Kevin

    2009-02-01

    Weight lifting and other forms of strength training are becoming more common because of an increased awareness of the need to maintain individual physical fitness. Emergency room data indicate that injuries caused by weight training have become more universal over time, likely because of increased participation rates. Neurologic injuries can result from weight lifting and related practices. Although predominantly peripheral nervous system injuries have been described, central nervous system disease may also occur. This article illustrates the types of neurologic disorders associated with weight lifting.

  6. Neurological signs and late-life depressive symptoms in a community population: the ESPRIT study.

    Science.gov (United States)

    Soremekun, Mishael; Stewart, Robert; Portet, Florence; Artero, Sylvaine; Ancelin, Marie-Laure; Ritchie, Karen

    2010-07-01

    Depression in the elderly is common and often resistant to treatment. It has been suggested that late-life depression may be related to underlying neurobiological changes. However, these observations are derived from diverse clinical samples and as yet have not been confirmed in a more representative population study. Our aim was to investigate associations between neurological signs as markers of underlying brain dysfunction and caseness for depression in an elderly community sample, controlling for physical health and comorbid/past neurological disorders. A cross-sectional analysis of 2102 older people without dementia from the ESPRIT project. Depressive symptomatology was ascertained using the CES-D and abnormal neurological signs/comorbidity from a full neurological examination according to ICD-10 criteria. Pyramidal, extrapyramidal, cranial nerve and sensory deficit signs were significantly associated with case-level depressive symptoms. However, all odds ratios were close to null values in participants who did not have previous neurological disorder. We confirmed previous findings of an association between neurological signs and case-level depressive symptoms in late life. However, this association may simply reflect the impact of more severe comorbid neurological disorder. (c) 2009 John Wiley & Sons, Ltd.

  7. Neurological manifestaions among Sudanese patients with multiple ...

    African Journals Online (AJOL)

    The study demonstrated that the most common non- neurological symptoms was locomotor symptoms (24%) ,while the most common neurological symptoms were backache and neck pain .The most common neurological findings were cord compression (8%) followed by peripheral neuropathy (2%) and CVA (2%). 22% of ...

  8. Meningoencephalitis caused by Streptococcus pneumoniae: a diagnostic and therapeutic challenge. Diagnosis with diffusion-weighted MRI leading to treatment with corticosteroids

    Energy Technology Data Exchange (ETDEWEB)

    Jorens, Philippe G.; Demey, Hendrik E. [University Hospital of Antwerp, UZA, Department of Intensive Care Medicine, Edegem (Belgium); Parizel, Paul M. [University of Antwerp, Department of Radiology, Edegem (Belgium); Smets, Katrien [University of Antwerp, Department of Neurology, Edegem (Belgium); General Hospital AZ Middelares, Department of Neurology, Sint-Niklaas (Belgium); Jadoul, Kris [General Hospital AZ Middelares, Department of Neurology, Sint-Niklaas (Belgium); Verbeek, M.M.; Wevers, R.A. [University Hospital of Nijmegen, Laboratory of Paediatrics and Neurology, Nijmegen (Netherlands); Cras, Patrick [University of Antwerp, Department of Neurology, Edegem (Belgium)

    2005-10-01

    Streptococcus pneumoniae is a common cause of bacterial meningitis but only rarely causes other infections such as brain abscess, encephalitis, encephalomyelitis or meningoencephalitis. We report on three adult patients with meningoencephalitis caused by S. pneumoniae. In all three, CT and MRI revealed widespread brain lesions, suggesting extensive parenchymal injury. Diffusion-weighted MRI showed lesions with restricted diffusion, reflecting local areas of ischaemia with cytotoxic oedema secondary to an immunologically mediated necrotising vasculitis and thrombosis. High levels of markers of neuronal, glial and myelin damage were found in the cerebrospinal fluid. According to the literature, brain parenchyma lesions in adults with pneumococcal meningoencephalitis are often associated with death or severe neurological deficit. Our patients were treated with pulse doses of glucocorticoids: this resulted in dramatic clinical improvement and an excellent final neurological recovery. (orig.)

  9. Women and Budget Deficits

    OpenAIRE

    Signe Krogstrup; Sébastien Wälti

    2007-01-01

    If women have different economic preferences than men, then female economic and political empowerment is likely to change policy and household decisions, and in turn macroeconomic outcomes. We test the hypothesis that female enfranchisement leads to lower government budget deficits due gender differences in preferences over fiscal outcomes. Estimating the impact of women's vote on budget deficits in a differences-in-differences regression for Swiss cantonal panel data, we find that including ...

  10. Erectile Dysfunction in Individuals with Neurologic Disability: A Hospital-based Cross-sectional Study

    OpenAIRE

    Salvatore Calabrò, Rocco; Gervasi, Giuseppe; Naro, Antonino; De Luca, Rosaria; Marullo, Michelangelo; Bramanti, Placido

    2016-01-01

    Objective: Neurogenic erectile dysfunction can be broadly defined as an inability to sustain or maintain a penile erection due to neurologic impairment. Sexual problems can occur due to any lesion affecting the central and peripheral nervous system. The aim of this study was to evaluate the prevalence and causes of erectile dysfunction in a group of hospital inpatients suffering from neurologic disorders.

  11. Horner Syndrome as the Only Focal Neurologic Manifestation of Hypothalamic Hemorrhage.

    Science.gov (United States)

    Sahin, Cansu B; Chaudhary, Neeraj; Trobe, Jonathan D

    2017-12-12

    A 70-year-old woman suffered an anterior dorsal hypothalamic hemorrhage that caused an ipsilateral Horner syndrome (HS) as the only focal neurologic manifestation. This is only the second reported case of hypothalamic hemorrhage producing HS. Because HS was the sole focal neurologic manifestation, its confirmation with topical apraclonidine drops was a valuable clue toward prompt localization of the patient's confusional state.

  12. Behavioural induced severe hypernatremia without neurological manifestations

    Directory of Open Access Journals (Sweden)

    Hassan Hossam

    2010-01-01

    Full Text Available Hypernatremia is a relatively common entity and is more prevalent among the elderly and critically ill. A number of medical conditions are commonly associated with hypernatremia, and these differ substantially among children and adults. Severe hypernatremia is usually associated with central nervous system manifestations and carries a high mortality rate. We report a case of a female patient who presented to the emergency department of the King Khalid University Hospital, Riyadh, Saudi Arabia with severe hypernatremia and without any associated co-morbid conditions or neurological manifestations. We did not find any etiological background despite extensive eva-luation other than under hydration due to decreased fluid intake, which was secondary to beha-vioural causes.

  13. Music therapy in neurological rehabilitation settings.

    Science.gov (United States)

    Galińska, Elżbieta

    2015-01-01

    The neurologic music therapy is a new scope of music therapy. Its techniques deal with dysfunctions resulting from diseases of the human nervous system. Music can be used as an alternative modality to access functions unavailable through non-musical stimulus. Processes in the brain activated by the influence of music can be generalized and transferred to non-musical functions. Therefore, in clinical practice, the translation of non-musical therapeutic exercises into analogous, isomorphic musical exercises is performed. They make use of the executive peculiarity of musical instruments and musical structures to prime, cue and coordinate movements. Among musical components, a repetitive rhythm plays a significant role. It regulates physiologic and behavioural functions through the mechanism of entrainment (synchronization of biological rhythms with musical rhythm based on acoustic resonance). It is especially relevant for patients with a deficient internal timing system in the brain. Additionally, regular rhythmic patterns facilitate memory encoding and decoding of non-musical information hence music is an efficient mnemonic tool. The music as a hierarchical, compound language of time, with its unique ability to access affective/motivational systems in the brain, provides time structures enhancing perception processes, mainly in the range of cognition, language and motor learning. It allows for emotional expression and improvement of the motivation for rehabilitation activities. The new technologies of rhythmic sensory stimulation (i.e. Binaural Beat Stimulation) or rhythmic music in combination with rhythmic light therapy appear. This multimodal forms of stimulation are used in the treatment of stroke, brain injury, dementia and other cognitive deficits. Clinical outcome studies provide evidence of the significant superiority of rehabilitation with music over the one without music.

  14. Obsessive–Compulsive Symptoms in Neurologic Disease: A Review

    Directory of Open Access Journals (Sweden)

    M. S. George

    1992-01-01

    Full Text Available Obsessive–compulsive disorder (OCD is an increasingly recognized disorder with a prevalence of 2–3% (Robins et al., 1984. Once thought to be psychodynamic in origin, OCD is now generally recognized as having a neurobiological cause. Although the exact pathophysiology of OCD in its pure form remains unknown, there are numerous reports of obsessive–compulsive symptoms arising in the setting of known neurological disease. In this paper, we review the reported cases of obsessive–compulsive symptoms associated with neurologic diseases and outline the known facts about the underlying neurobiology of OCD. Finally, we synthesize these findings into a proposed theory of the pathophysiology of OCD, in both its pure form and when it accompanies other neurological illness.

  15. Genetic analysis in neurology: the next 10 years.

    Science.gov (United States)

    Pittman, Alan; Hardy, John

    2013-06-01

    In recent years, neurogenetics research had made some remarkable advances owing to the advent of genotyping arrays and next-generation sequencing. These improvements to the technology have allowed us to determine the whole-genome structure and its variation and to examine its effect on phenotype in an unprecedented manner. The identification of rare disease-causing mutations has led to the identification of new biochemical pathways and has facilitated a greater understanding of the etiology of many neurological diseases. Furthermore, genome-wide association studies have provided information on how common genetic variability impacts on the risk for the development of various complex neurological diseases. Herein, we review how these technological advances have changed the approaches being used to study the genetic basis of neurological disease and how the research findings will be translated into clinical utility.

  16. Astaxanthin as a Potential Neuroprotective Agent for Neurological Diseases

    Directory of Open Access Journals (Sweden)

    Haijian Wu

    2015-09-01

    Full Text Available Neurological diseases, which consist of acute injuries and chronic neurodegeneration, are the leading causes of human death and disability. However, the pathophysiology of these diseases have not been fully elucidated, and effective treatments are still lacking. Astaxanthin, a member of the xanthophyll group, is a red-orange carotenoid with unique cell membrane actions and diverse biological activities. More importantly, there is evidence demonstrating that astaxanthin confers neuroprotective effects in experimental models of acute injuries, chronic neurodegenerative disorders, and neurological diseases. The beneficial effects of astaxanthin are linked to its oxidative, anti-inflammatory, and anti-apoptotic characteristics. In this review, we will focus on the neuroprotective properties of astaxanthin and explore the underlying mechanisms in the setting of neurological diseases.

  17. PET molecular imaging in stem cell therapy for neurological diseases

    Energy Technology Data Exchange (ETDEWEB)

    Wang, Jiachuan; Zhang, Hong [Second Affiliated Hospital of Zhejiang University School of Medicine, Department of Nuclear Medicine, Hangzhou, Zhejiang (China); Zhejiang University, Medical PET Center, Hangzhou (China); Institute of Nuclear Medicine and Molecular Imaging of Zhejiang University, Hangzhou (China); Key Laboratory of Medical Molecular Imaging of Zhejiang Province, Hangzhou (China); Tian, Mei [University of Texas, M.D. Anderson Cancer Center, Department of Experimental Diagnostic Imaging, Houston, TX (United States)

    2011-10-15

    Human neurological diseases such as Alzheimer's disease, Parkinson's disease, Huntington's disease, spinal cord injury and multiple sclerosis are caused by loss of different types of neurons and glial cells in the brain and spinal cord. At present, there are no effective therapies against these disorders. Discovery of the therapeutic potential of stem cells offers new strategies for the treatment of neurological diseases. Direct assessment of stem cells' survival, interaction with the host and impact on neuronal functions after transplantation requires advanced in vivo imaging techniques. Positron emission tomography (PET) is a potential molecular imaging modality to evaluate the viability and function of transplanted tissue or stem cells in the nervous system. This review focuses on PET molecular imaging in stem cell therapy for neurological diseases. (orig.)

  18. Insomnia in central neurologic diseases--occurrence and management

    DEFF Research Database (Denmark)

    Mayer, Geert; Jennum, Poul; Riemann, Dieter

    2011-01-01

    antidepressants may be an effective treatment for insomnia in stroke and Parkinson's disease (PD) patients. Melatonin and light treatment can stabilize the sleep-wake circadian rhythm and shorten sleep latency in dementias and PD. Cognitive behavioral therapy (CBT) can be effective in treating insomnia symptoms......The objective of this review is to highlight the impact of insomnia in central neurological disorders by providing information on its prevalence and give recommendations for diagnosis and treatment. Insomnia in neurological disorders is a frequent, but underestimated symptom. Its occurrence may...... the cause of insomnia must be clearly identified. First line treatment aims at the underlying neurologic disease. The few high quality treatment studies show that short term treatment with hypnotics may be recommended in most disorders after having ruled out high risk for adverse effects. Sedating...

  19. Dysprosody nonassociated with neurological diseases--a case report.

    Science.gov (United States)

    Pinto, José Antonio; Corso, Renato José; Guilherme, Ana Cláudia Rocha; Pinho, Sílvia Rebelo; Nóbrega, Monica de Oliveira

    2004-03-01

    Dysprosody also known as pseudo-foreign dialect, is the rarest neurological speech disorder. It is characterized by alterations in intensity, in the timing of utterance segments, and in rhythm, cadency, and intonation of words. The terms refers to changes as to duration, fundamental frequency, and intensity of tonic and atonic syllables of the sentences spoken, which deprive an individual's particular speech of its characteristics. The cause of this disease is usually associated with neurological pathologies such as brain vascular accidents, cranioencephalic traumatisms, and brain tumors. The authors report a case of dysprosody attended to at the Núcleo de Otorrinolaringologia e Cirurgia de Cabeça e Pescoço de São Paulo (NOSP). It is about a female patient with bilateral III degree Reinke's edema and normal neurological examinations that started presenting characteristics of the German dialect following a larynx microsurgery.

  20. Behavioral and neurological effects of symptomatic and asymptomatic lead exposure in children

    Energy Technology Data Exchange (ETDEWEB)

    Rummo, J.H.; Routh, D.K.; Rummo, N.J.; Brown, J.F.

    1979-03-01

    Forty-five children 4 to 8 y of age who had been exposed to environmental lead were studied, consisting of an acute encephalopathy group and groups with short- and long-term exposure but without encephalopathy. Control children were matched for age, sex, race, and socioeconomic status with lead-exposed subjects, but lived in post-1945 housing and had negative neurological history and blood tests. The encephalopathy group had a significantly higher incidence of neurological deficits, retarded mental development, and higher hyperactivity than control subjects. Children with short- and long-term exposure short of encephalopathy were somewhat inferior to matched control subjects, but not to a statistically significant extent.

  1. Colony-stimulating factor 1 receptor blockade prevents fractionated whole-brain irradiation-induced memory deficits.

    Science.gov (United States)

    Feng, Xi; Jopson, Timothy D; Paladini, Maria Serena; Liu, Sharon; West, Brian L; Gupta, Nalin; Rosi, Susanna

    2016-08-30

    Primary central nervous system (CNS) neoplasms and brain metastases are routinely treated with whole-brain radiation. Long-term survival occurs in many patients, but their quality of life is severely affected by the development of cognitive deficits, and there is no treatment to prevent these adverse effects. Neuroinflammation, associated with activation of brain-resident microglia and infiltrating monocytes, plays a pivotal role in loss of neurological function and has been shown to be associated with acute and long-term effects of brain irradiation. Colony-stimulating factor 1 receptor (CSF-1R) signaling is essential for the survival and differentiation of microglia and monocytes. Here, we tested the effects of CSF-1R blockade by PLX5622 on cognitive function in mice treated with three fractions of 3.3 Gy whole-brain irradiation. Young adult C57BL/6J mice were given three fractions of 3.3 Gy whole-brain irradiation while they were on diet supplemented with PLX5622, and the effects on periphery monocyte accumulation, microglia numbers, and neuronal functions were assessed. The mice developed hippocampal-dependent cognitive deficits at 1 and 3 months after they received fractionated whole-brain irradiation. The impaired cognitive function correlated with increased number of periphery monocyte accumulation in the CNS and decreased dendritic spine density in hippocampal granule neurons. PLX5622 treatment caused temporary reduction of microglia numbers, inhibited monocyte accumulation in the brain, and prevented radiation-induced cognitive deficits. Blockade of CSF-1R by PLX5622 prevents fractionated whole-brain irradiation-induced memory deficits. Therapeutic targeting of CSF-1R may provide a new avenue for protection from radiation-induced memory deficits.

  2. Medical Comorbidities in Attention Deficit Hyperactivity Disorder

    Directory of Open Access Journals (Sweden)

    Irem Yalug

    2009-09-01

    Full Text Available Attention Deficit Hyperactivity Disorder is one of the most common developmental disorders of childhood with a reported world-wide prevalence of 8 to 12 %. In studies conducted in our country the prevalence rates in community were reported to vary between 8.6 to 8.1 % while clinical prevalence rates were reported to vary between 8.6 to 29.44 %. Fifty to eighty percent of cases were reported to continue into adolescence while thirty to fifty percent may continue into adulthood. Attention deficit hyperactivity disorder is known to accompany subtle physical anomalies, allergic and neurologic disorders, obesity and eating disorders, traumatic injuries, risky sexual behavior, sleep disorders, substance and alcohol use, axis I and II disorders, occupational, legal and academic problems and increased treatment expenditures. Though the effects of this disorder continue throughout life, create burdens to the society along with its treatment as well as disabling the affected patients through their lives, and receive increasing attention in recent years, reviews focusing on problems associated with it are lacking. Therefore, this study aimed to summarize the results of previous studies conducted about medical comorbidities in attention deficit hyperactivity disorder.

  3. Acetylcholinesterase inhibition ameliorates deficits in motivational drive

    Directory of Open Access Journals (Sweden)

    Martinowich Keri

    2012-03-01

    Full Text Available Abstract Background Apathy is frequently observed in numerous neurological disorders, including Alzheimer's and Parkinson's, as well as neuropsychiatric disorders including schizophrenia. Apathy is defined as a lack of motivation characterized by diminished goal-oriented behavior and self-initiated activity. This study evaluated a chronic restraint stress (CRS protocol in modeling apathetic behavior, and determined whether administration of an anticholinesterase had utility in attenuating CRS-induced phenotypes. Methods We assessed behavior as well as regional neuronal activity patterns using FosB immunohistochemistry after exposure to CRS for 6 h/d for a minimum of 21 d. Based on our FosB findings and recent clinical trials, we administered an anticholinesterase to evaluate attenuation of CRS-induced phenotypes. Results CRS resulted in behaviors that reflect motivational loss and diminished emotional responsiveness. CRS-exposed mice showed differences in FosB accumulation, including changes in the cholinergic basal forebrain system. Facilitating cholinergic signaling ameliorated CRS-induced deficits in initiation and motivational drive and rescued immediate early gene activation in the medial septum and nucleus accumbens. Conclusions Some CRS protocols may be useful for studying deficits in motivation and apathetic behavior. Amelioration of CRS-induced behaviors with an anticholinesterase supports a role for the cholinergic system in remediation of deficits in motivational drive.

  4. Neurological comorbidity in children with neurofibromatosis type 1.

    Science.gov (United States)

    Hirabaru, Keiko; Matsuo, Muneaki

    2017-08-10

    The aim of this study was to determine the frequency of central nervous system comorbidities in children with neurofibromatosis type 1 (NF1). We performed a nationwide survey to investigate neurological comorbidities in 3-15-year-old children with NF1 in Japan by sending questionnaires to pediatricians and pediatric neurologists. A secondary questionnaire was sent to the parents of identified NF1 patients to assess neurological comorbidities including headache, attention deficit-hyperactivity disorder (ADHD) Rating Scale (RS), and the Social Responsiveness Scale 2. The primary survey identified 760 NF1 patients, and the parents of 565 patients were sent the secondary questionnaire. The parental response rate was 25.7% (145; 63 girls, 81 boys, one unspecified). Among the patients, 42.9% (55/128; 35 girls, 20 boys) were reported to exhibit intellectual problems. On the ADHD-RS, 40.2% (47/117) of NF1 patients aged 6-15 had ADHD (RS score >93rd percentile), with a rate of 47.7% in boys and 30.8% in girls. Furthermore, 20.2% of patients had suspected autism spectrum disorder (29/143; 10 girls, 19 boys), with Social Responsiveness Scale score ≥76. Headache was reported by 49.6% (61/123) of children over 5 years old, and 25.2% (31/123; 10 girls, 21 boys) reported migraine. Other neurological comorbidities included 20 cases of epilepsy (13.8%), 11 cases of optic nerve glioma (7.6%), five cases of brain tumor (3.4%), six cases of cerebrovascular disease (4.1%), and two cases of hydrocephalus (1.4%). Intellectual problems, ADHD, autism spectrum disorder, and migraine are major neurological comorbidities in NF1. © 2017 Japan Pediatric Society.

  5. Fiscal Deficits and Inflation in Nigeria | Ozurumba | Journal of ...

    African Journals Online (AJOL)

    This paper examines the causal relationship between inflation and fiscal deficits in Nigeria, covering the period 1970-2009. This was carried out by way of developing an estimation model of inflation and fiscal deficit, with a view to testing causes and effects as well as the relationship between them. The estimation technique ...

  6. Atypical Neurological Manifestations Of Hypokalemia

    Directory of Open Access Journals (Sweden)

    pal P K

    2004-01-01

    Full Text Available A part from the well-established syndrome of motor paralysis, hypokalemia may present with atypical neurological manifestations, which are not well documented in literature. Methods: We treated 30 patients of hypokalemia whose neurological manifestations improved after corrections of hypokalemia. A retrospective chart review of the clinical profile was done with emphasis on the evolution of symptoms and occurrence of unusual manifestations. Results: Twenty-eight patients had subacute quadriparesis with duration of symptoms varying from 10hrs to 7 days and two had slowly progressive quadriparesis. Fifty percent of patients had more than one attack of paralysis. Early asymmetric weakness (11, stiffness and abnormal posture of hands (7, predominant bibrachial weakness (4, distal paresthesias (4, hemiparesthesia (1, hyperreflexia(4, early severe weakness of neck muscles (3, chorea (1, trismus (1,and, retention of urine (1 were the unusual features observed. The means level of serum potassium on admission was 2.1+0.6mEq/L.and the serum creatine kinase was elevated in 14 out of 17 patients. All patients except two had complete recovery.

  7. [Oliver Sacks and literary neurology].

    Science.gov (United States)

    Guardiola, Elena; Banos, Josep E

    2014-03-16

    Popular medical literature attempts to discuss medical topics using a language that is, as far as possible, free of all medical jargon so as to make it more easily understandable by the general public. The very complexity of neurology makes it more difficult for the stories dealing with this specialty to be understood easily by an audience without any kind of medical training. This paper reviews the works written by Oliver Sacks involving the field of neurology aimed at the general public, and the main characteristics and the clinical situation discussed by the author are presented. Some biographical notes about Oliver Sacks are also included and the 11 books published by this author over the last 40 years are also analysed. In each case they are put into a historical context and the most outstanding aspects justifying what makes them an interesting read are commented on. In most cases, the genesis of the work is explained together with its most significant features. The works of Sacks contain a wide range of very interesting clinical situations that are usually explained by means of a language that is readily comprehensible to the general public. It also provides neurologists with a holistic view of different clinical situations, together with a discussion of their biographical, historical and developmental components.

  8. Specificity of Cognitive Impairment in Neurological Disease: A Methodological Critique of Parkinson’s Disease

    Directory of Open Access Journals (Sweden)

    H. J. Sagar

    1991-01-01

    Full Text Available Multiple cognitive deficits have been recognized in many neurological disorders but the specificity of the findings and the relationship to the underlying neuropathology remain obscure. Definitions of dementia have been proposed based on symptom profiles of the cognitive disorder and qualitative differences have been claimed between dementias of different aetiology. Some conditions have been claimed to show patterns of cognitive deficit that are distinguished from dementia and related to specific neuropathology or psychological processes, e.g. frontal lobe deficits in Parkinson's disease. Sometimes, a relationship has been established between certain cognitive deficits and particular neurochemical deficits which has led to the notion of specific drug treatment, e.g. cholinergic deficits and memory failure in Alzheimer's disease. However, these conclusions are often potentially flawed by methodological inadequacies. This critique presents some methodological issues relevant to the study of brain-behaviour and drug-behaviour relationships in syndromes of multiple cognitive deficit, using Parkinson's disease as the model. The following recommendations are made: rigid diagnostic criteria; representative patient groups; avoidance of arbitrary quantitative criteria to limit definitions of dementia; matching of groups for overall level of cognitive impairment in the search for qualitative cognitive differences related to neuropathology or effects of particular drugs; the use of suitable controls in patient groups, neuropsychological tests and treatment regimes; the use of specific quantitative tests of cognition, affect and motor disability; and longitudinal, compared with cross-sectional, study design.

  9. Rosmarinic acid protects against chronic ethanol-induced learning and memory deficits in rats.

    Science.gov (United States)

    Hasanein, Parisa; Seifi, Rosa; Hajinezhad, Mohammad Reza; Emamjomeh, Abbasali

    2017-11-01

    Ethanol consumption induces neurological disorders including cognitive dysfunction. Oxidative damage is considered a likely cause of cognitive deficits. We aimed to investigate the effects of rosmarinic acid (RA) in different doses for 30 days on chronic ethanol-induced cognitive dysfunction using the passive avoidance learning (PAL) and memory task in comparison with donepezil, a reference drug. We also evaluated the levels of superoxide dismutase (SOD), catalase (CAT), and lipid peroxidation in hippocampus as possible mechanisms. Memory impairment was induced by 15% w/v ethanol (2 g/kg, i.g.) administration for 30 days. RA (8, 16, and 32 mg/kg, i.g.) or donepezil (2 mg/kg, i.g.) was administered 30 minutes before ethanol. The acquisition trial was done 1 hour after the last administration of RA and donepezil. At the end, animals were weighed and hippocami were isolated for analyzing of oxidant/antioxidant markers. Ethanol caused cognition deficits in the PAL and memory task. While RA 16 and 32 mg/kg improved cognition in control rats, it prevented learning and memory deficits of alcoholic groups. RA 8 mg/kg did not influence cognitive function in both control and alcoholic rats. RA 32 mg/kg had comparable effects with donepezil in prevention of acquisition and retention memory impairment. The higher doses of RA not only prevented increased lipid peroxidation and nitrite content but also decreased SOD, CAT, GSH, and FRAP levels in alcoholic groups and exerted antioxidant effects in non-alcoholic rats. We showed that RA administration dose-dependently prevented cognitive impairment induced by chronic ethanol in PAL and memory and disturbed oxidant/antioxidant status as a possible mechanism. The antioxidant, anticholinesterase, and neuroprotective properties of RA may be involved in the observed effects. Therefore, RA represents a potential therapeutic option against chronic ethanol-induced amnesia which deserves consideration and further examination.

  10. Methylmalonate Induces Inflammatory and Apoptotic Potential: A Link to Glial Activation and Neurological Dysfunction.

    Science.gov (United States)

    Gabbi, Patricia; Ribeiro, Leandro Rodrigo; Jessié Martins, Gutierres; Cardoso, Alexandra Seide; Haupental, Fernanda; Rodrigues, Fernanda Silva; Machado, Alencar Kolinski; Sperotto Brum, Juliana; Medeiros Frescura Duarte, M M; Schetinger, Maria Rosa Chitolina; da Cruz, Ivana Beatrice Mânica; Flávia Furian, Ana; Oliveira, Mauro Schneider; Dos Santos, Adair Roberto Soares; Royes, Luiz Fernando Freire; Fighera, Michele Rechia; de Freitas, Mayara Lutchemeyer

    2017-03-01

    Methylmalonic acid (MMA) accumulates in tissues in methylmalonic acidemia, a heterogeneous group of inherited childhood diseases characterized by neurological dysfunction, oxidative stress and neuroinflammation; it is associated with degeneration of striatal neurons and cerebral cortical atrophy. It is presently unknown, however, whether transient exposure to MMA in the neonatal period is sufficient to trigger inflammatory and apoptotic processes that lead to brain structural damage. Here, newborn mice were given a single intracerebroventricular dose of MMA at 12 hours after birth. Maze testing of 21- and 40-day-old mice showed that MMA-injected animals exhibited deficit in the working memory test but not in the reference test. MMA-injected mice showed increased levels of the reactive oxygen species marker 2',7'-dichlorofluorescein diacetate, tumor necrosis factor, interleukin-1β, caspases 1, 3, and 8, and increased acetylcholinesterase activity in the cortex, hippocampus and striatum. This was associated with increased astrocyte and microglial immunoreactivity in all brain regions. These findings suggest that transient exposure to MMA may alter the redox state and cause neuroinflammatory/apoptotic processes and glial activation during critical periods of brain development. Similar processes may underlie brain dysfunction and cognitive impairment in patients with methylmalonic acidemia. © 2017 American Association of Neuropathologists, Inc. All rights reserved.

  11. A Hydatid Cyst of the Lumbar Spine: A Rare Cause of Paraplegia

    Directory of Open Access Journals (Sweden)

    Suhail Ur Rehman

    2017-05-01

    Full Text Available Introduction Hydatid cyst is a zoonotic disease, affecting humans and other mammals worldwide. It is caused by tapeworms of the genus Echinococcus, which is most frequently encountered in the liver and lungs. Although involvement of the central nervous system and spine is rare, it can lead to severe neurological deficits due to direct compression. Case Presentation We report a case of intradural extramedullary hydatid cyst in the lumbar region with a sudden onset, causing progressive paraplegia and areflexia over the past 20 days. After surgical removal, the cyst was sent for histopathological examination. The results showed inner laminated membranes and an outer fibrous layer, surrounded by foreign-body giant cells. The primary objective during surgery was to avoid perforation of the cyst, thereby reducing the risk of systemic dissemination and local seeding of the parasite. During the postoperative period, there was a steady improvement in the neurological deficit, and the patient was discharged with anthelmintics to prevent any distant dissemination. Conclusions An accurate and precise diagnosis is necessary when dealing with cystic pathologies.

  12. Mutations in a helix-1 motif of the ATP synthase c-subunit of Bacillus pseudofirmus OF4 cause functional deficits and changes in the c-ring stability and mobility on sodium dodecyl sulfate-polyacrylamide gel electrophoresis.

    Science.gov (United States)

    Liu, Jun; Fackelmayer, Oliver J; Hicks, David B; Preiss, Laura; Meier, Thomas; Sobie, Eric A; Krulwich, Terry A

    2011-06-21

    The ATP synthase of the alkaliphile Bacillus pseudofirmus OF4 has a tridecameric c-subunit rotor ring. Each c-subunit has an AxAxAxA motif near the center of the inner helix, where neutralophilic bacteria generally have a GxGxGxG motif. Here, we studied the impact of four single and six multiple Ala-to-Gly chromosomal mutations in the A16xAxAxA22 motif on the capacity for nonfermentative growth and, for most of the mutants, on ATP synthesis by ADP- and P(i)-loaded membrane vesicles at pH 7.5 and 10.5. Sodium dodecyl sulfate-polyacrylamide gel electrophoresis (SDS-PAGE) analyses of the holo-ATP synthases were used to probe stability of the mutant c-rotors and mobility properties of the c-rotors as well as the monomeric c-subunits that are released from them by trichloroacetic acid treatment. Mutants containing an Ala16-to-Gly mutation exhibited the most severe functional defects. Via SDS-PAGE, most of the mutant c-monomers exhibited increased mobility relative to the wild-type (WT) c-subunit, but among the intact c-rings, only Ala16-to-Gly mutants exhibited significantly increased mobility relative to that of the WT c-ring. The hypothesis that these c-rings have a decreased c-subunit stoichiometry is still untested, but the functional impact of an Ala16-to-Gly mutation clearly depended upon additional Ala-to-Gly mutation(s) and their positions. The A16/20G double mutant exhibited a larger functional deficit than both the A16G and A16/18G mutants. Most of the mutant c-rings showed in vitro instability relative to that of the WT c-ring. However, the functional deficits of mutants did not correlate well with the extent of c-ring stability loss, so this property is unlikely to be a major factor in vivo.

  13. Pseudoradial Nerve Palsy Caused by Acute Ischemic Stroke

    Directory of Open Access Journals (Sweden)

    Hassan Tahir MD

    2016-07-01

    Full Text Available Pseudoperipheral palsy has been used to characterize isolated monoparesis secondary to stroke. Isolated hand nerve palsy is a rare presentation for acute cerebral stroke. Our patient presented with clinical features of typical peripheral radial nerve palsy and a normal computed tomography scan of the head, which, without a detailed history and neurological examination, could have been easily misdiagnosed as a peripheral nerve lesion deferring further investigation for a stroke. We stress the importance of including cerebral infarction as a critical differential diagnosis in patients presenting with sensory-motor deficit in an isolated peripheral nerve pattern. A good history and physical exam can differentiate stroke from peripheral neuropathy as the cause of radial nerve palsy.

  14. Neurological Consequences of Cytomegalovirus Infection

    Science.gov (United States)

    ... that causes cold sores (herpes simplex virus), infectious mononucleosis (Epstein-Barr virus), and chickenpox/shingles (varicella zoster ... that causes cold sores (herpes simplex virus), infectious mononucleosis (Epstein-Barr virus), and chickenpox/shingles (varicella zoster ...

  15. Dysfunctional HCN ion channels in neurological diseases

    Directory of Open Access Journals (Sweden)

    Jacopo C. DiFrancesco

    2015-03-01

    Full Text Available Hyperpolarization-activated cyclic nucleotide-gated (HCN channels are expressed as four different isoforms (HCN1-4 in the heart and in the central and peripheral nervous systems. HCN channels are activated by membrane hyperpolarization at voltages close to resting membrane potentials and carry the hyperpolarization-activated current, dubbed If (funny current in heart and Ih in neurons. HCN channels contribute in several ways to neuronal activity and are responsible for many important cellular functions, including cellular excitability, generation and modulation of rhythmic activity, dendritic integration, transmission of synaptic potentials and plasticity phenomena. Because of their role, defective HCN channels are natural candidates in the search for potential causes of neurological disorders in humans. Several data, including growing evidence that some forms of epilepsy are associated with HCN mutations, support the notion of an involvement of dysfunctional HCN channels in different experimental models of the disease. Additionally, some anti-epileptic drugs are known to modify the activity of the Ih current. HCN channels are widely expressed in the peripheral nervous system and recent evidence has highlighted the importance of the HCN2 isoform in the transmission of pain. HCN channels are also present in the midbrain system, where they finely regulate the activity of dopaminergic neurons, and a potential role of these channels in the pathogenesis of Parkinson’s disease has recently emerged. The function of HCN channels is regulated by specific accessory proteins, which control the correct expression and modulation of the neuronal Ih current. Alteration of these proteins can severely interfere with the physiological channel function, potentially predisposing to pathological conditions. In this review we address the present knowledge of the association between HCN dysfunctions and neurological diseases, including clinical, genetic and

  16. [Post-ischemia neurologic recovery].

    Science.gov (United States)

    Guiraud-Chaumeil, Bernard; Pariente, Jérémie; Albucher, Jean-François; Loubinoux, Isabelle; Chollet, François

    2002-01-01

    Stroke is one of the most common affliction of patients with neurological symptoms. Rehabilitation of stroke patients is a difficult task. Our knowledge on rehabilitation has recently improved with the emergence of data from new neuroimaging techniques. A prospective, double blind, cross over, placebo, controlled study on 8 patients with pure motor hemiparesia, is conducted to determine the influence of a single dose of fluoxetine on motor performance and cerebral activation of patients recovering from stroke. Each patient undergoes two functional magnetic resonance imaging (fMRI) examinations, one under fluoxetine and one under placebo. A single dose of fluoxetine is enough to modulate cerebral sensori-motor activation and significantly improves motor skills of the affected side. Further studies are required to investigate the effect of chronic administration of fluoxetine on motor function.

  17. Neurology of foreign language aptitude

    Directory of Open Access Journals (Sweden)

    Adriana Biedroń

    2015-01-01

    Full Text Available This state-of-the art paper focuses on the poorly explored issue of foreign language aptitude, attempting to present the latest developments in this field and reconceptualizations of the construct from the perspective of neuroscience. In accordance with this goal, it first discusses general directions in neurolinguistic research on foreign language aptitude, starting with the earliest attempts to define the neurological substrate for talent, sources of difficulties in the neurolinguistic research on foreign language aptitude and modern research methods. This is followed by the discussion of the research on the phonology of foreign language aptitude with emphasis on functional and structural studies as well as their consequences for the knowledge of the concept. The subsequent section presents the studies which focus on lexical and morphosyntactic aspects of foreign language aptitude. The paper ends with a discussion of the limitations of contemporary research, the future directions of such research and selec ed methodological issues.

  18. Aphasia, Just a Neurological Disorder?

    Directory of Open Access Journals (Sweden)

    Mehmet Ozdemir

    2016-02-01

    Full Text Available Hashimoto%u2019s encephalopathy (HE is a rare disorder associated with autoimmune thyroiditis. Etiology of HE is not completely understood. High levels of serum antithyroid antibodies are seen in HE. Presentation with otoimmune thyroiditis, cognitive impairment, psychiatric and neurologic symptoms and absence of bacterial or viral enfections are characteristics of HE. HE is a steroid responsive encephalopathy. 60 years old male patient admitted to hospital with forget fulness continuing for 9 months and speech loss starting 2 days ago. Strong positivity of antithyroid antibodies increases the odds for HE. Thyroid function tests showed severe hypothyroidism. Electroencephalography and magnetic resonance imaging results were compatible with HE. HE is diagnosed with differantial diagnosis and exclusion of other reasons. This uncommon disorder is not recognised enough. High titres of serum antithyroid antiboides are always needed for diagnosis. Correct diagnosis requires awareness of wide range of cognitive and clinical presentations of HE.

  19. Porphyria and its neurologic manifestations.

    Science.gov (United States)

    Tracy, Jennifer A; Dyck, P James B

    2014-01-01

    Porphyrias are rare disorders resulting from a defect in the heme biosynthetic pathway. They can produce significant disease of both the peripheral and central nervous systems, in addition to other organ systems, with acute intermittent porphyria, hereditary coproporphyria, and variegate porphyria as the subtypes associated with neurologic manifestations. The presence of a motor-predominant peripheral neuropathy (axonal predominant), accompanied by gastrointestinal distress and neuropsychiatric manifestations, should be a strong clue to the diagnosis of porphyria. Clinical confirmation can be made through evaluation of urine porphyrins during an exacerbation of disease. While hematin is helpful for acute treatment, long-term effective management requires avoidance of overstimulation of the cytochrome P450 pathway, as well as other risk factor control. © 2014 Elsevier B.V. All rights reserved.

  20. Specific Language Impairment, Nonverbal IQ, Attention-Deficit/Hyperactivity Disorder, Autism Spectrum Disorder, Cochlear Implants, Bilingualism, and Dialectal Variants: Defining the Boundaries, Clarifying Clinical Conditions, and Sorting Out Causes.

    Science.gov (United States)

    Rice, Mabel L

    2016-02-01

    The purpose of this research forum article is to provide an overview of a collection of invited articles on the topic "specific language impairment (SLI) in children with concomitant health conditions or nonmainstream language backgrounds." Topics include SLI, attention-deficit/hyperactivity disorder, autism spectrum disorder, cochlear implants, bilingualism, and dialectal language learning contexts. The topic is timely due to current debates about the diagnosis of SLI. An overarching comparative conceptual framework is provided for comparisons of SLI with other clinical conditions. Comparisons of SLI in children with low-normal or normal nonverbal IQ illustrate the unexpected outcomes of 2 × 2 comparison designs. Comparative studies reveal unexpected relationships among speech, language, cognitive, and social dimensions of children's development as well as precise ways to identify children with SLI who are bilingual or dialect speakers. The diagnosis of SLI is essential for elucidating possible causal pathways of language impairments, risks for language impairments, assessments for identification of language impairments, linguistic dimensions of language impairments, and long-term outcomes. Although children's language acquisition is robust under high levels of risk, unexplained individual variations in language acquisition lead to persistent language impairments.

  1. Neuropep-1 ameliorates learning and memory deficits in an Alzheimer's disease mouse model, increases brain-derived neurotrophic factor expression in the brain, and causes reduction of amyloid beta plaques.

    Science.gov (United States)

    Shin, Min-Kyoo; Kim, Hong-Gi; Baek, Seung-Hyun; Jung, Woo-Ram; Park, Dong-Ik; Park, Jong-Sung; Jo, Dong-Gyu; Kim, Kil-Lyong

    2014-05-01

    Alzheimer's disease (AD) is a neurodegenerative disease characterized by amyloid beta (Aβ) deposits, hyperphosphorylated tau deposition, and cognitive dysfunction. Abnormalities in the expression of brain-derived neurotrophic factor (BDNF), which plays an important role in learning and memory formation, have been reported in the brains of AD patients. A BDNF modulating peptide (Neuropep-1) was previously identified by positional-scanning synthetic peptide combinatorial library. Here we examine the neuroprotective effects of Neuropep-1 on several in vitro neurotoxic insults, and triple-transgenic AD mouse model (3xTg-AD). Neuropep-1 protects cultured neurons against oligomeric Aβ1-42, 1-methyl-4-phenylpyridinium, and glutamate-induced neuronal cell death. Neuropep-1 injection also significantly rescues the spatial learning and memory deficits of 3xTg-AD mice compared with vehicle-treated control group. Neuropep-1 treatment markedly increases hippocampal and cortical BDNF levels. Furthermore, we found that Neuropep-1-injected 3xTg-AD mice exhibit dramatically reduced Aβ plaque deposition and Aβ levels without affecting tau pathology. Neuropep-1 treatment does not alter the expression or activity of full-length amyloid precursor protein, α-, β-, or γ-secretase, but levels of insulin degrading enzyme, an Aβ degrading enzyme, were increased. These findings suggest Neuropep-1 may be a therapeutic candidate for the treatment of AD. Copyright © 2014 Elsevier Inc. All rights reserved.

  2. Translational Assessment of Reward and Motivational Deficits in Psychiatric Disorders

    Science.gov (United States)

    Der-Avakian, Andre; Barnes, Samuel A.

    2016-01-01

    Deficits in reward and motivation are common symptoms characterizing several psychiatric and neurological disorders. Such deficits may include anhedonia, defined as loss of pleasure, as well as impairments in anticipatory pleasure, reward valuation, motivation/effort, and reward learning. This chapter describes recent advances in the development of behavioral tasks used to assess different aspects of reward processing in both humans and non-human animals. While earlier tasks were generally developed independently with limited cross-species correspondence, a newer generation of translational tasks has emerged that are theoretically and procedurally analogous across species and allow parallel testing, data analyses, and interpretation between human and rodent behaviors. Such enhanced conformity between cross-species tasks will facilitate investigation of the neurobiological mechanisms underlying discrete reward and motivated behaviors and is expected to improve our understanding and treatment of neuropsychiatric disorders characterized by reward and motivation deficits. PMID:26873017

  3. The core competencies for mental, neurological, and substance use disorder care in sub-Saharan Africa.

    OpenAIRE

    Collins, PY; Musisi, S; Frehywot, S; Patel, V

    2015-01-01

    The 2010 Global Burden of Disease Study points to a changing landscape in which non-communicable diseases, such as mental, neurological, and substance use (MNS) disorders, account for an increasing proportion of premature mortality and disability globally. Despite evidence of the need for care, a remarkable deficit of providers for MNS disorder service delivery persists in sub-Saharan Africa. This critical workforce can be developed from a range of non-specialist and specialist health workers...

  4. The relationship between insight and neurological dysfunction in first-episode psychosis.

    LENUS (Irish Health Repository)

    Hill, M

    2012-04-01

    Impaired insight is commonly seen in psychosis and some studies have proposed that is a biologically based deficit. Support for this view comes from the excess of neurological soft signs (NSS) observed in patients with psychoses and their neural correlates which demonstrate a degree of overlap with the regions of interest implicated in neuroimaging studies of insight. The aim was to examine the relationship between NSS and insight in a sample of 241 first-episode psychosis patients.

  5. Insights into the Pathology of the α2-Na(+)/K(+)-ATPase in Neurological Disorders; Lessons from Animal Models.

    Science.gov (United States)

    Isaksen, Toke J; Lykke-Hartmann, Karin

    2016-01-01

    A functional Na(+)/K(+)-ATPase consists of a catalytic α subunit and a regulatory β subunit. Four α isoforms of the Na(+)/K(+)-ATPase are found in mammals, each with a unique expression pattern and catalytic activity. The α2 isoform, encoded by the ATP1A2 gene, is primarily found in the central nervous system (CNS) and in heart-, skeletal- and smooth muscle tissues. In the CNS, the α2 isoform is mainly expressed in glial cells. In particular, the α2 isoform is found in astrocytes, important for astrocytic K(+) clearance and, consequently, the indirect uptake of neurotransmitters. Both processes are essential for proper brain activity, and autosomal dominantly mutations in the ATP1A2 gene cause the neurological disorder Familial hemiplegic migraine type 2 (FHM2). FHM2 is a severe subtype of migraine with aura including temporary numbness or weakness, and affecting only one side of the body. FHM2 patients often suffer from neurological comorbidities such as seizures, sensory disturbances, cognitive impairment, and psychiatric manifestations. The functional consequences of FHM2 disease mutations leads to a partial or complete loss of function of pump activity; however, a clear phenotype-genotype correlation has yet to be elucidated. Gene-modified mouse models targeting the Atp1a2 gene have proved instrumental in the understanding of the pathology of FHM2. Several Atp1a2 knockout (KO) mice targeting different exons have been reported. Homozygous Atp1a2 KO mice die shortly after birth due to respiratory malfunction resulting from abnormal Cl(-) homeostasis in brainstem neurons. Heterozygous KO mice are viable, but display altered behavior and neurological deficits such as altered spatial learning, decreased motor activity and enhanced fear/anxiety compared to wild type mice. FHM2 knock-in (KI) mouse models carrying the human in vivo disease mutations W887R and G301R have also been reported. Both models display altered cortical spreading depression (CSD) and point

  6. INSIGHTS INTO THE PATHOLOGY OF THE α2-Na+/K+-ATPase IN NEUROLOGICAL DISORDERS; LESSONS FROM ANIMAL MODELS

    Directory of Open Access Journals (Sweden)

    Toke Jost Isaksen

    2016-05-01

    Full Text Available A functional Na+/K+-ATPase consists of a catalytic α subunit and a regulatory β subunit. Four α isoforms of the Na+/K+-ATPase are found in mammals, each with a unique expression pattern and catalytic activity. The α2 isoform, encoded by the ATP1A2 gene, is primarily found in the central nervous system (CNS and in heart-, skeletal- and smooth muscle tissues. In the CNS, the α2 isoform is mainly expressed in neuroglial cells. In particular, the α2 isoform is found in astrocytes, and is important for astrocytic K+ clearance and, consequently, the indirect uptake of neurotransmitters. Both processes are essential for proper brain activity, and autosomal dominantly mutations in the ATP1A2 gene cause the neurological disorder Familial hemiplegic migraine type 2 (FHM2. FHM2 is a severe subtype of migraine with aura that involving temporary numbness or weakness, and affecting only one side of the body. FHM2 patients often suffer from neurological comorbidities such as seizures, sensory disturbances, cognitive impairment and psychiatric manifestations. The functional consequences of FHM2 disease mutations leads to a partial or complete loss of function of pump activity; however a clear phenotype-genotype correlation has yet to be elucidated. Gene-modified mouse models targeting the Atp1a2 gene have proved instrumental in the understanding of the pathology of FHM2. Several Atp1a2 knockout (KO mice targeting different exons have been reported. Homozygous Atp1a2 KO mice die shortly after birth due to respiratory malfunction resulting from abnormal Cl- homeostasis in brainstem neurons. Heterozygous KO mice are viable, but display altered behavior and neurological deficits such as altered spatial learning, decreased motor activity and enhanced fear/anxiety compared to wild type mice. FHM2 knock-in (KI mouse models carrying the human in vivo disease mutations W887R and G301R have also been reported. Both models display altered cortical spreading

  7. Pediatric neurology of the dog and cat.

    Science.gov (United States)

    Lavely, James A

    2006-05-01

    The neurologic examination in the puppy or kitten can be a challenging experience. Understanding the development of behavior reflexes and movement in puppies and kittens enables us to overcome some of these challenges and to recognize the neurologically abnormal patient. Subsequently,we can identify the neuroanatomic localization and generate a differential diagnosis list. This article first reviews the pediatric neurologic examination and then discusses diseases unique to these individuals.

  8. Sleep Disorders in Childhood Neurological Diseases

    Directory of Open Access Journals (Sweden)

    Abdullah Tolaymat

    2017-09-01

    Full Text Available Sleep problems are frequently addressed as a primary or secondary concern during the visit to the pediatric neurology clinic. Sleep disorders can mimic other neurologic diseases (e.g., epilepsy and movement disorders, and this adds challenges to the diagnostic process. Sleep disorders can significantly affect the quality of life and functionality of children in general and those with comorbid neurological diseases in particular. Understanding the pathophysiology of sleep disorders, recognizing the implications of sleep disorder in children with neurologic diseases and behavioral difficulties, and early intervention continue to evolve resulting in better neurocognitive outcomes.

  9. Challenges in neurological practice in developing countries.

    Science.gov (United States)

    Pandey, Sanjay

    2012-01-01

    The burden of neurological illness is much higher in developing countries. Neurological disorders in these countries are mainly due to poverty and malnutrition. Spectrums of diseases are also different in comparison with developed countries. Lack of resources, ignorance, and overpopulation make it very difficult and challenging to tackle this problem. Majority of the patients are seen by general practitioners who have little knowledge about neurological illnesses. Most of the countries have very few or no neurologist. There is a greater need of taking neurological care at primary care level where majority of the patients struggle with epilepsy, stroke and neuroinfections.

  10. Neurological and behavioral abnormalities, ventricular dilatation, altered cellular functions, inflammation, and neuronal injury in brains of mice due to common, persistent, parasitic infection.

    Science.gov (United States)

    Hermes, Gretchen; Ajioka, James W; Kelly, Krystyna A; Mui, Ernest; Roberts, Fiona; Kasza, Kristen; Mayr, Thomas; Kirisits, Michael J; Wollmann, Robert; Ferguson, David J P; Roberts, Craig W; Hwang, Jong-Hee; Trendler, Toria; Kennan, Richard P; Suzuki, Yasuhiro; Reardon, Catherine; Hickey, William F; Chen, Lieping; McLeod, Rima

    2008-10-23

    Worldwide, approximately two billion people are chronically infected with Toxoplasma gondii with largely unknown consequences. To better understand long-term effects and pathogenesis of this common, persistent brain infection, mice were infected at a time in human years equivalent to early to mid adulthood and studied 5-12 months later. Appearance, behavior, neurologic function and brain MRIs were studied. Additional analyses of pathogenesis included: correlation of brain weight and neurologic findings; histopathology focusing on brain regions; full genome microarrays; immunohistochemistry characterizing inflammatory cells; determination of presence of tachyzoites and bradyzoites; electron microscopy; and study of markers of inflammation in serum. Histopathology in genetically resistant mice and cytokine and NRAMP knockout mice, effects of inoculation of isolated parasites, and treatment with sulfadiazine or alphaPD1 ligand were studied. Twelve months after infection, a time equivalent to middle to early elderly ages, mice had behavioral and neurological deficits, and brain MRIs showed mild to moderate ventricular dilatation. Lower brain weight correlated with greater magnitude of neurologic abnormalities and inflammation. Full genome microarrays of brains reflected inflammation causing neuronal damage (Gfap), effects on host cell protein processing (ubiquitin ligase), synapse remodeling (Complement 1q), and also increased expression of PD-1L (a ligand that allows persistent LCMV brain infection) and CD 36 (a fatty acid translocase and oxidized LDL receptor that mediates innate immune response to beta amyloid which is associated with pro-inflammation in Alzheimer's disease). Immunostaining detected no inflammation around intra-neuronal cysts, practically no free tachyzoites, and only rare bradyzoites. Nonetheless, there were perivascular, leptomeningeal inflammatory cells, particularly contiguous to the aqueduct of Sylvius and hippocampus, CD4+ and CD8+ T cells

  11. Neurological and behavioral abnormalities, ventricular dilatation, altered cellular functions, inflammation, and neuronal injury in brains of mice due to common, persistent, parasitic infection

    Directory of Open Access Journals (Sweden)

    Hwang Jong-Hee

    2008-10-01

    Full Text Available Abstract Background Worldwide, approximately two billion people are chronically infected with Toxoplasma gondii with largely unknown consequences. Methods To better understand long-term effects and pathogenesis of this common, persistent brain infection, mice were infected at a time in human years equivalent to early to mid adulthood and studied 5–12 months later. Appearance, behavior, neurologic function and brain MRIs were studied. Additional analyses of pathogenesis included: correlation of brain weight and neurologic findings; histopathology focusing on brain regions; full genome microarrays; immunohistochemistry characterizing inflammatory cells; determination of presence of tachyzoites and bradyzoites; electron microscopy; and study of markers of inflammation in serum. Histopathology in genetically resistant mice and cytokine and NRAMP knockout mice, effects of inoculation of isolated parasites, and treatment with sulfadiazine or αPD1 ligand were studied. Results Twelve months after infection, a time equivalent to middle to early elderly ages, mice had behavioral and neurological deficits, and brain MRIs showed mild to moderate ventricular dilatation. Lower brain weight correlated with greater magnitude of neurologic abnormalities and inflammation. Full genome microarrays of brains reflected inflammation causing neuronal damage (Gfap, effects on host cell protein processing (ubiquitin ligase, synapse remodeling (Complement 1q, and also increased expression of PD-1L (a ligand that allows persistent LCMV brain infection and CD 36 (a fatty acid translocase and oxidized LDL receptor that mediates innate immune response to beta amyloid which is associated with pro-inflammation in Alzheimer's disease. Immunostaining detected no inflammation around intra-neuronal cysts, practically no free tachyzoites, and only rare bradyzoites. Nonetheless, there were perivascular, leptomeningeal inflammatory cells, particularly contiguous to the aqueduct of

  12. Cognitive deficits in schizophrenia

    Directory of Open Access Journals (Sweden)

    S Chattopadhyay

    2012-01-01

    Full Text Available The term schizophrenia was coined by Eugene Bleuler. Symptoms of schizophrenia are arranged into groups or clusters called as domains. The domains of dysfunctions are positive symptoms, negative symptoms, cognitive impairments, mood and suicidity, and aggression. Cognition is the sum total of mental processes that makes us acquire knowledge and keeps us aware of our surroundings and thus enables us to arrive at appropriate judgments. Cognitive deficits are recognized as enduring and persistent features in schizophrenia and can be neuro-cognitive or relating to social cognition. Neurocognitive deficits are deficits in speed of processing, attention / vigilance, working memory, verbal memory, visual memory, reasoning and problem solving, social cognition. Cognitive function can be assessed by various methods like experimental approach, neuropsychological and psychometric and ecologic approach. Cognitive deficits are present at onset of illness producing substantial impairment. Unlike psychotic symptoms, which remit with treatment, functional impairments remain stable over time. Detail understanding of such symptoms will help in disability limitation. Various cognitive remediation programmes are underway with such intent. Articles till March, 2012 were searched through PubMed and Google Scholar, which were studied in an attempt of understanding the topic. The information was structured and organized.

  13. Beyond the knowledge deficit

    DEFF Research Database (Denmark)

    Hansen, Janus Staffan; Holm, Lotte; Frewer, Lynn

    2003-01-01

    The paper reviews psychological and social scientific research on lay attitudes to food risks. Many experts (scientists, food producers and public health advisors) regard public unease about food risks as excessive. This expert-lay discrepancy is often attributed to a 'knowledge deficit' among lay...

  14. Clostridial disease associated with neurologic signs: tetanus, botulism, and enterotoxemia.

    Science.gov (United States)

    Rings, D Michael

    2004-07-01

    Clostridial infections are found worldwide in almost all species of animals and may involve a variety of body systems and present with a diversity of clinical signs. Most damage done through clostridial infections is due to the action of toxins released from the bacteria.Thus, disease caused by Clostridium spp should more correctly be called intoxication. Two prominent clostridial infections are associated with neurologic signs: Clostridium botulinum and C tetani. In both infections, the mechanism that is responsible for causing the problem is similar, despite the remarkable difference in clinical presentation. In addition, neurologic signs are described with C perfringens types C and D but are not the dominant feature of these diseases.

  15. Social-Cognitive Deficits in Schizophrenia.

    Science.gov (United States)

    Mier, Daniela; Kirsch, Peter

    Patients with schizophrenia not only suffer from prototypical psychotic symptoms such as delusions and hallucinations and from cognitive deficits, but also from tremendous deficits in social functioning. However, little is known about the interplay between the cognitive and the social-cognitive deficits in schizophrenia. Our chapter gives an overview on behavioral, as well as functional imaging studies on social cognition in schizophrenia. Main findings on cognitive and motivational deficits in schizophrenia are reviewed and introduced within the context of the dopamine hypothesis of schizophrenia. The reviewed findings suggest that disturbed "social brain" functioning in schizophrenia, depending on the specific context, can either lead to a neglect of the emotions and intentions of others or to the false attribution of these emotions and intentions in an emotionally neutral social content. We integrate these findings with the current knowledge about aberrant dopaminergic firing in schizophrenia by presenting a comprehensive model explaining core symptoms of the disorder. The main implication of the presented model is that neither cognitive-motivational, nor social-cognitive deficits alone cause schizophrenia symptoms, but that symptoms only emerge by the interplay of disturbed social brain functioning with aberrant dopaminergic firing.

  16. [Neurohagiography. Lamberto Caesaraugustanus, the cephalophoric: holy patron of Spanish neurology?].

    Science.gov (United States)

    Martín, A; Fernández-Armayor, V; Moreno, J M; Bustamante, C

    2002-10-01

    Until now Neurology has lacked a patron saint who, taking the most advantage of the rich cultural tradition inherited from our past and independently of the religious ideology of each one, can be helpful approach in the neurologist figure to different people. An Ad Hoc Committee from the Neurology History Study Group of the SEN has researched the medical hagiography with any kind of neurological relationship (neurohagiography), in order to make a hagiography study of every saint related to our speciality, with the added luck of proposing a patron for Neurology with hispanic origin. In this pioneer study of historiographic research different documents related with the medical hagiography have been studied, especially the Index ac Status Causarum, and information coming from different national ecclesiastic archives. A total of 342 saints share the patronage of 137 diseases, of which a 27,7% are related in some way to Neurology. Headache constitutes the prime cause of the invocations, with 20 saints. Another 11 saints plead for epilepsy; to these we also must add another six for so called possessed patients. Therefore, two of the three main causes of invocation (headache, fever and epilepsy) come up to chronic processes. Of all the saints with a hispanic origin candidates to the patronage of the neurologists San Lamberto Caesaraugustanus stands out, who died in the year 303 during Diocletian persecution. Belonging to the selected standing of "cephalophoric martyrs" (those beheahed who carry their own head in their hands), he was able to walk an important distance (about six kilometres) with his head split from the body, a fact only understood as a suprahuman phenomenon thanks to which he has becomes the brain transplant pioneer.

  17. Clinical features, proximate causes, and consequences of active convulsive epilepsy in Africa.

    Science.gov (United States)

    Kariuki, Symon M; Matuja, William; Akpalu, Albert; Kakooza-Mwesige, Angelina; Chabi, Martin; Wagner, Ryan G; Connor, Myles; Chengo, Eddie; Ngugi, Anthony K; Odhiambo, Rachael; Bottomley, Christian; White, Steven; Sander, Josemir W; Neville, Brian G R; Newton, Charles R J C; Twine, Rhian; Gómez Olivé, F Xavier; Collinson, Mark; Kahn, Kathleen; Tollman, Stephen; Masanja, Honratio; Mathew, Alexander; Pariyo, George; Peterson, Stefan; Ndyomughenyi, Donald; Bauni, Evasius; Kamuyu, Gathoni; Odera, Victor Mung'ala; Mageto, James O; Ae-Ngibise, Ken; Akpalu, Bright; Agbokey, Francis; Adjei, Patrick; Owusu-Agyei, Seth; Kleinschmidt, Immo; Doku, Victor C K; Odermatt, Peter; Nutman, Thomas; Wilkins, Patricia; Noh, John

    2014-01-01

    Epilepsy is common in sub-Saharan Africa (SSA), but the clinical features and consequences are poorly characterized. Most studies are hospital-based, and few studies have compared different ecological sites in SSA. We described active convulsive epilepsy (ACE) identified in cross-sectional community-based surveys in SSA, to understand the proximate causes, features, and consequences. We performed a detailed clinical and neurophysiologic description of ACE cases identified from a community survey of 584,586 people using medical history, neurologic examination, and electroencephalography (EEG) data from five sites in Africa: South Africa; Tanzania; Uganda; Kenya; and Ghana. The cases were examined by clinicians to discover risk factors, clinical features, and consequences of epilepsy. We used logistic regression to determine the epilepsy factors associated with medical comorbidities. Half (51%) of the 2,170 people with ACE were children and 69% of seizures began in childhood. Focal features (EEG, seizure types, and neurologic deficits) were present in 58% of ACE cases, and these varied significantly with site. Status epilepticus occurred in 25% of people with ACE. Only 36% received antiepileptic drugs (phenobarbital was the most common drug [95%]), and the proportion varied significantly with the site. Proximate causes of ACE were adverse perinatal events (11%) for onset of seizures before 18 years; and acute encephalopathy (10%) and head injury prior to seizure onset (3%). Important comorbidities were malnutrition (15%), cognitive impairment (23%), and neurologic deficits (15%). The consequences of ACE were burns (16%), head injuries (postseizure) (1%), lack of education (43%), and being unmarried (67%) or unemployed (57%) in adults, all significantly more common than in those without epilepsy. There were significant differences in the comorbidities across sites. Focal features are common in ACE, suggesting identifiable and preventable causes. Malnutrition and

  18. Clinical features, proximate causes, and consequences of active convulsive epilepsy in Africa

    Science.gov (United States)

    Kariuki, Symon M; Matuja, William; Akpalu, Albert; Kakooza-Mwesige, Angelina; Chabi, Martin; Wagner, Ryan G; Connor, Myles; Chengo, Eddie; Ngugi, Anthony K; Odhiambo, Rachael; Bottomley, Christian; White, Steven; Sander, Josemir W; Neville, Brian G R; Newton, Charles R J C

    2014-01-01

    Purpose Epilepsy is common in sub-Saharan Africa (SSA), but the clinical features and consequences are poorly characterized. Most studies are hospital-based, and few studies have compared different ecological sites in SSA. We described active convulsive epilepsy (ACE) identified in cross-sectional community-based surveys in SSA, to understand the proximate causes, features, and consequences. Methods We performed a detailed clinical and neurophysiologic description of ACE cases identified from a community survey of 584,586 people using medical history, neurologic examination, and electroencephalography (EEG) data from five sites in Africa: South Africa; Tanzania; Uganda; Kenya; and Ghana. The cases were examined by clinicians to discover risk factors, clinical features, and consequences of epilepsy. We used logistic regression to determine the epilepsy factors associated with medical comorbidities. Key Findings Half (51%) of the 2,170 people with ACE were children and 69% of seizures began in childhood. Focal features (EEG, seizure types, and neurologic deficits) were present in 58% of ACE cases, and these varied significantly with site. Status epilepticus occurred in 25% of people with ACE. Only 36% received antiepileptic drugs (phenobarbital was the most common drug [95%]), and the proportion varied significantly with the site. Proximate causes of ACE were adverse perinatal events (11%) for onset of seizures before 18 years; and acute encephalopathy (10%) and head injury prior to seizure onset (3%). Important comorbidities were malnutrition (15%), cognitive impairment (23%), and neurologic deficits (15%). The consequences of ACE were burns (16%), head injuries (postseizure) (1%), lack of education (43%), and being unmarried (67%) or unemployed (57%) in adults, all significantly more common than in those without epilepsy. Significance There were significant differences in the comorbidities across sites. Focal features are common in ACE, suggesting identifiable and

  19. Vegetative status characteristics in children with neurological pathology on the background of undifferentiated connective tissue dysplasia

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    Tyazka O.V.

    2016-03-01

    Full Text Available Background. Disorders of the autonomic nervous system are the most common pathological conditions detected in 20% - 85% of children and adolescents according to different authors' data. Assessment of the vegetative status in the period of intensive growth and differentiation of organs and tissues that is characteristic of childhood is of great practical importance. Identification of vegetative dysregulation is an important diagnostic measure in children's health status evaluation especially in patients with undifferentiated connective tissue dysplasia (UNDCT taking into account its genetic determinism and debut in childhood. Genetically determined biochemical disorders in the connective tissue followed by formation of characteristic pathological substrates cause dysregulation of sympathoadrenal system and correlate with UNDCT severity degree. Material and methods. There were 100 children aged from 5 to 16 years engaged in the investigation. All of them were treated in the neurological department of the City clinical hospital №4. All patients were divided into two groups: basic group, which included 50 children with neurological disorders and UNDC, and control one, which consisted of 50 children with neurological disorders without UNDCT. The survey included obstetric history analysis, anthropometry to determine the ratio of longitudinal and transverse dimensions (the index of Vervica; clinical and neurological examination (study of reflex&motor areas, sensory function, coordination; laboratory methods (clinical blood count and biochemical blood tests to determine the level of potassium and calcium ions, instrumental methods (electroencephalography, rheoencephalography, magnetic resonance imaging of the brain. Osokina's table was used for baseline autonomic tone assessment. The evaluation was conducted by counting the number of signs. Subsequently was performed the summation of the scores with the determination of the percentage of predominant

  20. Sociocultural issues and causes of cerebral palsy in Port Harcourt ...

    African Journals Online (AJOL)

    Background: Cerebral palsy (CP) is a common neurological disorder of childhood with significant neurological complications and associated comorbidities. The aim of this study was to determine the socio- cultural characteristics and causes of CP in children who presented to the Paediatric neurology clinic in Port Harcourt, ...

  1. Offsetting deficit conceptualisations: methodological considerations ...

    African Journals Online (AJOL)

    ... nature of student learning experiences in ways that accommodate the influence of various contextual realities brings researchers and their research agendas closer to offsetting deficit conceptualisation. Keywords: deficit discourses, higher education, knowledge recontextualisation, literacy practices, research design.

  2. Teaching the Tiger: A Handbook for Individuals Involved in the Education of Students with Attention Deficit Disorders, Tourette Syndrome or Obsessive-Compulsive Disorder.

    Science.gov (United States)

    Dornbush, Marilyn P.; Pruitt, Sheryl K.

    This book provides practical guidance concerning children with the neurological impairments of attention deficit disorder, Tourette syndrome, or obsessive-compulsive disorder. Section 1 focuses on helping those without neurological impairments understand these conditions. Topics covered include definitions, the deregulated arousal system,…

  3. Neurological Disorders in Medical Use of Cannabis: An Update.

    Science.gov (United States)

    Solimini, Renata; Rotolo, Maria Concetta; Pichini, Simona; Pacifici, Roberta

    2017-01-01

    Medical cannabis is increasingly used as a treatment or adjunct treatment with different levels of efficacy in several neurological disorders or related symptoms (such as multiple sclerosis, autism, Parkinson and Alzheimer disease, Tourette's syndrome, Huntington's disease, neuropathic pain, epilepsy, headache), as well as in other medical conditions (e.g. nausea and vomiting, glaucoma, appetite stimulation, cancer, inflammatory conditions, asthma). Nevertheless, a number of neurological adverse effects from use of medical cannabis on the short- and on the longterm have been reported, in addition to other adverse health events. It has been noticed that the use of medical cannabis can lead to a paradoxical effects depending on the amount of delta-9-tetrahydrocannabinol (THC) -like cannabinoids the preparation contain. Accordingly, some neurological disorders or symptoms (e.g. multiple sclerosis, seizures, epilepsy, headache) may be caused or exacerbated by the same treatment supposed to cure them. The current review presents an update of the neurological adverse effects resulting from the use of cannabis for medical purposes, highlighting the need to weigh the benefits and risks, when using cannabinoidbased treatments. Copyright© Bentham Science Publishers; For any queries, please email at epub@benthamscience.org.

  4. Toward a Neurology of Loneliness

    Science.gov (United States)

    Cacioppo, Stephanie; Capitanio, John P.; Cacioppo, John T.

    2016-01-01

    Social isolation has been recognized as a major risk factor for morbidity and mortality in humans for more than a quarter century. The brain is the key organ of social connections and processes, however, and the same objective social relationship can be experienced as caring and protective or as exploitive and isolating. We review evidence that the perception of social isolation (i.e., loneliness) impacts brain and behavior and is a risk factor for broad-based morbidity and mortality. However, the causal role of loneliness on neural mechanisms and mortality is difficult to test conclusively in humans. Mechanistic animal studies provide a lens through which to evaluate the neurological effects of a member of a social species living chronically on the social perimeter. Experimental studies show that social isolation produces significant changes in brain structures and processes in adult social animals. These effects are not uniform across the brain or across species but instead are most evident in brain regions that reflect differences in the functional demands of solitary versus social living for a particular species. The human and animal literatures have developed independently, however, and significant gaps also exist. The current review underscores the importance of integrating human and animal research to delineate the mechanisms through which social relationships impact the brain, health, and well-being. PMID:25222636

  5. Gluten sensitivity and neurological manifestations

    Directory of Open Access Journals (Sweden)

    Agostino Berio

    2015-12-01

    Full Text Available The authors report on six cases of gluten-sensitivity, also defined non-celiac gluten sensitivity, characterized by abdominal features (diarrhea, bloating, pain, genetic positivity for predisposition to celiac disease (DQB1* 02 in all cases; DQA1*05 in three; DQA1*02 in two, DQB1*03 in two, negative anti-t-Transglutaminase antibodies, normal mucosa on biopsy in four cases, type 1 of Marsh in one case. The subjects presented frequent central nervous system (CNS symptoms: headache in three patients, somnolence in one, electroencephalogram aspecific alterations in three (in two of them with previous seizures, leptomeningeal cyst in one, intracranial calcification in one, cerebral gliosis in two. After a gluten-free diet, all intestinal and clinical CNS features remitted, but re-appeared after gluten reintroduction. On the basis of the neurological signs, the authors stress the relevance of immune innate system in the pathogenesis of these cases with possible subsequent evolution on immune adaptive system involvement.

  6. Endocannabinoid System in Neurological Disorders.

    Science.gov (United States)

    Ranieri, Roberta; Laezza, Chiara; Bifulco, Maurizio; Marasco, Daniela; Malfitano, Anna M

    2016-01-01

    Several studies support the evidence that the endocannabinoid system and cannabimimetic drugs might have therapeutic potential in numerous pathologies. These pathologies range from neurological disorders, atherosclerosis, stroke, cancer to obesity/metabolic syndrome and others. In this paper we review the endocannabinoid system signaling and its alteration in neurodegenerative disorders like multiple sclerosis, Alzheimer's disease, Parkinson's disease and Huntington's disease and discuss the main findings about the use of cannabinoids in the therapy of these pathologies. Despite different etiologies, neurodegenerative disorders exhibit similar mechanisms like neuro-inflammation, excitotoxicity, deregulation of intercellular communication, mitochondrial dysfunction and disruption of brain tissue homeostasis. Current treatments ameliorate the symptoms but are not curative. Interfering with the endocannabinoid signaling might be a valid therapeutic option in neuro-degeneration. To this aim, pharmacological intervention to modulate the endocannabinoid system and the use of natural and synthetic cannabimimetic drugs have been assessed. CB1 and CB2 receptor signaling contributes to the control of Ca2+ homeostasis, trophic support, mitochondrial activity, and inflammatory conditions. Several studies and patents suggest that the endocannabinoid system has neuro-protective properties and might be a target in neurodegenerative diseases.

  7. Task analysis in neurosciences programme design - neurological ...

    African Journals Online (AJOL)

    Defining educational objectives is the key to achieving the goal of professional competence in students. The technique of task analysis was selected to determine components of competence in clinical neurology appropriate to the needs of primary care. A survey of neurological problems in general practice revealed that ...

  8. Archives: African Journal of Neurological Sciences

    African Journals Online (AJOL)

    Items 1 - 28 of 28 ... Archives: African Journal of Neurological Sciences. Journal Home > Archives: African Journal of Neurological Sciences. Log in or Register to get access to full text downloads. Username, Password, Remember me, or Register · Journal Home · ABOUT THIS JOURNAL · Advanced Search · Current Issue ...

  9. Suspecting Neurological Dysfunction From E Mail Messages ...

    African Journals Online (AJOL)

    A non medical person suspected and confirmed neurological dysfunction in an individual, based only on e mail messages sent by the individual. With email communication becoming rampant “peculiar” email messages may raise the suspicion of neurological dysfunction. Organic pathology explaining the abnormal email ...

  10. Neurological and neurosurgical manifestations of human ...

    African Journals Online (AJOL)

    adults in Abidjan, Cote d'Ivoire and in Kinshasa and among inpatients in Ugandan hospitals. Ninety per cent of deaths ... various parts of the continent. Neurological manifestations. The spectrum of neurological diseases reported in ... Primary effects of HIV. HEADACHE. Case report. A Malawian 46-year-old male senior ...

  11. Child Neurology Education for Pediatric Residents.

    Science.gov (United States)

    Albert, Dara V F; Patel, Anup D; Behnam-Terneus, Maria; Sautu, Beatriz Cunill-De; Verbeck, Nicole; McQueen, Alisa; Fromme, H Barrett; Mahan, John D

    2017-03-01

    The aim of this study was to evaluate whether the current state of child neurology education during pediatric residency provides adequate preparation for pediatric practice. A survey was sent to recent graduates from 3 pediatric residency programs to assess graduate experience, perceived level of competence, and desire for further education in child neurology. Responses from generalists versus subspecialists were compared. The response rate was 32%, half in general pediatric practice. Only 22% feel very confident in approaching patients with neurologic problems. This may represent the best-case scenario as graduates from these programs had required neurology experiences, whereas review of Accreditation Council of Graduate Medical Education-accredited residency curricula revealed that the majority of residencies do not. Pediatric neurologic problems are common, and pediatric residency graduates do encounter such problems in practice. The majority of pediatricians report some degree of confidence; however, some clear areas for improvement are apparent.

  12. Efficacy of intraoperative neurologic monitoring in surgery involving a vertical expandable prosthetic titanium rib for early-onset spinal deformity.

    Science.gov (United States)

    Skaggs, David L; Choi, Paul D; Rice, Christie; Emans, John; Song, Kit M; Smith, John T; Campbell, Robert M

    2009-07-01

    The vertical expandable prosthetic titanium rib (VEPTR) device is used in the treatment of thoracic insufficiency syndrome and certain types of early-onset spinal deformity. The purpose of this study was to evaluate the risk of neurologic injury during surgical procedures involving use of the VEPTR and to determine the efficacy of intraoperative spinal cord neuromonitoring. Data were collected prospectively during a multicenter study. Surgical procedures were divided into three categories: primary device implantation, device exchange, and device lengthening. Further retrospective evaluation was undertaken in cases of neurologic injury or changes detected with neuromonitoring. There were 1736 consecutive VEPTR procedures at six centers: 327 (in 299 patients) consisted of a primary device implantation, 224 were a device exchange, and 1185 were a device lengthening. Perioperative clinical neurologic injury was noted in eight (0.5%) of the 1736 cases: these injuries were identified after five (1.5%) of the 327 procedures for primary device implantation, three (1.3%) of the 224 device exchanges, and none of the 1185 device-lengthening procedures. Of the eight cases of neurologic injury, six involved the upper extremity and two involved the lower extremity. The neurologic deficit was temporary in seven patients and permanent in one patient, who had persistent neurogenic arm and hand pain. Intraoperative neuromonitoring demonstrated changes during six (0.3%) of the 1736 procedures: five (1.5%) of the 327 procedures for primary device implantation and one (0.08%) of the 1185 device-lengthening procedures. The surgery was altered in all six cases, with resolution of the monitoring changes in five cases and persistent signal changes and a neurologic deficit (upper-extremity brachial plexopathy) in one. Two patients had false-negative results of monitoring of somatosensory evoked potentials, and one had false-negative results of monitoring of somatosensory evoked potentials

  13. Motor Deficits Following Pediatric Mild Traumatic Brain Injury: Implications for School Psychologists

    Science.gov (United States)

    Davis, Andrew S.; Moore, Brittney; Rice, Valerie; Decker, Scott

    2015-01-01

    Mild traumatic brain injury (mTBI), sometimes referred to as concussion, is one of the most common acquired neurological problems of childhood. When children return to school following mTBI, school psychologists should be actively involved in the determination of neurocognitive and functional deficits for the purpose of designing strength-based…

  14. Regional cortical hyper perfusion on perfusion CT during postical motor deficit: A case report

    Energy Technology Data Exchange (ETDEWEB)

    Baik, Hye Jin [Dept. of Radiology, Haeundae Paik Hospital, Inje University College of Medicine, Busan (Korea, Republic of)

    2013-08-15

    Postictal neurologic deficit is a well-known complication mimicking the manifestation of a stroke. We present a case of a patient with clinical evidence of Todd's paralysis correlating with reversible postictal parenchymal changes on perfusion CT and magnetic resonance (MR) imaging. In this case, perfusion CT and MR imaging were helpful in the differential diagnosis of stroke-mimicking conditions.

  15. Extended Attention Span Training System: Video Game Neurotherapy for Attention Deficit Disorder.

    Science.gov (United States)

    Pope, Alan T.; Bogart, Edward H.

    1996-01-01

    Describes the Extended Attention Span Training (EAST) system for modifying attention deficits, which takes the concept of biofeedback one step further by making a video game more difficult as the player's brain waves indicate that attention is waning. Notes contributions of this technology to neuropsychology and neurology, where the emphasis is on…

  16. Cognitive-Linguistic Deficit and Speech Intelligibility in Chronic Progressive Multiple Sclerosis

    Science.gov (United States)

    Mackenzie, Catherine; Green, Jan

    2009-01-01

    Background: Multiple sclerosis is a disabling neurological disease with varied symptoms, including dysarthria and cognitive and linguistic impairments. Association between dysarthria and cognitive-linguistic deficit has not been explored in clinical multiple sclerosis studies. Aims: In patients with chronic progressive multiple sclerosis, the…

  17. Could a neurological disease be a part of Mozart's pathography?

    Science.gov (United States)

    Ivkić, Goran; Erdeljić, Viktorija

    2011-01-01

    As expected, since we recently celebrated the 250th anniversary of birth of Wolfgang Amadeus Mozart, there has been again a renewal of interest in his short but intensive life, as well as in the true reason of his untimely dead. Mozart lived and died in time when the medical knowledge was based mostly on subjective observations, without the established basics of standardized medical terminology and methodology. This leaves a great space for hypothesizing about his health problems, as well as about the cause of his death. The medical academic community attributed to Mozart approximately 150 different medical diagnoses. There is much speculation on the possible causes of Mozart's death: uremia, infection, rheumatic fever, trichinellosis, etc. Recently some authors have raised the question about a possible concomitant neurological disease. According to available records, Mozart has shown some elements of cyclotimic disorder, epilepsy and Gilles de la Tourette syndrome. Furthermore, the finding of a temporal fracture on (allegedly) Mozart's skull, gives a way to speculations about the possibility of a chronic subdural hematoma and its compressive effect on the temporal lobe. Despite numerous theories on Mozart's pathography that also include a concomitant neurological disorder, the medical and history records about Mozart's health status indicate that he probably had suffered from an infective illness, followed most likely by the reactivation of rheumatic fever, which was followed by strong immunologic reaction in the last days of his life. Taking all the above into consideration, it is reasonably to conclude that Mozart's neurological disturbances were caused by the intensity of the infective disease, and not primarily by a neurological disease.

  18. Motor Deficits are Triggered by Reperfusion-Reoxygenation Injury as Diagnosed by MRI and by a Mechanism Involving Oxidants

    Science.gov (United States)

    Drobyshevsky, Alexander; Luo, Kehuan; Derrick, Matthew; Yu, Lei; Du, Hongyan; Prasad, P.V.; Vasquez-Vivar, Jeannette; Batinic-Haberle, Ines; Tan, Sidhartha

    2012-01-01

    The early antecedents of cerebral palsy (CP) are unknown but are suspected to be due to hypoxia-ischemia (H-I). In our rabbit model of CP, the MRI biomarker, ADC on diffusion-weighted imaging, predicted which fetuses will develop postnatal hypertonia. Surviving H-I fetuses experience reperfusion-reoxygenation but a sub-population manifested a continued decline of ADC during early reperfusion-reoxygenation, which possibly represented greater brain injury (RepReOx). We hypothesized that oxidative stress in reperfusion-reoxygenation is a critical trigger for postnatal hypertonia. We investigated if RepReOx predicted postnatal neurobehavior, indicated oxidative stress, and if targeting antioxidants at RepReOx ameliorated motor deficits, which included testing of a new superoxide dismutase mimic (MnTnHex-2-PyP). Rabbit dams, 79% gestation (E25), were subjected to 40-min uterine ischemia. Fetal brain ADC was followed during H-I, immediate reperfusion-reoxygenation, and 4-72 hours after H-I. Endpoints were postnatal neurological outcome at E32, ADC at end of, ADC nadir during H-I and reperfusion-reoxygenation, and area under ADC during first 20-min reperfusion-reoxygenation. Antioxidants targeting RepReOx were administered before and/or after uterine ischemia. The new MRI-ADC biomarker for RepReOx improved prediction of postnatal hypertonia. Greater superoxide production, mitochondrial injury and oligodendroglial loss occurred in fetal brains exhibiting RepReOx than in those without. The antioxidants, MnTnHex-2-PyP, and Ascorbate and Trolox combination, significantly decreased postnatal motor deficits and extent of RepReOx. The etiological link between early injury and later motor deficits can thus be investigated by MRI and allows us to distinguish between critical oxidative stress that causes motor deficits from non-critical oxidative stress that does not. PMID:22514312

  19. Attention deficits and divorce.

    Science.gov (United States)

    Bouchard, Geneviève; Saint-Aubin, Jean

    2014-09-01

    Building on previous work on the role of attention deficits associated with the regulation of executive control in psychiatric disorders, we examine whether these attention deficits are related to an interpersonal disturbance, the experience of divorce. Attentional capacities of 95 randomly selected couples from the general population were measured with a well-established task, the Attentional Network Task, which assesses the efficiency of 3 attention networks (that is, alerting, orienting, and executive control). Among the 190 participants, 32 had experienced a divorce in the past. ANCOVAs were used to compare divorced people in marital or cohabiting unions with people in first unions in their performance on this purely cognitive task. Our findings indicate that divorced people who are currently living in a cohabiting relationship show significantly lower executive control than other adults living as couples, after controlling for sex, age, income, and education. This subgroup of divorced people not only exhibit greater difficulty in responding to some stimuli while ignoring irrelevant ones but also manifest cognitive deficits in conflict resolution. This study highlights the links between attention and the long-term maintenance of intimate relationships. Our results may have important implications for the identification of people at risk for divorce.

  20. Neurologic abnormalities in mouse models of the lysosomal storage disorders mucolipidosis II and mucolipidosis III γ.

    Directory of Open Access Journals (Sweden)

    Rachel A Idol

    Full Text Available UDP-GlcNAc:lysosomal enzyme N-acetylglucosamine-1-phosphotransferase is an α2β2γ2 hexameric enzyme that catalyzes the synthesis of the mannose 6-phosphate targeting signal on lysosomal hydrolases. Mutations in the α/β subunit precursor gene cause the severe lysosomal storage disorder mucolipidosis II (ML II or the more moderate mucolipidosis III alpha/beta (ML III α/β, while mutations in the γ subunit gene cause the mildest disorder, mucolipidosis III gamma (ML III γ. Here we report neurologic consequences of mouse models of ML II and ML III γ. The ML II mice have a total loss of acid hydrolase phosphorylation, which results in depletion of acid hydrolases in mesenchymal-derived cells. The ML III γ mice retain partial phosphorylation. However, in both cases, total brain extracts have normal or near normal activity of many acid hydrolases reflecting mannose 6-phosphate-independent lysosomal targeting pathways. While behavioral deficits occur in both models, the onset of these changes occurs sooner and the severity is greater in the ML II mice. The ML II mice undergo progressive neurodegeneration with neuronal loss, astrocytosis, microgliosis and Purkinje cell depletion which was evident at 4 months whereas ML III γ mice have only mild to moderate astrocytosis and microgliosis at 12 months. Both models accumulate the ganglioside GM2, but only ML II mice accumulate fucosylated glycans. We conclude that in spite of active mannose 6-phosphate-independent targeting pathways in the brain, there are cell types that require at least partial phosphorylation function to avoid lysosomal dysfunction and the associated neurodegeneration and behavioral impairments.