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Sample records for brain injury chronic

  1. Chronic cerebrovascular dysfunction after traumatic brain injury.

    Science.gov (United States)

    Jullienne, Amandine; Obenaus, Andre; Ichkova, Aleksandra; Savona-Baron, Catherine; Pearce, William J; Badaut, Jerome

    2016-07-01

    Traumatic brain injuries (TBI) often involve vascular dysfunction that leads to long-term alterations in physiological and cognitive functions of the brain. Indeed, all the cells that form blood vessels and that are involved in maintaining their proper function can be altered by TBI. This Review focuses on the different types of cerebrovascular dysfunction that occur after TBI, including cerebral blood flow alterations, autoregulation impairments, subarachnoid hemorrhage, vasospasms, blood-brain barrier disruption, and edema formation. We also discuss the mechanisms that mediate these dysfunctions, focusing on the cellular components of cerebral blood vessels (endothelial cells, smooth muscle cells, astrocytes, pericytes, perivascular nerves) and their known and potential roles in the secondary injury cascade. © 2016 Wiley Periodicals, Inc. PMID:27117494

  2. Chronic Traumatic Encephalopathy: The Neuropathological Legacy of Traumatic Brain Injury.

    Science.gov (United States)

    Hay, Jennifer; Johnson, Victoria E; Smith, Douglas H; Stewart, William

    2016-05-23

    Almost a century ago, the first clinical account of the punch-drunk syndrome emerged, describing chronic neurological and neuropsychiatric sequelae occurring in former boxers. Thereafter, throughout the twentieth century, further reports added to our understanding of the neuropathological consequences of a career in boxing, leading to descriptions of a distinct neurodegenerative pathology, termed dementia pugilistica. During the past decade, growing recognition of this pathology in autopsy studies of nonboxers who were exposed to repetitive, mild traumatic brain injury, or to a single, moderate or severe traumatic brain injury, has led to an awareness that it is exposure to traumatic brain injury that carries with it a risk of this neurodegenerative disease, not the sport or the circumstance in which the injury is sustained. Furthermore, the neuropathology of the neurodegeneration that occurs after traumatic brain injury, now termed chronic traumatic encephalopathy, is acknowledged as being a complex, mixed, but distinctive pathology, the detail of which is reviewed in this article. PMID:26772317

  3. A prospective study to evaluate a new residential community reintegration programme for severe chronic brain injury: the Brain Integration Programme.

    NARCIS (Netherlands)

    Geurtsen, G.J.; Martina, J.D.; Heugten, C.M. van; Geurts, A.C.H.

    2008-01-01

    PURPOSE: To assess the effectiveness of a residential community reintegration programme for participants with chronic sequelae of severe acquired brain injury that hamper community functioning. DESIGN: Prospective cohort study. SUBJECTS: Twenty-four participants with acquired brain injury (traumatic

  4. Neurotherapy for chronic headache following traumatic brain injury

    Institute of Scientific and Technical Information of China (English)

    David V Nelson; Mary Lee Esty

    2015-01-01

    Background:Chronic headache following traumatic brain injury (TBI) sustained in military service, while common, is highly challenging to treat with existing pharmacologic and non-pharmacologic interventions, and it may be complicated by co-morbid posttraumatic stress. Recently, a novel form of brainwave-based intervention known as the Flexyx Neurotherapy System (FNS), which involves minute pulses of electromagnetic energy stimulation of brainwave activity, has been suggested as a means to address symptoms of TBI. This study reports on a clinical series of patients with chronic headache following service-connected TBI treated with FNS. Methods: Nine veterans of the wars in Afghanistan and Iraq with moderate to severe chronic headaches following service-connected TBI complicated by posttraumatic stress symptoms were treated in 20 individual FNS sessions at the Brain Wellness and Biofeedback Center of Washington (in Bethesda, Maryland, USA). They periodically completed measures including the Brief Pain Inventory-Headache (BPI-HA), previous week worst and average pain ratings, the Posttraumatic Stress Disorder Checklist-Military version (PCL-M), and an individual treatment session numerical rating scale (NRS) for the degree of cognitive dysfunction. Data analyses included beginning-to-end of treatmentt-test comparisons for the BPI-HA, PCL-M, and cognitive dysfunction NRS. Results: All beginning-to-end of treatmentt-test comparisons for the BPI-HA, PCL-M, and cognitive dysfunction NRS indicated statistically significant decreases. All but one participant experienced a reduction in headaches along with reductions in posttraumatic stress and perceived cognitive dysfunction, with a subset experiencing the virtual elimination of headaches. One participant obtained modest headache relief but no improvements in posttraumatic stress or cognitive dysfunction. Conclusions: FNS may be a potentially efficacious treatment for chronic posttraumatic headache sustained in military

  5. Functional brain study of chronic traumatic head injury

    International Nuclear Information System (INIS)

    Explosive aggressive behaviour is a significant clinical and medico-legal problem in patients suffering from head injury. However, experts in neuropsychiatry have proposed a specific category for this disorder: the organic aggressive syndrome:. The basic reason for proposing this diagnosis is that it describes the specificity of the violent conduct secondary to 'brain damage' with greater precision. Early diagnosis and treatment of the injury is critical. The impact of hnetium-99m-hexamethylpropuleneamine oxime (HMPAO) was examined for measuring brain damage in correlation to neuropsychological performance in patients with traumatic brain injury (TBI). We thus report the case of a twelve-year-old child with a history of CET, who presents with serious episodes of heteroaggressiveness and suggest the usefulness of single photon emission computerized tomography (SPECT) to establish the validity of this psychiatric diagnosis. The appearance of modern functional neuro-image techniques (SPECT) may help to increase the validity of clinical diagnoses in the field of psychiatry in general and of forensic psychiatry in particularly, as the related findings may be used as demarcation criteria to establish syndromic diagnoses (Au)

  6. Clinical Utility of '99mTc-HMPAO Brain SPECT Findings in Chronic Head Injury

    International Nuclear Information System (INIS)

    Minima deterioration of cerebral perfusion or microanatomical changes were undetectable on conventional Brain CT or MRI. So evaluation of focal functional changes of the brain parenchyme is essential in chronic head injury patients, who did not show focal anatomical changes on these radiological studies. However, the patients who had longstanding neurologic sequelae following head injury, there had been no available imaging modalities for evaluating these patients precisely. Therefore we tried to detect the focal functional changes on the brain parenchyme using 99mTc-HMPAO Brain SPECT on the patients of chronic head injuries. Twenty three patients who had suffered from headache, memory dysfunction, personality change and insomnia lasting more than six months following head injury were included in our cases, which showed no anatomical abnormalities on Brain CT or MRI. At first they underwent psychological test whether the symptoms were organic or not. Also we were able to evaluate the cerebral perfusion changes with 99mTc-HMPAO Brain SPECT in 22 patients among the 23, which five patients were focal and 17 patients were nonfocally diffuse perfusion changes. Thus we can predict the perfusion changes such as local vascular deterioration or functional defects using 99mTc-HMPAO Brain SPECT in the patients who had suffered from post-traumatic sequelae, which changes were undetectable on Brain CT or MRI.

  7. Systems biomarkers as acute diagnostics and chronic monitoring tools for traumatic brain injury

    Science.gov (United States)

    Wang, Kevin K. W.; Moghieb, Ahmed; Yang, Zhihui; Zhang, Zhiqun

    2013-05-01

    Traumatic brain injury (TBI) is a significant biomedical problem among military personnel and civilians. There exists an urgent need to develop and refine biological measures of acute brain injury and chronic recovery after brain injury. Such measures "biomarkers" can assist clinicians in helping to define and refine the recovery process and developing treatment paradigms for the acutely injured to reduce secondary injury processes. Recent biomarker studies in the acute phase of TBI have highlighted the importance and feasibilities of identifying clinically useful biomarkers. However, much less is known about the subacute and chronic phases of TBI. We propose here that for a complex biological problem such as TBI, multiple biomarker types might be needed to harness the wide range of pathological and systemic perturbations following injuries, including acute neuronal death, neuroinflammation, neurodegeneration and neuroregeneration to systemic responses. In terms of biomarker types, they range from brain-specific proteins, microRNA, genetic polymorphism, inflammatory cytokines and autoimmune markers and neuro-endocrine hormones. Furthermore, systems biology-driven biomarkers integration can help present a holistic approach to understanding scenarios and complexity pathways involved in brain injury.

  8. Systematic review of the risk of dementia and chronic cognitive impairment after mild traumatic brain injury

    DEFF Research Database (Denmark)

    Godbolt, Alison K; Cancelliere, Carol; Hincapié, Cesar A;

    2014-01-01

    OBJECTIVE: To synthesize the best available evidence regarding the risk of dementia and chronic cognitive impairment (CCI) after mild traumatic brain injury (MTBI). DATA SOURCES: MEDLINE and other databases were searched (2001-2012) using a previously published search strategy and predefined crit...

  9. Family needs in the chronic phase after severe brain injury in Denmark

    DEFF Research Database (Denmark)

    Doser, Karoline; Norup, Anne

    2014-01-01

    caregiving for the patient was completed. The relatives completed the revised version of the Family Needs Questionnaire, a questionnaire consisting of 37 items related to different needs following brain injury. Results: Significant changes in status were found in employment (z = -3.464, p = 0.001) and co-habitation...... were only met in 41-50% of the total sample. Conclusion: Occupational and co-habitation status of the relatives was significantly affected by brain injury. A high number of relatives reported family needs not satisfied in the chronic phase. This requires an interventional approach for families to get...

  10. Chronic ibuprofen administration worsens cognitive outcome following traumatic brain injury in rats.

    Science.gov (United States)

    Browne, Kevin D; Iwata, Akira; Putt, M E; Smith, Douglas H

    2006-10-01

    Traumatic brain injury (TBI) can induce progressive neurodegeneration in association with chronic inflammation. Since chronic treatment with the non-steroidal anti-inflammatory drug (NSAID), ibuprofen, improves functional and histopathologic outcome in a mouse model of Alzheimer's disease (AD), we investigated whether it would also improve long-term outcome following TBI. Anesthetized adult rats were subjected to fluid percussion brain injury. Over the following 4 months the injured animals received ibuprofen per os (formulated in feed) at the approximate doses of 20 mg/kg body wt/day (n=13), 40 mg/kg body wt/day (n=13), or control (feed only, n=12). Sham animals underwent surgery without injury or ibuprofen treatment (n=9). At 4 months post-injury, a Morris water maze task revealed a profound learning dysfunction in all three injured groups compared to the sham group. Surprisingly, the learning ability of injured animals treated with either chronic ibuprofen regimen was significantly worsened compared to non-treated injured animals. However, there was no difference in the extent of progressive atrophy of the cortex or hippocampus between treated and non-treated injured animals. These data may have important implications for TBI patients who are often prescribed NSAIDs for chronic pain. PMID:16764859

  11. Facial Affect Recognition Training Through Telepractice: Two Case Studies of Individuals with Chronic Traumatic Brain Injury

    OpenAIRE

    John Williamson; Emi Isaki

    2015-01-01

    The use of a modified Facial Affect Recognition (FAR) training to identify emotions was investigated with two case studies of adults with moderate to severe chronic (> five years) traumatic brain injury (TBI).  The modified FAR training was administered via telepractice to target social communication skills.  Therapy consisted of identifying emotions through static facial expressions, personally reflecting on those emotions, and identifying sarcasm and emotions within social stories and ro...

  12. Damage to Myelin and Oligodendrocytes: A Role in Chronic Outcomes Following Traumatic Brain Injury?

    Directory of Open Access Journals (Sweden)

    William L. Maxwell

    2013-09-01

    Full Text Available There is increasing evidence in the experimental and clinical traumatic brain injury (TBI literature that loss of central myelinated nerve fibers continues over the chronic post-traumatic phase after injury. However, the biomechanism(s of continued loss of axons is obscure. Stretch-injury to optic nerve fibers in adult guinea-pigs was used to test the hypothesis that damage to the myelin sheath and oligodendrocytes of the optic nerve fibers may contribute to, or facilitate, the continuance of axonal loss. Myelin dislocations occur within internodal myelin of larger axons within 1–2 h of TBI. The myelin dislocations contain elevated levels of free calcium. The volume of myelin dislocations increase with greater survival and are associated with disruption of the axonal cytoskeleton leading to secondary axotomy. Waves of Ca2+ depolarization or spreading depression extend from the initial locus injury for perhaps hundreds of microns after TBI. As astrocytes and oligodendrocytes are connected via gap junctions, it is hypothesized that spreading depression results in depolarization of central glia, disrupt axonal ionic homeostasis, injure axonal mitochondria and allow the onset of axonal degeneration throughout an increasing volume of brain tissue; and contribute toward post-traumatic continued loss of white matter.

  13. Pilot study: Computer-based virtual anatomical interactivity for rehabilitation of individuals with chronic acquired brain injury

    OpenAIRE

    C. Douglas Simmons, PhD, OTR/L, FAOTA; Sajay Arthanat, PhD, OTR/L, ATP; Vincent J. Macri, BA, MA

    2014-01-01

    Deficiencies in upper-limb motor function and executive functioning can compromise an affected individual’s ability to complete everyday activities. Impaired motor and executive functioning therefore pose a risk to increasing numbers of veterans who have been diagnosed with acquired brain injury. This article reports on changes in upper-limb motor function and executive functioning of 12 adult participants with chronic acquired brain injury using a novel, computer-based, motor and cognitive r...

  14. Facial Affect Recognition Training Through Telepractice: Two Case Studies of Individuals with Chronic Traumatic Brain Injury

    Directory of Open Access Journals (Sweden)

    John Williamson

    2015-07-01

    Full Text Available The use of a modified Facial Affect Recognition (FAR training to identify emotions was investigated with two case studies of adults with moderate to severe chronic (> five years traumatic brain injury (TBI.  The modified FAR training was administered via telepractice to target social communication skills.  Therapy consisted of identifying emotions through static facial expressions, personally reflecting on those emotions, and identifying sarcasm and emotions within social stories and role-play.  Pre- and post-therapy measures included static facial photos to identify emotion and the Prutting and Kirchner Pragmatic Protocol for social communication.  Both participants with chronic TBI showed gains on identifying facial emotions on the static photos.               

  15. Diffuse traumatic brain injury affects chronic corticosterone function in the rat

    Directory of Open Access Journals (Sweden)

    Rachel K Rowe

    2016-07-01

    Full Text Available As many as 20–55% of patients with a history of traumatic brain injury (TBI experience chronic endocrine dysfunction, leading to impaired quality of life, impaired rehabilitation efforts and lowered life expectancy. Endocrine dysfunction after TBI is thought to result from acceleration–deceleration forces to the brain within the skull, creating enduring hypothalamic and pituitary neuropathology, and subsequent hypothalamic–pituitary endocrine (HPE dysfunction. These experiments were designed to test the hypothesis that a single diffuse TBI results in chronic dysfunction of corticosterone (CORT, a glucocorticoid released in response to stress and testosterone. We used a rodent model of diffuse TBI induced by midline fluid percussion injury (mFPI. At 2months postinjury compared with uninjured control animals, circulating levels of CORT were evaluated at rest, under restraint stress and in response to dexamethasone, a synthetic glucocorticoid commonly used to test HPE axis regulation. Testosterone was evaluated at rest. Further, we assessed changes in injury-induced neuron morphology (Golgi stain, neuropathology (silver stain and activated astrocytes (GFAP in the paraventricular nucleus (PVN of the hypothalamus. Resting plasma CORT levels were decreased at 2months postinjury and there was a blunted CORT increase in response to restraint induced stress. No changes in testosterone were measured. These changes in CORT were observed concomitantly with altered complexity of neuron processes in the PVN over time, devoid of neuropathology or astrocytosis. Results provide evidence that a single moderate diffuse TBI leads to changes in CORT function, which can contribute to the persistence of symptoms related to endocrine dysfunction. Future experiments aim to evaluate additional HP-related hormones and endocrine circuit pathology following diffuse TBI.

  16. Diffuse traumatic brain injury affects chronic corticosterone function in the rat.

    Science.gov (United States)

    Rowe, Rachel K; Rumney, Benjamin M; May, Hazel G; Permana, Paska; Adelson, P David; Harman, S Mitchell; Lifshitz, Jonathan; Thomas, Theresa C

    2016-07-01

    As many as 20-55% of patients with a history of traumatic brain injury (TBI) experience chronic endocrine dysfunction, leading to impaired quality of life, impaired rehabilitation efforts and lowered life expectancy. Endocrine dysfunction after TBI is thought to result from acceleration-deceleration forces to the brain within the skull, creating enduring hypothalamic and pituitary neuropathology, and subsequent hypothalamic-pituitary endocrine (HPE) dysfunction. These experiments were designed to test the hypothesis that a single diffuse TBI results in chronic dysfunction of corticosterone (CORT), a glucocorticoid released in response to stress and testosterone. We used a rodent model of diffuse TBI induced by midline fluid percussion injury (mFPI). At 2months postinjury compared with uninjured control animals, circulating levels of CORT were evaluated at rest, under restraint stress and in response to dexamethasone, a synthetic glucocorticoid commonly used to test HPE axis regulation. Testosterone was evaluated at rest. Further, we assessed changes in injury-induced neuron morphology (Golgi stain), neuropathology (silver stain) and activated astrocytes (GFAP) in the paraventricular nucleus (PVN) of the hypothalamus. Resting plasma CORT levels were decreased at 2months postinjury and there was a blunted CORT increase in response to restraint induced stress. No changes in testosterone were measured. These changes in CORT were observed concomitantly with altered complexity of neuron processes in the PVN over time, devoid of neuropathology or astrocytosis. Results provide evidence that a single moderate diffuse TBI leads to changes in CORT function, which can contribute to the persistence of symptoms related to endocrine dysfunction. Future experiments aim to evaluate additional HP-related hormones and endocrine circuit pathology following diffuse TBI. PMID:27317610

  17. Chronic impact of traumatic brain injury on outcome and quality of life: a narrative review.

    Science.gov (United States)

    Stocchetti, Nino; Zanier, Elisa R

    2016-01-01

    Traditionally seen as a sudden, brutal event with short-term impairment, traumatic brain injury (TBI) may cause persistent, sometimes life-long, consequences. While mortality after TBI has been reduced, a high proportion of severe TBI survivors require prolonged rehabilitation and may suffer long-term physical, cognitive, and psychological disorders. Additionally, chronic consequences have been identified not only after severe TBI but also in a proportion of cases previously classified as moderate or mild. This burden affects the daily life of survivors and their families; it also has relevant social and economic costs.Outcome evaluation is difficult for several reasons: co-existing extra-cranial injuries (spinal cord damage, for instance) may affect independence and quality of life outside the pure TBI effects; scales may not capture subtle, but important, changes; co-operation from patients may be impossible in the most severe cases. Several instruments have been developed for capturing specific aspects, from generic health status to specific cognitive functions. Even simple instruments, however, have demonstrated variable inter-rater agreement.The possible links between structural traumatic brain damage and functional impairment have been explored both experimentally and in the clinical setting with advanced neuro-imaging techniques. We briefly report on some fundamental findings, which may also offer potential targets for future therapies.Better understanding of damage mechanisms and new approaches to neuroprotection-restoration may offer better outcomes for the millions of survivors of TBI. PMID:27323708

  18. Traumatic Brain Injury

    Science.gov (United States)

    Traumatic brain injury (TBI) happens when a bump, blow, jolt, or other head injury causes damage to the brain. Every year, millions of people in the U.S. suffer brain injuries. More than half are bad enough that ...

  19. Traumatic Brain Injury

    Science.gov (United States)

    Traumatic brain injury (TBI) happens when a bump, blow, jolt, or other head injury causes damage to the brain. Every year, millions of people in the U.S. suffer brain injuries. More than half are bad enough that people ...

  20. Functional Magnetic Resonance Imaging of Chronic Dysarthric Speech after Childhood Brain Injury: Reliance on a Left-Hemisphere Compensatory Network

    Science.gov (United States)

    Morgan, Angela T.; Masterton, Richard; Pigdon, Lauren; Connelly, Alan; Liegeois, Frederique J.

    2013-01-01

    Severe and persistent speech disorder, dysarthria, may be present for life after brain injury in childhood, yet the neural correlates of this chronic disorder remain elusive. Although abundant literature is available on language reorganization after lesions in childhood, little is known about the capacity of motor speech networks to reorganize…

  1. Improved Cognitive Function After Transcranial, Light-Emitting Diode Treatments in Chronic, Traumatic Brain Injury: Two Case Reports

    OpenAIRE

    Naeser, Margaret A.; Saltmarche, Anita; Krengel, Maxine H.; Hamblin, Michael R.; Knight, Jeffrey A.

    2011-01-01

    Objective: Two chronic, traumatic brain injury (TBI) cases, where cognition improved following treatment with red and near-infrared light-emitting diodes (LEDs), applied transcranially to forehead and scalp areas, are presented. Background: Significant benefits have been reported following application of transcranial, low-level laser therapy (LLLT) to humans with acute stroke and mice with acute TBI. These are the first case reports documenting improved cognitive function in chronic, TBI pati...

  2. Association of chronic vascular changes with functional outcome after traumatic brain injury in rats.

    Science.gov (United States)

    Hayward, Nick M E A; Immonen, Riikka; Tuunanen, Pasi I; Ndode-Ekane, Xavier Ekolle; Gröhn, Olli; Pitkänen, Asla

    2010-12-01

    We tested the hypothesis that vascular remodeling in the cortex, hippocampus, and thalamus is associated with long-term functional recovery after traumatic brain injury (TBI). We induced TBI with lateral fluid-percussion (LFP) injury in adult rats. Animals were followed-up for 9 months, during which we tested motor performance using a neuroscore test, spatial learning and memory with a Morris water maze, and seizure susceptibility with a pentylenetetrazol (PTZ) test. At 8 months, they underwent structural MRI, and cerebral blood flow (CBF) was assessed by arterial spin labeling (ASL) MRI. Then, rats were perfused for histology to assess the density of blood vessels. In the perilesional cortex, the CBF decreased by 56% (p water maze correlated with enhanced thalamic vessel density (r = -0.81, p < 0.01). Finally, enhanced seizure susceptibility was associated with reduced CBF in the ipsilateral hippocampus (r = 0.78, p < 0.05) and increased vascular density in the thalamus (r = 0.69, p < 0.05). There was little interaction between the behavioral measures. The present study demonstrates that each of the investigated brain areas has a unique pattern of vascular abnormalities. Chronic alterations in CBF could not be attributed to changes in vascular density. Association of thalamic hypervascularity to epileptogenesis warrants further studies. Finally, hippocampal hypoperfusion may predict later seizure susceptibility in the LFP injury model of TBI, which could be of value for pre-clinical antiepileptogenesis trials. PMID:20839948

  3. Transcranial LED therapy for cognitive dysfunction in chronic, mild traumatic brain injury: two case reports

    Science.gov (United States)

    Naeser, Margaret A.; Saltmarche, Anita; Krengel, Maxine H.; Hamblin, Michael R.; Knight, Jeffrey A.

    2010-02-01

    Two chronic, traumatic brain injury (TBI) cases are presented, where cognitive function improved following treatment with transcranial light emitting diodes (LEDs). At age 59, P1 had closed-head injury from a motor vehicle accident (MVA) without loss of consciousness and normal MRI, but unable to return to work as development specialist in internet marketing, due to cognitive dysfunction. At 7 years post-MVA, she began transcranial LED treatments with cluster heads (2.1" diameter with 61 diodes each - 9x633nm, 52x870nm; 12-15mW per diode; total power, 500mW; 22.2 mW/cm2) on bilateral frontal, temporal, parietal, occipital and midline sagittal areas (13.3 J/cm2 at scalp, estimated 0.4 J/cm2 to brain cortex per area). Prior to transcranial LED, focused time on computer was 20 minutes. After 2 months of weekly, transcranial LED treatments, increased to 3 hours on computer. Performs nightly home treatments (now, 5 years, age 72); if stops treating >2 weeks, regresses. P2 (age 52F) had history of closed-head injuries related to sports/military training and recent fall. MRI shows fronto-parietal cortical atrophy. Pre-LED, was not able to work for 6 months and scored below average on attention, memory and executive function. Performed nightly transcranial LED treatments at home (9 months) with similar LED device, on frontal and parietal areas. After 4 months of LED treatments, returned to work as executive consultant, international technology consulting firm. Neuropsychological testing (post- 9 months of transcranial LED) showed significant improvement in memory and executive functioning (range, +1 to +2 SD improvement). Case 2 reported reduction in PTSD symptoms.

  4. Functional outcome following rehabilitation in chronic severe traumatic brain injury patients: A prospective study

    Directory of Open Access Journals (Sweden)

    Anupam Gupta

    2012-01-01

    Full Text Available Objective: The objective was to assess functional outcome of rehabilitation in chronic severe traumatic brain injury (TBI in-patients. Setting: The study was performed at university tertiary research hospital. Study Design: A prospective cross-sectional study Materials and Methods: Forty patients (34 men with mean age of 30.1 years (range 6--60, SD 10.8, severe TBI (Glasgow coma scale 3--8, duration of coma > 6 hours, post-traumatic amnesia> 1 day postinjury were admitted in rehabilitation unit minimum 3 months (mean 7.7±4.6 months, range 3--22 months following injury falling in Glasgow outcome scale (GOS of 3. Functional recovery was assessed using the Barthel Index (BI score and disability rating scores (DRS. Data Analysis: Paired Student′s t-test was used for the assessment of functional recovery using mean BI scores at admission and discharge. The Wilcoxon nonparametric test was used for the assessment of functional recovery by comparing admission and discharge DRS scores. Results: Mean duration of stay was 30.8 days (range 18--91, SD15.6. Significant functional recovery observed in patients comparing BI and DRS scores at admission and discharge (mean BI admission 50.5±25.4, range 0--85 vs. mean discharge BI score 61.1±25.3, range 0--95, P<0.001, mean DRS admission score 7.57±4.1, range 2.5--21.0 vs. mean discharge DRS score 6.36±4.3, range 1.0-21.0, P<0.001. Conclusion: Patients with severe TBI continue to show functional recovery even in chronic phase with rehabilitation. They are left with significant residual physical and cognitive deficits and would require long-term care and assistance from care givers for the daily activities, as suggested by the mean DRS score at discharge.

  5. Cognitive Gains from Gist Reasoning Training in Adolescents with Chronic-Stage Traumatic Brain Injury

    Directory of Open Access Journals (Sweden)

    Lori G. Cook

    2014-06-01

    Full Text Available Adolescents with traumatic brain injury (TBI typically demonstrate good recovery of previously acquired skills. However, higher-order and later emergent cognitive functions are often impaired and linked to poor outcomes in academic and social/behavioral domains. Few control trials exist that test cognitive treatment effectiveness at chronic recovery stages. The current pilot study compared the effects of two forms of cognitive training, gist reasoning (top-down versus rote memory learning (bottom-up, on ability to abstract meanings, recall facts, and utilize core executive functions (i.e., working memory, inhibition in 20 adolescents (ages 12-20 who were six months or longer post-TBI. Participants completed eight 45-minute sessions over one month. After training, the gist reasoning group (n = 10 exhibited significant improvement in ability to abstract meanings and increased fact recall. This group also showed significant generalizations to untrained executive functions of working memory and inhibition. The memory training group (n = 10 failed to show significant gains in ability to abstract meaning or on other untrained specialized executive functions, although improved fact recall approached significance. These preliminary results suggest that relatively short-term training (6 hours utilizing a top-down reasoning approach is more effective than a bottom-up rote learning approach in achieving gains in higher-order cognitive abilities in adolescents at chronic stages of TBI. These findings need to be replicated in a larger study; nonetheless, the preliminary data suggest that traditional cognitive intervention schedules need to extend to later-stage training opportunities. Chronic-stage, higher-order cognitive trainings may serve to elevate levels of cognitive performance in adolescents with TBI.

  6. Filling in the gaps: Anticipatory control of eye movements in chronic mild traumatic brain injury

    Directory of Open Access Journals (Sweden)

    Mithun Diwakar

    2015-01-01

    Full Text Available A barrier in the diagnosis of mild traumatic brain injury (mTBI stems from the lack of measures that are adequately sensitive in detecting mild head injuries. MRI and CT are typically negative in mTBI patients with persistent symptoms of post-concussive syndrome (PCS, and characteristic difficulties in sustaining attention often go undetected on neuropsychological testing, which can be insensitive to momentary lapses in concentration. Conversely, visual tracking strongly depends on sustained attention over time and is impaired in chronic mTBI patients, especially when tracking an occluded target. This finding suggests deficient internal anticipatory control in mTBI, the neural underpinnings of which are poorly understood. The present study investigated the neuronal bases for deficient anticipatory control during visual tracking in 25 chronic mTBI patients with persistent PCS symptoms and 25 healthy control subjects. The task was performed while undergoing magnetoencephalography (MEG, which allowed us to examine whether neural dysfunction associated with anticipatory control deficits was due to altered alpha, beta, and/or gamma activity. Neuropsychological examinations characterized cognition in both groups. During MEG recordings, subjects tracked a predictably moving target that was either continuously visible or randomly occluded (gap condition. MEG source-imaging analyses tested for group differences in alpha, beta, and gamma frequency bands. The results showed executive functioning, information processing speed, and verbal memory deficits in the mTBI group. Visual tracking was impaired in the mTBI group only in the gap condition. Patients showed greater error than controls before and during target occlusion, and were slower to resynchronize with the target when it reappeared. Impaired tracking concurred with abnormal beta activity, which was suppressed in the parietal cortex, especially the right hemisphere, and enhanced in left caudate and

  7. The role of Tc-99m HMPAO brain perfusion SPECT in the psychiatric disability evaluation of patients with chronic traumatic brain injury

    International Nuclear Information System (INIS)

    We studied whether brain perfusion SPECT is useful in the psychiatric disability evaluation of patients with chronic traumatic brain injury (TBI). Sixty-nine patients (M:F=58:11, age 39 ± 14 years) who underwent Tc-99m HMPAO brain SPECT, brain MRI and neuropsychological (NP) tests during hospitalization in psychiatric wards for the psychiatric disability evaluation were included; the severity of injury was mild in 31, moderate in 17 and severe in 21. SPECT, MRI, NP tests were performed 6 ∼ 61 months (mean 23 months) post-injury. Diagnostic accuracy of SPECT and MRI to show hypoperfusion or abnormal signal intensity in patients with cognitive impairment represented by NP test results were compared. Forty-two patients were considered to have cognitive impairment on NP tests and 27 not. Brain SPECT showed 71% sensitivity and 85% specificity, while brain MRI showed 62% sensitivity and 93% specificity (p>0.05, McNemar test). SPECT found more cortical lesions and MRI was superior in detecting white matter lesions. sensitivity and specificity of 31 mild TBI patients were 45%, 90% for SPECT and 27%, 100% for MRI (p>0.05, McNemar test). Among 41 patients with normal brain MRI, SEPCT showed 63% sensitivity (50% for mild TBI) and 88% specificity (85% for malingerers). Brain SPECT has a supplementary role to neuropsychological tests in the psychiatric disability evaluation of chronic TBI patients by detecting more cortical lesions than MRI

  8. Chronic visual dysfunction after blast-induced mild traumatic brain injury

    OpenAIRE

    M. Teresa Magone, MD; Ellen Kwon, OD; Soo Y. Shin, MD

    2014-01-01

    The purpose of this study was to investigate the long-term visual dysfunction in patients after blast-induced mild traumatic brain injury (mbTBI) using a retrospective case series of 31 patients with mbTBI (>12 mo prior) without eye injuries. Time since mbTBI was 50.5 +/– 19.8 mo. Age at the time of injury was 30.0 +/– 8.3 yr. Mean corrected visual acuity was 20/20. Of the patients, 71% (n = 22) experienced loss of consciousness; 68% (n = 15) of patients in this subgroup were dismounted durin...

  9. Neuropathophysiology of Brain Injury.

    Science.gov (United States)

    Quillinan, Nidia; Herson, Paco S; Traystman, Richard J

    2016-09-01

    Every year in the United States, millions of individuals incur ischemic brain injury from stroke, cardiac arrest, or traumatic brain injury. These acquired brain injuries can lead to death or long-term neurologic and neuropsychological impairments. The mechanisms of ischemic and traumatic brain injury that lead to these deficiencies result from a complex interplay of interdependent molecular pathways, including excitotoxicity, acidotoxicity, ionic imbalance, oxidative stress, inflammation, and apoptosis. This article reviews several mechanisms of brain injury and discusses recent developments. Although much is known from animal models of injury, it has been difficult to translate these effects to humans. PMID:27521191

  10. Chronic Repetitive Mild Traumatic Brain Injury Results in Reduced Cerebral Blood Flow, Axonal Injury, Gliosis, and Increased T-Tau and Tau Oligomers.

    Science.gov (United States)

    Ojo, Joseph O; Mouzon, Benoit; Algamal, Moustafa; Leary, Paige; Lynch, Cillian; Abdullah, Laila; Evans, James; Mullan, Michael; Bachmeier, Corbin; Stewart, William; Crawford, Fiona

    2016-07-01

    Exposure to repetitive mild traumatic brain injury (mTBI) is a risk factor for chronic traumatic encephalopathy, which is characterized by patchy deposition of hyperphosphorylated tau aggregates in neurons and astrocytes at the depths of cortical sulci. We developed an mTBI paradigm to explore effects of repetitive concussive-type injury over several months in mice with a human tau genetic background (hTau). Two injuries were induced in the hTau mice weekly over a period of 3 or 4 months and the effects were compared with those in noninjured sham animals. Behavioral and in vivo measures and detailed neuropathological assessments were conducted 6 months after the first injury. Our data confirm impairment in cerebral blood flow and white matter damage. This was accompanied by a 2-fold increase in total tau levels and mild increases in tau oligomers/conformers and pTau (Thr231) species in brain gray matter. There was no evidence of neurofibrillary/astroglial tangles, neuropil threads, or perivascular foci of tau immunoreactivity. There were neurobehavioral deficits (ie, disinhibition and impaired cognitive performance) in the mTBI animals. These data support the relevance of this new mTBI injury model for studying the consequences of chronic repetitive mTBI in humans, and the role of tau in TBI. PMID:27251042

  11. Chronic visual dysfunction after blast-induced mild traumatic brain injury

    Directory of Open Access Journals (Sweden)

    M. Teresa Magone, MD

    2014-03-01

    Full Text Available The purpose of this study was to investigate the long-term visual dysfunction in patients after blast-induced mild traumatic brain injury (mbTBI using a retrospective case series of 31 patients with mbTBI (>12 mo prior without eye injuries. Time since mbTBI was 50.5 +/– 19.8 mo. Age at the time of injury was 30.0 +/– 8.3 yr. Mean corrected visual acuity was 20/20. Of the patients, 71% (n = 22 experienced loss of consciousness; 68% (n = 15 of patients in this subgroup were dismounted during the blast injury. Overall, 68% (n = 21 of patients had visual complaints. The most common complaints were photophobia (55% and difficulty with reading (32%. Of all patients, 25% were diagnosed with convergence insufficiency and 23% had accommodative insufficiency. Patients with more than one mbTBI had a higher rate of visual complaints (87.5%. Asymptomatic patients had a significantly longer time (62.5 +/– 6.2 mo since the mbTBI than symptomatic patients (42.0 +/– 16.4 mo, p < 0.004. Long-term visual dysfunction after mbTBI is common even years after injury despite excellent distance visual acuity and is more frequent if more than one incidence of mbTBI occurred. We recommend obtaining a careful medical history, evaluation of symptoms, and binocular vision assessment during routine eye examinations in this prepresbyopic patient population.

  12. Chronic visual dysfunction after blast-induced mild traumatic brain injury.

    Science.gov (United States)

    Magone, M Teresa; Kwon, Ellen; Shin, Soo Y

    2014-01-01

    The purpose of this study was to investigate the long-term visual dysfunction in patients after blast-induced mild traumatic brain injury (mbTBI) using a retrospective case series of 31 patients with mbTBI (>12 mo prior) without eye injuries. Time since mbTBI was 50.5 +/- 19.8 mo. Age at the time of injury was 30.0 +/- 8.3 yr. Mean corrected visual acuity was 20/20. Of the patients, 71% (n = 22) experienced loss of consciousness; 68% (n = 15) of patients in this subgroup were dismounted during the blast injury. Overall, 68% (n = 21) of patients had visual complaints. The most common complaints were photophobia (55%) and difficulty with reading (32%). Of all patients, 25% were diagnosed with convergence insufficiency and 23% had accommodative insufficiency. Patients with more than one mbTBI had a higher rate of visual complaints (87.5%). Asymptomatic patients had a significantly longer time (62.5 +/- 6.2 mo) since the mbTBI than symptomatic patients (42.0 +/- 16.4 mo, p < 0.004). Long-term visual dysfunction after mbTBI is common even years after injury despite excellent distance visual acuity and is more frequent if more than one incidence of mbTBI occurred. We recommend obtaining a careful medical history, evaluation of symptoms, and binocular vision assessment during routine eye examinations in this prepresbyopic patient population. PMID:24805895

  13. Proinflammatory cytokine expression contributes to brain injury provoked by chronic monocyte activation.

    OpenAIRE

    Sirén, A. L.; McCarron, R.; Wang, L.; Garcia-Pinto, P.; Ruetzler, C.; Martin, D.; Hallenbeck, J. M.

    2001-01-01

    BACKGROUND: We have proposed that an increased interaction between monocyte/macrophages and blood vessel endothelium predisposes subjects to strokes. The effect of chronic monocyte activation on the development of cerebral infarcts was thus studied in rats after provocation of a modified local Swartzman reaction, in brain vasculature. MATERIALS AND METHODS: Two weeks after an IV bolus of bacillus Calmette-Guérin (BCG), we studied spontaneous superoxide production, integrin expression, endothe...

  14. SECONDARY BRAIN INJURY

    OpenAIRE

    Ida Ayu Basmatika

    2013-01-01

    Secondary brain injury is a condision that occurs at some times after the primary impact and can be largely prevented and treated. Most brain injury ends with deadly consequences which is caused by secondary damage to the brain. Traumatic brain injured still represents the leading cause of morbidity and mortality in individuals under the age of 45 years in the world. The classification of secondary brain injured is divided into extracranial and intracranial causes. The cause of extracranial s...

  15. Severe Traumatic Brain Injury

    Science.gov (United States)

    ... inflicted traumatic brain injury (ITBI), is a leading cause of child maltreatment deaths in the United States. Meeting the ... Awareness Additional Prevention Resources Childhood Injuries Concussion in Children and Teens Injuries from Violence Injuries from Motor Vehicle Crashes Teen Driver Safety ...

  16. Phosphodiesterase inhibition rescues chronic cognitive deficits induced by traumatic brain injury.

    Science.gov (United States)

    Titus, David J; Sakurai, Atsushi; Kang, Yuan; Furones, Concepcion; Jergova, Stanislava; Santos, Rosmery; Sick, Thomas J; Atkins, Coleen M

    2013-03-20

    Traumatic brain injury (TBI) modulates several cell signaling pathways in the hippocampus critical for memory formation. Previous studies have found that the cAMP-protein kinase A signaling pathway is downregulated after TBI and that treatment with a phosphodiesterase (PDE) 4 inhibitor rolipram rescues the decrease in cAMP. In the present study, we examined the effect of rolipram on TBI-induced cognitive impairments. At 2 weeks after moderate fluid-percussion brain injury or sham surgery, adult male Sprague Dawley rats received vehicle or rolipram (0.03 mg/kg) 30 min before water maze acquisition or cue and contextual fear conditioning. TBI animals treated with rolipram showed a significant improvement in water maze acquisition and retention of both cue and contextual fear conditioning compared with vehicle-treated TBI animals. Cue and contextual fear conditioning significantly increased phosphorylated CREB levels in the hippocampus of sham animals, but not in TBI animals. This deficit in CREB activation during learning was rescued in TBI animals treated with rolipram. Hippocampal long-term potentiation was reduced in TBI animals, and this was also rescued with rolipram treatment. These results indicate that the PDE4 inhibitor rolipram rescues cognitive impairments after TBI, and this may be mediated through increased CREB activation during learning. PMID:23516287

  17. Evaluating the effectiveness of reasoning training in military and civilian chronic traumatic brain injury patients: study protocol

    Directory of Open Access Journals (Sweden)

    Krawczyk Daniel C

    2013-01-01

    Full Text Available Abstract Background Individuals who sustain traumatic brain injuries (TBIs often continue to experience significant impairment of cognitive functions mediated by the prefrontal cortex well into chronic stages of recovery. Traditional brain training programs that focus on improving specific skills fall short of addressing integrative functions that draw upon multiple higher-order processes critical for social and vocational integration. In the current study, we compare the effects of two short-term, intensive, group-based cognitive rehabilitation programs for individuals with chronic TBI. One program emphasizes learning about brain functions and influences on cognition, while the other program adopts a top-down approach to improve abstract reasoning abilities that are largely reliant on the prefrontal cortex. These treatment programs are evaluated in civilian and military veteran TBI populations. Methods/design One hundred individuals are being enrolled in this double-blinded clinical trial (all measures and data analyses will be conducted by blinded raters and analysts. Each individual is randomly assigned to one of two treatment conditions, with each condition run in groups of five to seven individuals. The primary anticipated outcomes are improvement in abstract reasoning and everyday life functioning, measured through behavioral tasks and questionnaires, and attention modulation, as measured by functional neuroimaging. Secondary expected outcomes include improvements in the cognitive processes of working memory, attention, and inhibitory control. Discussion Results of this trial will determine whether cognitive rehabilitation aimed at teaching TBI-relevant information about the brain and cognition versus training in TBI-affected thinking abilities (e.g., memory, attention, and executive functioning can improve outcomes in chronic military and civilian TBI patient populations. It should shed light on the nature of improvements and the

  18. Neurodegeneration after mild and repetitive traumatic brain injury: Chronic traumatic encepalopathy

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    Stanescu Ioana

    2015-09-01

    Full Text Available Repetitive brain trauma is associated with a progressive neurological deterioration, now termed as chronic traumatic encephalopathy (CTE. Although research on the long-term effects of TBI is advancing quickly, the incidence and prevalence of post-traumatic neurodegeneration and CTE are unknown. The incidence and prevalence of chronic traumatic encephalopathy and the genetic risk factors critical to its development are currently under research. CTE can be diagnosed only by post mortem neuropathological examination of the brain. Great efforts are being made to better understand the clinical signs and symptoms of CTE, obtained in most cases retrospectively from families of affected persons.Patients with CTE are described as having behavioral, mood, cognitive and motor impairments, occurring after a long latency from the traumatic events. Recent pathogenetic studies have provided new insights to CTE mechanisms, offering important clues in understanding neurodegenerative process and relations between physical factors and pathologic protein deposition. Further research is needed to better identify the genetic and environmental risk factors for CTE, as well as rehabilitation and treatment strategies.

  19. Mild traumatic brain injury.

    NARCIS (Netherlands)

    Vos, P.E.; Alekseenko, Y.; Battistin, L.; Ehler, E.; Gerstenbrand, F.; Muresanu, D.F.; Potapov, A.; Stepan, C.A.; Traubner, P.; Vecsei, L.; Wild, K. von

    2012-01-01

    Traumatic Brain Injury (TBI) is among the most frequent neurological disorders. Of all TBIs 90% are considered mild with an annual incidence of 100-300/100.000. Intracranial complications of Mild Traumatic Brain Injury (MTBI) are infrequent (10%), requiring neurosurgical intervention in a minority o

  20. Theory of mind mediates the prospective relationship between abnormal social brain network morphology and chronic behavior problems after pediatric traumatic brain injury.

    Science.gov (United States)

    Ryan, Nicholas P; Catroppa, Cathy; Beare, Richard; Silk, Timothy J; Crossley, Louise; Beauchamp, Miriam H; Yeates, Keith Owen; Anderson, Vicki A

    2016-04-01

    Childhood and adolescence coincide with rapid maturation and synaptic reorganization of distributed neural networks that underlie complex cognitive-affective behaviors. These regions, referred to collectively as the 'social brain network' (SBN) are commonly vulnerable to disruption from pediatric traumatic brain injury (TBI); however, the mechanisms that link morphological changes in the SBN to behavior problems in this population remain unclear. In 98 children and adolescents with mild to severe TBI, we acquired 3D T1-weighted MRIs at 2-8 weeks post-injury. For comparison, 33 typically developing controls of similar age, sex and education were scanned. All participants were assessed on measures of Theory of Mind (ToM) at 6 months post-injury and parents provided ratings of behavior problems at 24-months post-injury. Severe TBI was associated with volumetric reductions in the overall SBN package, as well as regional gray matter structural change in multiple component regions of the SBN. When compared with TD controls and children with milder injuries, the severe TBI group had significantly poorer ToM, which was associated with more frequent behavior problems and abnormal SBN morphology. Mediation analysis indicated that impaired theory of mind mediated the prospective relationship between abnormal SBN morphology and more frequent chronic behavior problems. Our findings suggest that sub-acute alterations in SBN morphology indirectly contribute to long-term behavior problems via their influence on ToM. Volumetric change in the SBN and its putative hub regions may represent useful imaging biomarkers for prediction of post-acute social cognitive impairment, which may in turn elevate risk for chronic behavior problems. PMID:26796967

  1. Clinical Management of a Patient with Chronic Recurrent Vertigo Following a Mild Traumatic Brain Injury

    Directory of Open Access Journals (Sweden)

    Eric G. Johnson

    2009-01-01

    Full Text Available Vertigo, was provoked and right torsional up-beat nystagmus was observed in a 47-year-old patient when she was placed into the right Hallpike-Dix test position using infrared goggle technology. The clinical diagnosis was benign paroxysmal positional vertigo (BPPV, specifically right posterior canalithiasis, resulting from a mild traumatic brain injury (TBI suffered approximately six-months earlier. Previous medical consultations did not include vestibular system examination, and Meclizine was prescribed to suppress her chief complaint of vertigo. Ultimately, the patient was successfully managed by performing two canalith repositioning maneuvers during a single clinical session. The patient reported 100% resolution of symptoms upon reexamination the following day, and the Hallpike-Dix test was negative. Continued symptom resolution was subjectively reported 10 days postintervention via telephone consultation. This case report supports previous publications concerning the presence of BPPV following TBI and the need for inclusion of vestibular system examination during medical consultation.

  2. Cerebral perfusion and neuropsychological follow up in mild traumatic brain injury: acute versus chronic disturbances?

    Science.gov (United States)

    Metting, Zwany; Spikman, Jacoba M; Rödiger, Lars A; van der Naalt, Joukje

    2014-04-01

    In a subgroup of patients with mild traumatic brain injury (TBI) residual symptoms, interfering with outcome and return to work, are found. With neuropsychological assessment cognitive deficits can be demonstrated although the pathological underpinnings of these cognitive deficits are not fully understood. As the admission computed tomography (CT) often is normal, perfusion CT imaging may be a useful indicator of brain dysfunction in the acute phase after injury in these patients. In the present study, directly after admission perfusion CT imaging was performed in mild TBI patients with follow-up neuropsychological assessment in those with complaints and a normal non-contrast CT. Neuropsychological tests comprised the 15 Words test Immediate Recall, Trailmaking test part B, Zoo Map test and the FEEST, which were dichotomized into normal and abnormal. Perfusion CT results of patients with normal neuropsychological test scores were compared to those with abnormal test scores. In total eighteen patients were included. Those with an abnormal score on the Zoo Map test had a significant lower CBV in the right frontal and the bilateral parieto-temporal white matter. Patients with an abnormal score on the FEEST had a significant higher MTT in the bilateral frontal white matter and a significant decreased CBF in the left parieto-temporal grey matter. No significant relation between the perfusion CT parameters and the 15 Words test and the Trailmaking test part B was present. In conclusion, impairments in executive functioning and emotion perception assessed with neuropsychological tests during follow up were related to differences in cerebral perfusion at admission in mild TBI. The pathophysiological concept of these findings is discussed. PMID:24556319

  3. High prevalence of chronic pituitary and target-organ hormone abnormalities after blast-related mild traumatic brain injury

    Directory of Open Access Journals (Sweden)

    CharlesW.Wilkinson

    2012-02-01

    Full Text Available Studies of traumatic brain injury from all causes have found evidence of chronic hypopituitarism, defined by deficient production of one or more pituitary hormones at least one year after injury, in 25-50% of cases. Most studies found the occurrence of posttraumatic hypopituitarism (PTHP to be unrelated to injury severity. Growth hormone deficiency (GHD and hypogonadism were reported most frequently. Hypopituitarism, and in particular adult GHD, is associated with symptoms that resemble those of PTSD, including fatigue, anxiety, depression, irritability, insomnia, sexual dysfunction, cognitive deficiencies, and decreased quality of life. However, the prevalence of PTHP after blast-related mild TBI (mTBI, an extremely common injury in modern military operations, has not been characterized. We measured concentrations of 12 pituitary and target-organ hormones in two groups of male US Veterans of combat in Iraq or Afghanistan. One group consisted of participants with blast-related mTBI whose last blast exposure was at least one year prior to the study. The other consisted of Veterans with similar military deployment histories but without blast exposure. Eleven of 26, or 42% of participants with blast concussions were found to have abnormal hormone levels in one or more pituitary axes, a prevalence similar to that found in other forms of TBI. Five members of the mTBI group were found with markedly low age-adjusted insulin-like growth factor-I (IGF-I levels indicative of probable GHD, and three had testosterone and gonadotropin concentrations consistent with hypogonadism. If symptoms characteristic of both PTHP and PTSD can be linked to pituitary dysfunction, they may be amenable to treatment with hormone replacement. Routine screening for chronic hypopituitarism after blast concussion shows promise for appropriately directing diagnostic and therapeutic decisions that otherwise may remain unconsidered and for markedly facilitating recovery and

  4. Pilot study: Computer-based virtual anatomical interactivity for rehabilitation of individuals with chronic acquired brain injury

    Directory of Open Access Journals (Sweden)

    C. Douglas Simmons, PhD, OTR/L, FAOTA

    2014-06-01

    Full Text Available Deficiencies in upper-limb motor function and executive functioning can compromise an affected individual’s ability to complete everyday activities. Impaired motor and executive functioning therefore pose a risk to increasing numbers of veterans who have been diagnosed with acquired brain injury. This article reports on changes in upper-limb motor function and executive functioning of 12 adult participants with chronic acquired brain injury using a novel, computer-based, motor and cognitive rehabilitation program called PreMotor Exercise Games (PEGs. Manual muscle, goniometric range of motion, and dynamometer assessments were used to determine motor functioning while the Executive Function Performance Test measured cognitive functioning. A three-level repeated measures design was conducted to determine changes pre- and postintervention. Participants demonstrated significant improvement in shoulder (p = 0.01 and wrist (p = 0.01 range of motion and clinically relevant improvement for elbow range of motion. Participants demonstrated clinically relevant improvement in shoulder, elbow, and wrist strength. Finally, participants demonstrated significant improvement in executive functioning (p < 0.05. Using PEGs as a modality for both motor and cognitive intervention is a potentially beneficial adjunct to rehabilitation and warrants further study.

  5. Repeated mild traumatic brain injury causes chronic neuroinflammation, changes in hippocampal synaptic plasticity, and associated cognitive deficits

    Science.gov (United States)

    Aungst, Stephanie L; Kabadi, Shruti V; Thompson, Scott M; Stoica, Bogdan A; Faden, Alan I

    2014-01-01

    Repeated mild traumatic brain injury (mTBI) can cause sustained cognitive and psychiatric changes, as well as neurodegeneration, but the underlying mechanisms remain unclear. We examined histologic, neurophysiological, and cognitive changes after single or repeated (three injuries) mTBI using the rat lateral fluid percussion (LFP) model. Repeated mTBI caused substantial neuronal cell loss and significantly increased numbers of activated microglia in both ipsilateral and contralateral hippocampus on post-injury day (PID) 28. Long-term potentiation (LTP) could not be induced on PID 28 after repeated mTBI in ex vivo hippocampal slices from either hemisphere. N-Methyl-D-aspartate (NMDA) receptor-mediated responses were significantly attenuated after repeated mTBI, with no significant changes in α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) receptor-mediated responses. Long-term potentiation was elicited in slices after single mTBI, with potentiation significantly increased in ipsilateral versus contralateral hippocampus. After repeated mTBI, rats displayed cognitive impairments in the Morris water maze (MWM) and novel object recognition (NOR) tests. Thus, repeated mTBI causes deficits in the hippocampal function and changes in excitatory synaptic neurotransmission, which are associated with chronic neuroinflammation and neurodegeneration. PMID:24756076

  6. Repeated mild traumatic brain injury causes chronic neuroinflammation, changes in hippocampal synaptic plasticity, and associated cognitive deficits.

    Science.gov (United States)

    Aungst, Stephanie L; Kabadi, Shruti V; Thompson, Scott M; Stoica, Bogdan A; Faden, Alan I

    2014-07-01

    Repeated mild traumatic brain injury (mTBI) can cause sustained cognitive and psychiatric changes, as well as neurodegeneration, but the underlying mechanisms remain unclear. We examined histologic, neurophysiological, and cognitive changes after single or repeated (three injuries) mTBI using the rat lateral fluid percussion (LFP) model. Repeated mTBI caused substantial neuronal cell loss and significantly increased numbers of activated microglia in both ipsilateral and contralateral hippocampus on post-injury day (PID) 28. Long-term potentiation (LTP) could not be induced on PID 28 after repeated mTBI in ex vivo hippocampal slices from either hemisphere. N-Methyl-D-aspartate (NMDA) receptor-mediated responses were significantly attenuated after repeated mTBI, with no significant changes in α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) receptor-mediated responses. Long-term potentiation was elicited in slices after single mTBI, with potentiation significantly increased in ipsilateral versus contralateral hippocampus. After repeated mTBI, rats displayed cognitive impairments in the Morris water maze (MWM) and novel object recognition (NOR) tests. Thus, repeated mTBI causes deficits in the hippocampal function and changes in excitatory synaptic neurotransmission, which are associated with chronic neuroinflammation and neurodegeneration. PMID:24756076

  7. Protection of Effective Component Group from Xiaoshuan Tongluo on Brain Injury after Chronic Hypoperfusion in Rats

    Institute of Scientific and Technical Information of China (English)

    TAN Chu-bing; WANG Hong-qing; TIAN Shuo; GAO Mei; XU Wei-ren; CHEN Ruo-yun; DU Guan-hua

    2011-01-01

    Objective To investigate the protective effects of purified effective component group in extract from Xiaoshuan Tongluo(CGXT)formula on chronic brain ischemia in rats.Methods CGXT 75,150,and 300 mg/kg or vehicle were ig administered daily for four weeks to rats with bilateral common carotid arteries ligation(BCCAL).From the day 24 to 28 after BCCAL,Morris water maze was performed to assess the learning and memory impairment of rats.Four weeks after BCCAL,brain gray and white matter damage were assessed.Results In Morris test,the mean escape latency of rats in the CGXT(150 and 300 mg/kg)groups was significantly shorter than that in the vehicle group.CGXT also attenuated the neuronal damage in hippocampus and cortex and reduced the pathological damage in the optic tract and corpus callosum.Conclusion CGXT could improve learning and memory impairment resulted from BCCAL in rats.These results provide the experimental basis for the clinical use of CGXT in stroke treatment and may help in investigation of multimodal therapy strategies in ischemic cerebrovascular diseases including stroke.

  8. Disruption of caudate working memory activation in chronic blast-related traumatic brain injury

    Directory of Open Access Journals (Sweden)

    Mary R. Newsome

    2015-01-01

    Full Text Available Mild to moderate traumatic brain injury (TBI due to blast exposure is frequently diagnosed in veterans returning from the wars in Iraq and Afghanistan. However, it is unclear whether neural damage resulting from blast TBI differs from that found in TBI due to blunt-force trauma (e.g., falls and motor vehicle crashes. Little is also known about the effects of blast TBI on neural networks, particularly over the long term. Because impairment in working memory has been linked to blunt-force TBI, the present functional magnetic resonance imaging (fMRI study sought to investigate whether brain activation in response to a working memory task would discriminate blunt-force from blast TBI. Twenty-five veterans (mean age = 29.8 years, standard deviation = 6.01 years, 1 female who incurred TBI due to blast an average of 4.2 years prior to enrollment and 25 civilians (mean age = 27.4 years, standard deviation = 6.68 years, 4 females with TBI due to blunt-force trauma performed the Sternberg Item Recognition Task while undergoing fMRI. The task involved encoding 1, 3, or 5 items in working memory. A group of 25 veterans (mean age = 29.9 years, standard deviation = 5.53 years, 0 females and a group of 25 civilians (mean age = 27.3 years, standard deviation = 5.81 years, 0 females without history of TBI underwent identical imaging procedures and served as controls. Results indicated that the civilian TBI group and both control groups demonstrated a monotonic relationship between working memory set size and activation in the right caudate during encoding, whereas the blast TBI group did not (p < 0.05, corrected for multiple comparisons using False Discovery Rate. Blast TBI was also associated with worse performance on the Sternberg Item Recognition Task relative to the other groups, although no other group differences were found on neuropsychological measures of episodic memory, inhibition, and general processing speed. These results

  9. Alterations of cerebral blood flow and cerebrovascular reserve in patients with chronic traumatic brain injury accompanying deteriorated intelligence

    International Nuclear Information System (INIS)

    The purpose of this study was to evaluate alterations of regional cerbral blood flow (CBF) and cerebrovascular reserve (CVR), and correlation between these alternations and cognitive dysfunctin in patients with chronic traumatic brain injury (TBI) and normal brain MRI findings. Thirty TBI patients and 19 healthy volunteers underwent rest/acetazolaminde brain SPECT using Tc-99m HMPAO. Korean-Wechsler Adult Intelligence scale test was also performed in the patient group. Statistical analysis was performed with statistical parametric mapping software (SPM '97). CBF was diminished in the left hemisphere including Wernicke's area in all patients with lower verbal scale scores. In addition, a reduction in CBF in the right frontal, temporal and parietal cortices was related with depressed scores in information, digital span, arithmetic and similarities. In patients with lower performance scale scores, CBF was mainly diminished in the right hemisphere including superior temporal and supramarginal gyri, premotor, primary somatomotor and a part of prefrontal cortices, left frontal lobe and supramarginal gyrus. CVR was diminished in sixty-four Brodmann's areas compared to control. A reduction in CVR was demonstrated bilaterally in the frontal and temporal lobes in patients with lower scores in both verbal and performance tests, and in addition, both inferior parietal and occipital lobes in information subset. Alterations of CBF and CVR were demonstrated in the symptomatic TBI patients with normal MRI finding. These alterations were correlated with the change of intelligence, of which the complex functions are subserved by multiple interconnected cortical structures.=20

  10. Detection of Growth Hormone Deficiency in Adults with Chronic Traumatic Brain Injury.

    Science.gov (United States)

    Kreber, Lisa A; Griesbach, Grace S; Ashley, Mark J

    2016-09-01

    This study examined the prevalence of growth hormone deficiency (GHD) in patients with traumatic brain injury (TBI) during the post-acute phase of recovery and whether GHD was associated with increased disability, decreased independence, and depression. A secondary objective was to determine the accuracy of insulin-like growth factor-1 (IGF-1) levels in predicting GHD in patients with TBI. Anterior pituitary function was assessed in 235 adult patients with TBI through evaluation of fasting morning hormone levels. GH levels were assessed through provocative testing, specifically the glucagon stimulation test. GHD was diagnosed in a significant number of patients, with 45% falling into the severe GHD (≤3 μg/L) category. IGF-1 levels were not predictive of GHD. Patients with GHD were more disabled and less independent compared with those patients who were not GHD. Those patients with more severe GHD also showed decreased levels of cortisol and testosterone. Symptoms of depression were also more prevalent in this group. In addition, patients with severe GHD had delayed admission to post-acute rehabilitation. This study confirms the high prevalence of GHD in patients with TBI and the necessity to monitor clinical symptoms and perform provocative testing to definitively diagnose GHD. PMID:26414093

  11. SECONDARY BRAIN INJURY

    Directory of Open Access Journals (Sweden)

    Ida Ayu Basmatika

    2013-03-01

    Full Text Available Secondary brain injury is a condision that occurs at some times after the primary impact and can be largely prevented and treated. Most brain injury ends with deadly consequences which is caused by secondary damage to the brain. Traumatic brain injured still represents the leading cause of morbidity and mortality in individuals under the age of 45 years in the world. The classification of secondary brain injured is divided into extracranial and intracranial causes. The cause of extracranial such as hipoxia, hypotensi, hyponatremia, hypertermia, hypoglycemia or hyperglycemia. The cause of intracranial such as extradural, subdural, intraserebral, intraventrikular, dan subarachnoid hemorrhage. Beside that secondary injury can also be caused by edema and infection. Post-traumatic cerebral injured is characterized by direct tissue damage, impaired regulation of cerebral blood flow (cerebral blood flow / CBF, and disruption of metabolism. Manifestations of secondary brain injured include increased intracranial pressure, ischemic brain damage, cerebral hypoxia and hypercarbi, as well as disruption of cerebral autoregulation. The first priority is to stabilize the patient's cervical spine injury, relieve and maintain airway, ensure adequate ventilation (breathing, and making venous access for fluid resuscitation pathways (circulation and assessing the level of awareness and disability. This steps is crucial in patients with head injured to prevent hypoxia and hypotension, which is the main cause of secondary brain injury.

  12. Fibroblast growth factor-2 induced by enriched environment enhances angiogenesis and motor function in chronic hypoxic-ischemic brain injury.

    Directory of Open Access Journals (Sweden)

    Jung Hwa Seo

    Full Text Available This study aimed to investigate the effects of enriched environment (EE on promoting angiogenesis and neurobehavioral function in an animal model of chronic hypoxic-ischemic (HI brain injury. HI brain damage was induced in seven day-old CD-1® mice by unilateral carotid artery ligation and exposure to hypoxia (8% O2 for 90 min. At six weeks of age, the mice were randomly assigned to either EE or standard cages (SC for two months. Rotarod, forelimb-use asymmetry, and grip strength tests were performed to evaluate neurobehavioral function. In order to identify angiogenic growth factors regulated by EE, an array-based multiplex ELISA assay was used to measure the expression in frontal cortex, striatum, and cerebellum. Among the growth factors, the expression of fibroblast growth factor-2 (FGF-2 was confirmed using western blotting. Platelet endothelial cell adhesion molecule-1 (PECAM-1 and α-smooth muscle actin (α-SMA were also evaluated using immunohistochemistry. As a result, mice exposed to EE showed significant improvements in rotarod and ladder walking performances compared to SC controls. The level of FGF-2 was significantly higher in the frontal cortex of EE mice at 8 weeks after treatment in multiplex ELISA and western blot. On the other hand, FGF-2 in the striatum significantly increased at 2 weeks after exposure to EE earlier than in the frontal cortex. Expression of activin A was similarly upregulated as FGF-2 expression pattern. Particularly, all animals treated with FGF-2 neutralizing antibody abolished the beneficial effect of EE on motor performance relative to mice not given anti-FGF-2. Immunohistochemistry showed that densities of α-SMA(+ and PECAM-1(+ cells in frontal cortex, striatum, and hippocampus were significantly increased following EE, suggesting the histological findings exhibit a similar pattern to the upregulation of FGF-2 in the brain. In conclusion, EE enhances endogenous angiogenesis and neurobehavioral functions

  13. Brain injury - discharge

    Science.gov (United States)

    ... 5, 2014. Chuang K, Stroud, NL, Zafonte R. Rehabilitation of patients with traumatic brain injury. In: Winn HR, ed. Youman's Neurological Surgery . 6th ed. Philadelphia, PA: Elsevier Saunders; 2011: ...

  14. Pediatric Traumatic Brain Injury.

    Science.gov (United States)

    Schaller, Alexandra L; Lakhani, Saquib A; Hsu, Benson S

    2015-10-01

    The purpose of this article is to provide a better understanding of pediatric traumatic brain injury and its management. Within the pediatric age group, ages 1 to 19, injuries are the number one cause of death with traumatic brain injury being involved in almost 50 percent of these cases. This, along with the fact that the medical system spends over $1 billion annually on pediatric traumatic brain injury, makes this issue both timely and relevant to health care providers. Over the course of this article the epidemiology, physiology, pathophysiology, and treatment of pediatric traumatic brain injury will be explored. Emphasis will be placed on the role of the early responder and the immediate interventions that should be considered and/or performed. The management discussed in this article follows the most recent recommendations from the 2012 edition of the Guidelines for the Acute Medical Management of Severe Traumatic Brain Injury in Infants, Children, and Adolescents. Despite the focus of this article, it is important not to lose sight of the fact that an ounce of prevention is worth a pound--or, to be more precise and use the average human's brain measurements, just above three pounds--of cure. PMID:26630835

  15. Utility of fractional anisotropy imaging analyzed by statistical parametric mapping for detecting minute brain lesions in chronic-stage patients who had mild or moderate traumatic brain injury

    International Nuclear Information System (INIS)

    Diffusion tensor imaging (DTI) has recently evolved as valuable technique to investigate diffuse axonal injury (DAI). This study examined whether fractional anisotropy (FA) images analyzed by statistical parametric mapping (FA-SPM images) are superior to T2*-weighted gradient recalled echo (T2*GRE) images or fluid-attenuated inversion recovery (FLAIR) images for detecting minute lesions in traumatic brain injury (TBI) patients. DTI was performed in 25 patients with cognitive impairments in the chronic stage after mild or moderate TBI. The FA maps obtained from the DTI were individually compared with those from age-matched healthy control subjects using voxel-based analysis and FA-SPM images (p<0.001). Abnormal low-intensity areas on T2*GRE images (T2* lesions) were found in 10 patients (40.0%), abnormal high-intensity areas on FLAIR images in 4 patients (16.0%), and areas with significantly decreased FA on FA-SPM image in 16 patients (64.0%). Nine of 10 patients with T2* lesions had FA-SPM lesions. FA-SPM lesions topographically included most T2* lesions in the white matter and the deep brain structures, but did not include T2* lesions in the cortex/near-cortex or lesions containing substantial hemosiderin regardless of location. All 4 patients with abnormal areas on FLAIR images had FA-SPM lesions. FA-SPM imaging is useful for detecting minute lesions because of DAI in the white matter and the deep brain structures, which may not be visualized on T2*GRE or FLAIR images, and may allow the detection of minute brain lesions in patients with post-traumatic cognitive impairment. (author)

  16. Hysteria following brain injury.

    OpenAIRE

    Eames, P

    1992-01-01

    Of 167 patients referred to a unit treating severe behaviour disorders after brain injury, 54 showed clinical features closely resembling those of gross hysteria as described by Charcot. Close correlation was found with very diffuse insults (hypoxia and hypoglycaemia), but not with severity of injury or with family or personal history of hysterical or other psychiatric disorder. The findings may have implications for the understanding of the nature of hysteria.

  17. Significant Improvements in Cognitive Performance Post-Transcranial, Red/Near-Infrared Light-Emitting Diode Treatments in Chronic, Mild Traumatic Brain Injury: Open-Protocol Study

    OpenAIRE

    Naeser, Margaret A.; Zafonte, Ross; Krengel, Maxine H.; MARTIN, PAULA I; Frazier, Judith; Michael R Hamblin; Knight, Jeffrey A.; Meehan, William P.; BAKER, ERROL H.

    2014-01-01

    This pilot, open-protocol study examined whether scalp application of red and near-infrared (NIR) light-emitting diodes (LED) could improve cognition in patients with chronic, mild traumatic brain injury (mTBI). Application of red/NIR light improves mitochondrial function (especially in hypoxic/compromised cells) promoting increased adenosine triphosphate (ATP) important for cellular metabolism. Nitric oxide is released locally, increasing regional cerebral blood flow. LED therapy is noninvas...

  18. TRAUMATIC BRAIN INJURY (TBI) DATABASE

    Science.gov (United States)

    The Traumatic Brain Injury National Data Center (TBINDC) at Kessler Medical Rehabilitation Research and Education Center is the coordinating center for the research and dissemination efforts of the Traumatic Brain Injury Model Systems (TBIMS) program funded by the National Instit...

  19. Radiation Injury to the Brain

    Science.gov (United States)

    ... Hits since January 2003 RADIATION INJURY TO THE BRAIN Radiation treatments affect all cells that are targeted. ... fractions, duration of therapy, and volume of [healthy brain] nervous tissue irradiated influence the likelihood of injury. ...

  20. Traumatic Brain Injury (TBI)

    Science.gov (United States)

    ... A. (2008). Mild traumatic brain injury in U.S. soldiers returning from Iraq. New England Journal of Medicine, 358, 453–463. ... and Spotlights U.S. hospitals miss followup for suspected child abuse Q&A with NICHD Acting Director Catherine ...

  1. Brain Injury Association of America

    Science.gov (United States)

    ... Only) 1-800-444-6443 Welcome to the Brain Injury Association of America (BIAA) Brain injury is not an event or an outcome. ... misunderstood, under-funded neurological disease. People who sustain brain injuries must have timely access to expert trauma ...

  2. Chronic avulsive injuries of childhood

    International Nuclear Information System (INIS)

    Children and adolescents are prone to avulsive injuries related to a combination of their propensity for great strength, ability to sustain extreme levels of activity, and immature growing apophyses. Appropriate interpretation of imaging studies showing chronic avulsive injuries is essential so that the irregularity and periostitis that can be associated with chronic avulsions is not misinterpreted as probable malignancy. This article reviews the chronic avulsive injuries of childhood. (orig.)

  3. Chronic avulsive injuries of childhood

    Energy Technology Data Exchange (ETDEWEB)

    Donnelly, L.F.; Helms, C.A. [Dept. of Radiology, Duke Univ. Medical Center, Durham, NC (United States); Bisset, G.S. III [Dept. of Radiology, Duke Univ. Medical Center, Durham, NC (United States)]|[Department of Pediatrics, Duke University Medical Center, Durham, NC (United States); Squire, D.L. [Department of Pediatrics, Duke University Medical Center, Durham, NC (United States)

    1999-03-01

    Children and adolescents are prone to avulsive injuries related to a combination of their propensity for great strength, ability to sustain extreme levels of activity, and immature growing apophyses. Appropriate interpretation of imaging studies showing chronic avulsive injuries is essential so that the irregularity and periostitis that can be associated with chronic avulsions is not misinterpreted as probable malignancy. This article reviews the chronic avulsive injuries of childhood. (orig.) With 12 figs., 8 refs.

  4. PERSONALITY CHANGES IN BRAIN INJURY

    OpenAIRE

    Garcia, Patricia Gracia; Mielke, Michelle M.; Rosenberg, Paul; Bergey, Alyssa; Rao, Vani

    2011-01-01

    Traumatic brain injury (TBI) is frequently complicated by alterations in mood and behaviour and changes in personality. We report mild personality changes post-TBI as a possible indicator of traumatic brain injury, but not of injury severity or psychiatric complications.

  5. NONINVASIVE BRAIN STIMULATION IN TRAUMATIC BRAIN INJURY

    OpenAIRE

    Demirtas-Tatlidede, Asli; Vahabzadeh-Hagh, Andrew M.; Bernabeu, Montserrat; Tormos, Jose M.; Pascual-Leone, Alvaro

    2012-01-01

    Brain stimulation techniques have evolved in the last few decades with more novel methods capable of painless, noninvasive brain stimulation. While the number of clinical trials employing noninvasive brain stimulation continues to increase in a variety of medication-resistant neurological and psychiatric diseases, studies evaluating their diagnostic and therapeutic potential in traumatic brain injury (TBI) are largely lacking. This review introduces different techniques of noninvasive brain s...

  6. A systematic review of the risk of dementia and chronic cognitive impairment after mild traumatic brain injury. Results of the International Collaboration on MTBI Prognosis (ICoMP)

    DEFF Research Database (Denmark)

    Godbolt, Allison; Cancelliere, Carol; Hincapié, Cesar A;

    2014-01-01

    Objective: To synthesize the best available evidence regarding the risk of dementia and chronic cognitive impairment (CCI), following mild traumatic brain injury (MTBI). Data sources: MEDLINE and other databases were searched (2001–2012), using a previously published search strategy and pre....... Children with MTBI and intracranial pathology (‘complicated’ MTBI) performed worse than children without intracranial pathology. Children showed higher rates of cognitive symptoms 1 year after MTBI than a control group. Conclusions: There is a lack of evidence of increased risk of dementia after MTBI. In...

  7. Development and testing of two lifestyle interventions for persons with chronic mild-to-moderate traumatic brain injury: Acceptability and feasibility.

    Science.gov (United States)

    Bay, Esther; Ribbens-Grimm, Christine; Chan, Roxane R

    2016-05-01

    This clinical methods discursive highlights the development, piloting, and evaluation of two group interventions designed for persons who experienced chronic traumatic brain injury (TBI). Intervention science for this population is limited and lacking in rigor. Our innovative approach to customize existing interventions and develop parallel delivery methods guided by Allostatic Load theory is presented and preliminary results described. Overall, parallel group interventions delivered by trained leaders with mental health expertise were acceptable and feasible for persons who reported being depressed, stressed, and symptomatic. They reported being satisfied with the overall programs and mostly satisfied with the individual classes. Attendance was over the anticipated 70% expected rate and changes in daily living habits were reported by participants. These two group interventions show promise in helping persons to self manage their chronic stress and symptomatology. PMID:27091260

  8. Evaluation after Traumatic Brain Injury

    Science.gov (United States)

    Trudel, Tina M.; Halper, James; Pines, Hayley; Cancro, Lorraine

    2010-01-01

    It is important to determine if a traumatic brain injury (TBI) has occurred when an individual is assessed in a hospital emergency room after a car accident, fall, or other injury that affects the head. This determination influences decisions about treatment. It is essential to screen for the injury, because the sooner they begin appropriate…

  9. Controversies in preterm brain injury.

    Science.gov (United States)

    Penn, Anna A; Gressens, Pierre; Fleiss, Bobbi; Back, Stephen A; Gallo, Vittorio

    2016-08-01

    In this review, we highlight critical unresolved questions in the etiology and mechanisms causing preterm brain injury. Involvement of neurons, glia, endogenous factors and exogenous exposures is considered. The structural and functional correlates of interrupted development and injury in the premature brain are under active investigation, with the hope that the cellular and molecular mechanisms underlying developmental abnormalities in the human preterm brain can be understood, prevented or repaired. PMID:26477300

  10. Traumatic Brain Injury (TBI): Moderate or Severe

    Science.gov (United States)

    Traumatic Brain Injury (TBI) Moderate or Severe Definition A TBI is classified as moderate or severe when a patient experiences ... skull and enters the brain Defense and Veterans Brain Injury Center PATFIAE MN TI LSI ES Traumatic Brain ...

  11. Traumatic brain injury, neuroimaging, and neurodegeneration

    Directory of Open Access Journals (Sweden)

    Erin D. Bigler

    2013-08-01

    Full Text Available Depending on severity, traumatic brain injury (TBI induces immediate neuropathological effects that in the mildest form may be transient but as severity increases results in neural damage and degeneration. The first phase of neural degeneration is explainable by the primary acute and secondary neuropathological effects initiated by the injury; however, neuroimaging studies demonstrate a prolonged period of pathological changes that progressively occur even during the chronic phase. This review examines how neuroimaging may be used in TBI to understand (1 the dynamic changes that occur in brain development relevant to understanding the effects of TBI and how these relate to developmental stage when the brain is injured, (2 how TBI interferes with age-typical brain development and the effects of aging thereafter, and (3 how TBI results in greater frontotemporolimbic damage, results in cerebral atrophy, and is more disruptive to white matter neural connectivity. Neuroimaging quantification in TBI demonstrates degenerative effects from brain injury over time. An adverse synergistic influence of TBI with aging may predispose the brain injured individual for the development of neuropsychiatric and neurodegenerative disorders long after surviving the brain injury.

  12. Traumatic Brain Injury Registry (TBI)

    Data.gov (United States)

    Department of Veterans Affairs — As the number of Operation Enduring Freedom/Operation Iraqi Freedom (OEF/OIF) Traumatic Brain Injury (TBI) patients has grown, so has the need to track and monitor...

  13. Traumatic Brain Injury (TBI) Data and Statistics

    Science.gov (United States)

    ... Submit Search The CDC Injury Prevention & Control: Traumatic Brain Injury & Concussion Note: Javascript is disabled or is not ... please visit this page: About CDC.gov . Traumatic Brain Injury & Concussion Basic Information Get the Facts Signs and ...

  14. Pediatric minor traumatic brain injury.

    Science.gov (United States)

    Gordon, Kevin E

    2006-12-01

    The literature surrounding minor traumatic brain injury is complex, methodologically challenging, and controversial. Although we lack a consistent standardized definition, the annual rate is likely in excess of 200 per 100,000 children. The proportion of children with minor traumatic brain injury who will require neurosurgery is certainly return to play is currently recommended. The recurrence risk for subsequent concussions is elevated, but there is limited documentation of the effectiveness of preventative efforts. Much remains to be learned. PMID:17178354

  15. Sleep in traumatic brain injury.

    Science.gov (United States)

    Vermaelen, James; Greiffenstein, Patrick; deBoisblanc, Bennett P

    2015-07-01

    More than one-half million patients are hospitalized annually for traumatic brain injury (TBI). One-quarter demonstrate sleep-disordered breathing, up to 50% experience insomnia, and half have hypersomnia. Sleep disturbances after TBI may result from injury to sleep-regulating brain tissue, nonspecific neurohormonal responses to systemic injury, ICU environmental interference, and medication side effects. A diagnosis of sleep disturbances requires a high index of suspicion and appropriate testing. Treatment starts with a focus on making the ICU environment conducive to normal sleep. Treating sleep-disordered breathing likely has outcome benefits in TBI. The use of sleep promoting sedative-hypnotics and anxiolytics should be judicious. PMID:26118920

  16. Traumatic Brain Injury Inpatient Rehabilitation

    Science.gov (United States)

    Im, Brian; Schrer, Marcia J.; Gaeta, Raphael; Elias, Eileen

    2010-01-01

    Traumatic brain injuries (TBI) can cause multiple medical and functional problems. As the brain is involved in regulating nearly every bodily function, a TBI can affect any part of the body and aspect of cognitive, behavioral, and physical functioning. However, TBI affects each individual differently. Optimal management requires understanding the…

  17. Mental Trauma Experienced by Caregivers of patients with Diffuse Axonal Injury or Severe Traumatic Brain Injury

    OpenAIRE

    Syed Tajuddin Syed Hassan; Husna Jamaludin; Rosna Abd Raman; Haliza Mohd Riji; Khaw Wan Fei

    2013-01-01

    Context: As with care giving and rehabilitation in chronic illnesses, the concern with traumatic brain injury (TBI), particularly with diffuse axonal injury (DAI), is that the caregivers are so overwhelmingly involved in caring and rehabilitation of the victim that in the process they become traumatized themselves. This review intends to shed light on the hidden and silent trauma sustained by the caregivers of severe brain injury survivors. Motor vehicle accident (MVA) is the highest contribu...

  18. Brain Temperature: Physiology and Pathophysiology after Brain Injury

    OpenAIRE

    Ségolène Mrozek; Fanny Vardon; Thomas Geeraerts

    2012-01-01

    The regulation of brain temperature is largely dependent on the metabolic activity of brain tissue and remains complex. In intensive care clinical practice, the continuous monitoring of core temperature in patients with brain injury is currently highly recommended. After major brain injury, brain temperature is often higher than and can vary independently of systemic temperature. It has been shown that in cases of brain injury, the brain is extremely sensitive and vulnerable to small variatio...

  19. Diffusion tensor tractography-based analysis of the cingulum: clinical utility and findings in traumatic brain injury with chronic sequels

    Energy Technology Data Exchange (ETDEWEB)

    Kurki, Timo [Turku University Hospital, Department of Radiology, Turku (Finland); MRI Unit, Terveystalo Pulssi Medical Centre, Turku (Finland); Himanen, Leena; Vuorinen, Elina; Myllyniemi, Anna; Saarenketo, Anna-Riitta [NeuTera Neuropsychologist Centre, Turku (Finland); Kauko, Tommi [University of Turku, Department of Biostatistics, Turku (Finland); Brandstack, Nina [Turku University Hospital, Department of Radiology, Turku (Finland); Helsinki University Hospital, Department of Radiology, Helsinki (Finland); Tenovuo, Olli [Turku University Hospital and University of Turku, Department of Rehabilitation and Brain Trauma, Turku (Finland)

    2014-10-15

    To evaluate the clinical utility of quantitative diffusion tensor tractography (DTT) and tractography-based core analysis (TBCA) of the cingulum by defining the reproducibility, normal values, and findings in traumatic brain injury (TBI). Eighty patients with TBI and normal routine MRI and 78 controls underwent MRI at 3T. To determine reproducibility, 12 subjects were scanned twice. Superior (SC) and inferior (IC) cingulum were analyzed separately by DTT (fractional anisotropy (FA) thresholds 0.15 and 0.30). TBCA was performed from volumes defined by tractography with gradually changed FA thresholds. FA values were correlated with clinical and neuropsychological data. The lowest coefficient of variation was obtained at DTT threshold 0.30 (2.0 and 2.4 % for SC and IC, respectively), but in proportion to standard deviations of normal controls, the reproducibility of TBCA was better in SC and similar to that of DTT in IC. In patients with TBI, volume reduction with loss of peripheral fibers was relatively common; mean FA was mostly normal in these tractograms. The frequency of FA reductions (>2 SD) was in DTT smaller than in TBCA, in which FA decrease was present in 42 (13.1 %) of the 320 measurements. Central FA values in SC predicted visuoperceptual ability, and those in left IC predicted cognitive speed, language, and communication ability (p < 0.05). Tractography-based measurements have sufficient reproducibility for demonstration of severe abnormalities of the cingulum. TBCA is preferential for clinical FA analysis, because it measures corresponding areas in patients and controls without inaccuracies due to trauma-induced structural changes. (orig.)

  20. Diffusion tensor tractography-based analysis of the cingulum: clinical utility and findings in traumatic brain injury with chronic sequels

    International Nuclear Information System (INIS)

    To evaluate the clinical utility of quantitative diffusion tensor tractography (DTT) and tractography-based core analysis (TBCA) of the cingulum by defining the reproducibility, normal values, and findings in traumatic brain injury (TBI). Eighty patients with TBI and normal routine MRI and 78 controls underwent MRI at 3T. To determine reproducibility, 12 subjects were scanned twice. Superior (SC) and inferior (IC) cingulum were analyzed separately by DTT (fractional anisotropy (FA) thresholds 0.15 and 0.30). TBCA was performed from volumes defined by tractography with gradually changed FA thresholds. FA values were correlated with clinical and neuropsychological data. The lowest coefficient of variation was obtained at DTT threshold 0.30 (2.0 and 2.4 % for SC and IC, respectively), but in proportion to standard deviations of normal controls, the reproducibility of TBCA was better in SC and similar to that of DTT in IC. In patients with TBI, volume reduction with loss of peripheral fibers was relatively common; mean FA was mostly normal in these tractograms. The frequency of FA reductions (>2 SD) was in DTT smaller than in TBCA, in which FA decrease was present in 42 (13.1 %) of the 320 measurements. Central FA values in SC predicted visuoperceptual ability, and those in left IC predicted cognitive speed, language, and communication ability (p < 0.05). Tractography-based measurements have sufficient reproducibility for demonstration of severe abnormalities of the cingulum. TBCA is preferential for clinical FA analysis, because it measures corresponding areas in patients and controls without inaccuracies due to trauma-induced structural changes. (orig.)

  1. Significant improvements in cognitive performance post-transcranial, red/near-infrared light-emitting diode treatments in chronic, mild traumatic brain injury: open-protocol study.

    Science.gov (United States)

    Naeser, Margaret A; Zafonte, Ross; Krengel, Maxine H; Martin, Paula I; Frazier, Judith; Hamblin, Michael R; Knight, Jeffrey A; Meehan, William P; Baker, Errol H

    2014-06-01

    This pilot, open-protocol study examined whether scalp application of red and near-infrared (NIR) light-emitting diodes (LED) could improve cognition in patients with chronic, mild traumatic brain injury (mTBI). Application of red/NIR light improves mitochondrial function (especially in hypoxic/compromised cells) promoting increased adenosine triphosphate (ATP) important for cellular metabolism. Nitric oxide is released locally, increasing regional cerebral blood flow. LED therapy is noninvasive, painless, and non-thermal (cleared by the United States Food and Drug Administration [FDA], an insignificant risk device). Eleven chronic, mTBI participants (26-62 years of age, 6 males) with nonpenetrating brain injury and persistent cognitive dysfunction were treated for 18 outpatient sessions (Monday, Wednesday, Friday, for 6 weeks), starting at 10 months to 8 years post- mTBI (motor vehicle accident [MVA] or sports-related; and one participant, improvised explosive device [IED] blast injury). Four had a history of multiple concussions. Each LED cluster head (5.35 cm diameter, 500 mW, 22.2 mW/cm(2)) was applied for 10 min to each of 11 scalp placements (13 J/cm(2)). LEDs were placed on the midline from front-to-back hairline; and bilaterally on frontal, parietal, and temporal areas. Neuropsychological testing was performed pre-LED, and at 1 week, and 1 and 2 months after the 18th treatment. A significant linear trend was observed for the effect of LED treatment over time for the Stroop test for Executive Function, Trial 3 inhibition (p=0.004); Stroop, Trial 4 inhibition switching (p=0.003); California Verbal Learning Test (CVLT)-II, Total Trials 1-5 (p=0.003); and CVLT-II, Long Delay Free Recall (p=0.006). Participants reported improved sleep, and fewer post-traumatic stress disorder (PTSD) symptoms, if present. Participants and family reported better ability to perform social, interpersonal, and occupational functions. These open-protocol data suggest that placebo

  2. The Impact of Traumatic Brain Injury on the Aging Brain.

    Science.gov (United States)

    Young, Jacob S; Hobbs, Jonathan G; Bailes, Julian E

    2016-09-01

    Traumatic brain injury (TBI) has come to the forefront of both the scientific and popular culture. Specifically, sports-related concussions or mild TBI (mTBI) has become the center of scientific scrutiny with a large amount of research focusing on the long-term sequela of this type of injury. As the populace continues to age, the impact of TBI on the aging brain will become clearer. Currently, reports have come to light that link TBI to neurodegenerative disorders such as Alzheimer's and Parkinson's diseases, as well as certain psychiatric diseases. Whether these associations are causations, however, is yet to be determined. Other long-term sequelae, such as chronic traumatic encephalopathy (CTE), appear to be associated with repetitive injuries. Going forward, as we gain better understanding of the pathophysiological process involved in TBI and subclinical head traumas, and individual traits that influence susceptibility to neurocognitive diseases, a clearer, more comprehensive understanding of the connection between brain injury and resultant disease processes in the aging brain will become evident. PMID:27432348

  3. Traumatic brain injury-induced sleep disorders.

    Science.gov (United States)

    Viola-Saltzman, Mari; Musleh, Camelia

    2016-01-01

    Sleep disturbances are frequently identified following traumatic brain injury, affecting 30%-70% of persons, and often occur after mild head injury. Insomnia, fatigue, and sleepiness are the most frequent sleep complaints after traumatic brain injury. Sleep apnea, narcolepsy, periodic limb movement disorder, and parasomnias may also occur after a head injury. In addition, depression, anxiety, and pain are common brain injury comorbidities with significant influence on sleep quality. Two types of traumatic brain injury that may negatively impact sleep are acceleration/deceleration injuries causing generalized brain damage and contact injuries causing focal brain damage. Polysomnography, multiple sleep latency testing, and/or actigraphy may be utilized to diagnose sleep disorders after a head injury. Depending on the disorder, treatment may include the use of medications, positive airway pressure, and/or behavioral modifications. Unfortunately, the treatment of sleep disorders associated with traumatic brain injury may not improve neuropsychological function or sleepiness. PMID:26929626

  4. Brain injury - discharge

    Science.gov (United States)

    ... injuries do not happen. This includes making the bathroom safe, for either a child or an adult , and protecting against falls . Family and caregivers may need to help the person with the following: Exercising ...

  5. Neurobiology of premature brain injury

    OpenAIRE

    Salmaso, Natalina; Jablonska, Beata; Scafidi, Joseph; Vaccarino, Flora M.; Gallo, Vittorio

    2014-01-01

    Every year in the United States, an estimated 500,000 babies are born preterm (before 37 completed weeks of gestation), and this number is rising, along with the recognition of brain injuries due to preterm delivery. A common underlying pathogenesis appears to be perinatal hypoxia induced by immature lung development, which causes injury to vulnerable neurons and glia. Abnormal growth and maturation of susceptible cell types, particularly neurons and oligodendrocytes, in preterm babies with v...

  6. Brain injury requires lung protection

    OpenAIRE

    Lopez-Aguilar, Josefina; Blanch, Lluis

    2015-01-01

    The paper entitled “The high-mobility group protein B1-Receptor for advanced glycation endproducts (HMGB1-RAGE) axis mediates traumatic brain injury (TBI)-induced pulmonary dysfunction in lung transplantation” published recently in Science Translational Medicine links lung failure after transplantation with alterations in the axis HMGB1-RAGE after TBI, opening a new field for exploring indicators for the early detection of patients at risk of developing acute lung injury (ALI). The lung is on...

  7. Missile injuries of the brain

    International Nuclear Information System (INIS)

    Data was analyzed relating to a consecutive series of 16 patients of penetrating brain injuries received at forward defense lines. Characteristics studied were the cause of injury, level of consciousness and various neurological deficits presented on initial examination, CT scan findings, the surgical procedures performed and the final outcome after one year of follow-up. One out of 16 patients, died due to severe associated injuries to abdominal viscera and major vessels. Meningitis occurred in one patient during the immediate postoperative period. All patients with motor weakness speech deficits and incontinence showed significant improvement. Hearing loss of one ear persisted in one patient. Two patients developed delayed onset seizures. It is concluded that, patients with penetrating brain injuries should be evacuated to the tertiary care neurosurgical centres as soon as possible. In operation only obviously necrotic brain and easily accessible metal and bone pieces should be removed. There is no need to explore the normal brain as it would only result in increased neurological deficits. The patients with such injuries should receive broad-spectrum antibiotics to prevent the infective complications. (author)

  8. Brain Injury Safety Tips and Prevention

    Science.gov (United States)

    ... this? Submit Button Brain Injury Safety Tips and Prevention Recommend on Facebook Tweet Share Compartir There are ... More HEADS UP Video: Brain Injury Safety and Prevention frame support disabled and/or not supported in ...

  9. Family needs after brain injury

    DEFF Research Database (Denmark)

    Norup, Anne; Perrin, Paul B; Cuberos-Urbano, Gustavo;

    2015-01-01

    OBJECTIVE: The objective of this study was to explore differences by country in the importance of family needs after traumatic brain injury (TBI), as well as differences in met/unmet needs. METHOD: Two hundred and seventy-one family members of an individual with TBI in Mexico, Colombia, Spain...

  10. Hypopituitarism in Traumatic Brain Injury

    DEFF Research Database (Denmark)

    Klose, Marianne; Feldt-Rasmussen, Ulla

    2015-01-01

    While hypopituitarism after traumatic brain injury (TBI) was previously considered rare, it is now thought to be a major cause of treatable morbidity among TBI survivors. Consequently, recommendations for assessment of pituitary function and replacement in TBI were recently introduced. Given the...

  11. Cerebral circulation and metabolism in the patients with higher brain dysfunction caused by chronic minor traumatic brain injury. A study by the positron emission tomography in twenty subjects with normal MRI findings

    International Nuclear Information System (INIS)

    Many individuals are affected on their higher brain functions, such as intelligence, memory, and attention, even after minor traumatic brain injury (MTBI). Although higher brain dysfunction is based on impairment of the cerebral circulation and metabolism, the precise relationship between them remains unknown. This study was undertaken to investigate the relationship between the cerebral circulation or cerebral metabolism and higher brain dysfunction. Twenty subjects with higher brain dysfunction caused by chronic MTBI were studied. They had no abnormal MRI findings. The full-scale intelligence quotient (FIQ) were quantitatively evaluated by the Wechsler Adult Intelligence Scale-Revised (WAIS-R), and the subjects were classified into the normal group and the impaired group. Concurrent with the evaluation of FIQ, positron emission tomography (PET) was performed by the steady state method with 15O gases inhalation. Regional cerebral blood flow (rCBF), oxygen extraction fraction (OEF) and cerebral metabolic rate of oxygen (CMRO2) were calculated in the bilateral frontal, parietal, temporal, and occipital lobe. First, of all twenty subjects, we investigated rCBF, OEF and CMRO2 in all regions. Then we compared rCBF, OEF, and CMRO2 between the normal group and the impaired group based on FIQ score. We also studied the change of FIQ score of 13 subjects 9.3 months after the first evaluation. In addition, we investigated the change of rCBF, OEF and CMRO2 along with the improvement of FIQ score. Although rCBF and OEF of all subjects were within the normal range in all regions, CMRO2 of more than half of subjects was under the lower normal limit in all regions except in the right occipital lobe, showing the presence of ''relative luxury perfusion''. Comparison of rCBF, OEF and CMRO2 between normal group and impaired group revealed that CMRO2 of the impaired group was significantly lower than that of the normal group in the bilateral frontal, temporal, and occipital lobe

  12. Knowledge of Traumatic Brain Injury among Educators

    Science.gov (United States)

    Ernst, William J.; Gallo, Adrienne B.; Sellers, Amanda L.; Mulrine, Jessica; MacNamara, Luciana; Abrahamson, Allison; Kneavel, Meredith

    2016-01-01

    The purpose of this study is to determine knowledge of traumatic brain injury among educators. Few studies have examined knowledge of traumatic brain injury in this population and fewer still have included a substantial proportion of general education teachers. Examining knowledge of traumatic brain injury in educators is important as the vast…

  13. Assessment of Students with Traumatic Brain Injury

    Science.gov (United States)

    Chesire, David J.; Buckley, Valerie A.; Canto, Angela I.

    2011-01-01

    The incidence of brain injuries, as well as their impact on individuals who sustain them, has received growing attention from American media in recent years. This attention is likely the result of high profile individuals suffering brain injuries. Greater public awareness of traumatic brain injuries (TBIs) has also been promoted by sources such as…

  14. Preconditioning for traumatic brain injury

    Science.gov (United States)

    Yokobori, Shoji; Mazzeo, Anna T; Hosein, Khadil; Gajavelli, Shyam; Dietrich, W. Dalton; Bullock, M. Ross

    2016-01-01

    Traumatic brain injury (TBI) treatment is now focused on the prevention of primary injury and reduction of secondary injury. However, no single effective treatment is available as yet for the mitigation of traumatic brain damage in humans. Both chemical and environmental stresses applied before injury, have been shown to induce consequent protection against post-TBI neuronal death. This concept termed “preconditioning” is achieved by exposure to different pre-injury stressors, to achieve the induction of “tolerance” to the effect of the TBI. However, the precise mechanisms underlying this “tolerance” phenomenon are not fully understood in TBI, and therefore even less information is available about possible indications in clinical TBI patients. In this review we will summarize TBI pathophysiology, and discuss existing animal studies demonstrating the efficacy of preconditioning in diffuse and focal type of TBI. We will also review other non-TBI preconditionng studies, including ischemic, environmental, and chemical preconditioning, which maybe relevant to TBI. To date, no clinical studies exist in this field, and we speculate on possible futureclinical situation, in which pre-TBI preconditioning could be considered. PMID:24323189

  15. Traumatic brain injury-induced sleep disorders

    Directory of Open Access Journals (Sweden)

    Viola-Saltzman M

    2016-02-01

    Full Text Available Mari Viola-Saltzman, Camelia Musleh Department of Neurology, NorthShore University HealthSystem, Evanston, IL, USA Abstract: Sleep disturbances are frequently identified following traumatic brain injury, affecting 30%–70% of persons, and often occur after mild head injury. Insomnia, fatigue, and sleepiness are the most frequent sleep complaints after traumatic brain injury. Sleep apnea, narcolepsy, periodic limb movement disorder, and parasomnias may also occur after a head injury. In addition, depression, anxiety, and pain are common brain injury comorbidities with significant influence on sleep quality. Two types of traumatic brain injury that may negatively impact sleep are acceleration/deceleration injuries causing generalized brain damage and contact injuries causing focal brain damage. Polysomnography, multiple sleep latency testing, and/or actigraphy may be utilized to diagnose sleep disorders after a head injury. Depending on the disorder, treatment may include the use of medications, positive airway pressure, and/or behavioral modifications. Unfortunately, the treatment of sleep disorders associated with traumatic brain injury may not improve neuropsychological function or sleepiness. Keywords: traumatic brain injury, insomnia, hypersomnia, sleep apnea, periodic limb movement disorder, fatigue

  16. TRAUMATIC BRAIN INJURY SURVEILLANCE SYSTEM (TBISS)

    Science.gov (United States)

    The National Center for Injury Prevention and Control (NCIPC), Centers for Disease Control and Prevention (CDC) had developed and maintains a surveillance system to understand the magnitude and characteristics of hospitalized and fatal traumatic brain injuries in the United State...

  17. How woodpecker avoids brain injury?

    Science.gov (United States)

    Wu, C. W.; Zhu, Z. D.; Zhang, W.

    2015-07-01

    It has long been recognized that woodpecker is an excellent anti-shock organism, as its head and brain can bear high deceleration up to 1500 g under fast pecking. To investigate the mechanism of brain protection of woodpecker, we built a finite element model of a whole woodpecker using computed topography scanning technique and geometry modeling. Numerical results show that the periodical changing Young's modulus around the skull affects the stress wave propagation in head and makes the stress lowest at the position of the brain. Modal analysis reveals the application of pre-tension force to the hyoid bone can increase the natural frequency of woodpecker's head. The large gap between the natural and working frequencies enable the woodpecker to effectively protect its brain from the resonance injury. Energy analyses indicate the majority of the impact energy (99.7%) is stored in the bulk of body and is utilized in the next pecking. There is only a small fraction of it enters into the head (0.3%). The whole body of the woodpecker gets involved in the energy conversion and forms an efficient anti-shock protection system for the brain.

  18. [Mild brain injuries in emergency medicine].

    Science.gov (United States)

    Liimatainen, Suvi; Niskakangas, Tero; Ohman, Juha

    2011-01-01

    Diagnostics and correct classification of mild brain injuries is challenging. Problems caused by insufficient documentation at the acute phase become more obvious in situations in which legal insurance issues are to be considered. A small proportion of patients with mild brain injury suffer from prolonged symptoms. Medical recording and classification of the brain injury at the initial phase should therefore be carried out in a structured manner. The review deals with the diagnostic problems of mild brain injuries and presents a treatment protocol for adult patients at the acute phase, aiming at avoiding prolonged problems. PMID:22238915

  19. Quality of Life Following Brain Injury: Perspectives from Brain Injury Association of America State Affiliates

    Science.gov (United States)

    Degeneffe, Charles Edmund; Tucker, Mark

    2012-01-01

    Objective: to examine the perspectives of brain injury professionals concerning family members' feelings about the quality of life experienced by individuals with brain injuries. Participants: participating in the study were 28 individuals in leadership positions with the state affiliates of the Brain Injury Association of America (BIAA). Methods:…

  20. Brain protection by magnesium ion against radioaction brain injury

    International Nuclear Information System (INIS)

    Radiation brain injury is a serious complication among the radiotherapy of brain tumors. It is demonstrated that the protective action of magnesium ion in the brain injury from some experimental studies recent years, which is the prospective neuro protective agents overall merits. This article is summarized the causes and the variance of magnesium ion in the brain tissue afterwards the radioactive brain injury, additionally the defense mechanism of magnesium ion from the aspects of inflammation reduction, encephaledema alleviation, anti-apoptosis and improvement of nerve function. (authors)

  1. Late exercise reduces neuroinflammation and cognitive dysfunction after traumatic brain injury

    OpenAIRE

    Piao, Chun-Shu; Stoica, Bogdan A.; Wu, Junfang; Sabirzhanov, Boris; Zhao, Zaorui; Cabatbat, Rainier; Loane, David J.; Faden, Alan I.

    2013-01-01

    Delayed secondary biochemical and cellular changes after traumatic brain injury continue for months to years, and are associated with chronic neuroinflammation and progressive neurodegeneration. Physical activity can reduce inflammation and facilitate recovery after brain injury. Here, we investigated the time-dependent effects, and underlying mechanisms of post-traumatic exercise initiation on outcome after moderate traumatic brain injury using a well-characterized mouse controlled cortical ...

  2. Support Network Responses to Acquired Brain Injury

    Science.gov (United States)

    Chleboun, Steffany; Hux, Karen

    2011-01-01

    Acquired brain injury (ABI) affects social relationships; however, the ways social and support networks change and evolve as a result of brain injury is not well understood. This study explored ways in which survivors of ABI and members of their support networks perceive relationship changes as recovery extends into the long-term stage. Two…

  3. Treatment of very severe brain injuries

    Institute of Scientific and Technical Information of China (English)

    杨振九; 杨佳勇; 冯承宣; 宋伟健; 孙强

    2004-01-01

    Objective: To sum up the experience in treating very severe traumatic brain injuries.Methods: Retrospective analysis of 68 patients with very severe traumatic brain injuries treated in our hospital from 1997 to 2002 was done.Results: Forty-one (60%) patients died. In the 50 patients treated surgically 27 (40%) survived, 8 recovered well, 9 had moderate disability and 10 had sever deficits. The 18 patients treated non-operatively all died.Conclusions: Much attention should be given to the observation of the changes of severe brain injuries with cranial base injury. Timely operative decompression, basic life support, keeping effective brain blood perfusion and effective oxygen supply, improving cerebral microcirculation and preventing or controlling complications are the main methods to raise the successful rate of treating very severe brain injuries and the life quality of the patients.

  4. Respiratory mechanics in brain injury: A review

    OpenAIRE

    Koutsoukou, Antonia; Katsiari, Maria; Orfanos, Stylianos E; Kotanidou, Anastasia; Daganou, Maria; Kyriakopoulou, Magdalini; Koulouris, Nikolaos G.; Rovina, Nikoletta

    2016-01-01

    Several clinical and experimental studies have shown that lung injury occurs shortly after brain damage. The responsible mechanisms involve neurogenic pulmonary edema, inflammation, the harmful action of neurotransmitters, or autonomic system dysfunction. Mechanical ventilation, an essential component of life support in brain-damaged patients (BD), may be an additional traumatic factor to the already injured or susceptible to injury lungs of these patients thus worsening lung injury, in case ...

  5. Effect of AVP on brain edema following traumatic brain injury

    Institute of Scientific and Technical Information of China (English)

    XU Miao; SU Wei; HUANG Wei-dong; LU Yuan-qiang; XU Qiu-ping; CHEN Zhao-jun

    2007-01-01

    Objective: To evaluate plasma arginine vasopressin (AVP) level in patients with traumatic brain injury and investigate the role of AVP in the process of brain edema. Methods: A total of 30 patients with traumatic brain injury were involved in our study. They were divided into two groups by Glasgow Coma Scale: severe traumatic brain injury group (STBI, GCS≤ 8) and moderate traumatic brain injury group (MTBI, GCS>8).Samples of venous blood were collected in the morning at rest from 15 healthy volunteers (control group)and within 24 h after traumatic brain injury from these patients for AVP determinations by radioimmunoassay. The severity and duration of the brain edema were estimated by head CT scan.Results: plasma AVP levels (ng/L) were (mean±SD): control, 3.06±1.49; MTBI, 38.12±7.25; and STBI, 66.61±17.10.The plasma level of AVP was significantly increased within 24 h after traumatic brain injury and followed by the reduction of GCS, suggesting the deterioration of cerebral injury (P<0.01). And the AVP level was correlated with the severity (STBI r=0.919, P<0.01; MTBI r=0.724, P<0.01) and the duration of brain edema (STBI r=0.790, P<0.01; MTBI r=0.712, P<0.01). Conclusions: The plasma AVP level is closely associated with the severity of traumatic brain injury. AVP may play an important role in pathogenesis of brain edema after traumatic brain injury.

  6. Loss of neuronal integrity: a cause of hypometabolism in patients with traumatic brain injury without MRI abnormality in the chronic stage

    International Nuclear Information System (INIS)

    Traumatic brain injury (TBI) causes brain dysfunction in many patients. However, some patients have severe brain dysfunction but display no abnormalities on magnetic resonance imaging (MRI). There have been some reports of hypometabolism even in such patients. The purpose of this study was to investigate the relationship between metabolic abnormality and loss of neuronal integrity in TBI patients with some symptoms but without MRI abnormalities. The study population comprised ten patients with TBI and ten normal volunteers. All of the patients were examined at least 1 year after the injury. 15O-labelled gas PET and [11C]flumazenil (FMZ) positron emission tomography (PET) were carried out. The cerebral metabolic rate of oxygen (CMRO2) and binding potential (BP) images of FMZ were calculated. Axial T2WI, T2*WI and FLAIR images were obtained. Coronal images were added in some cases. All of the patients had normal MRI findings, and all showed areas with abnormally low CMRO2. Low uptake on BP images was observed in six patients (60%). No lesions that showed low uptake on BP images were without low CMRO2. On the other hand, there were 14 lesions with low CMRO2 but without BP abnormalities. These results indicate that there are metabolic abnormalities in TBI patients with some symptoms after brain injury but without abnormalities on MRI. Some of the hypometabolic lesions showed low BP, indicating a loss of neuronal integrity. Thus, FMZ PET may have potential to distinguish hypometabolism caused by neuronal loss from that caused by other factors. (orig.)

  7. Intranasal epidermal growth factor treatment rescues neonatal brain injury

    Science.gov (United States)

    Scafidi, Joseph; Hammond, Timothy R.; Scafidi, Susanna; Ritter, Jonathan; Jablonska, Beata; Roncal, Maria; Szigeti-Buck, Klara; Coman, Daniel; Huang, Yuegao; McCarter, Robert J.; Hyder, Fahmeed; Horvath, Tamas L.; Gallo, Vittorio

    2014-02-01

    There are no clinically relevant treatments available that improve function in the growing population of very preterm infants (less than 32 weeks' gestation) with neonatal brain injury. Diffuse white matter injury (DWMI) is a common finding in these children and results in chronic neurodevelopmental impairments. As shown recently, failure in oligodendrocyte progenitor cell maturation contributes to DWMI. We demonstrated previously that the epidermal growth factor receptor (EGFR) has an important role in oligodendrocyte development. Here we examine whether enhanced EGFR signalling stimulates the endogenous response of EGFR-expressing progenitor cells during a critical period after brain injury, and promotes cellular and behavioural recovery in the developing brain. Using an established mouse model of very preterm brain injury, we demonstrate that selective overexpression of human EGFR in oligodendrocyte lineage cells or the administration of intranasal heparin-binding EGF immediately after injury decreases oligodendroglia death, enhances generation of new oligodendrocytes from progenitor cells and promotes functional recovery. Furthermore, these interventions diminish ultrastructural abnormalities and alleviate behavioural deficits on white-matter-specific paradigms. Inhibition of EGFR signalling with a molecularly targeted agent used for cancer therapy demonstrates that EGFR activation is an important contributor to oligodendrocyte regeneration and functional recovery after DWMI. Thus, our study provides direct evidence that targeting EGFR in oligodendrocyte progenitor cells at a specific time after injury is clinically feasible and potentially applicable to the treatment of premature children with white matter injury.

  8. [Imaging of brain changes in chronic pain].

    Science.gov (United States)

    Vartiainen, Nuutti; Forss, Nina

    2014-01-01

    Modern methods of brain imaging have enabled objective measurements of functional and structural brain changes associated with chronic pain conditions. According to recent investigations, chronic pain is not only associated with abnormally strong or prolonged activity of regions processing acute pain, but also with activation of brain networks that are characteristic for each pain state, changes in cortical remodeling, as well as local reduction of grey matter in several regions of the brain. Brain changes associated with chronic pain facilitate the understanding of mechanisms of various chronic pain conditions. PMID:25211820

  9. Changes in T lymphocyte subsets after severe traumatic brain injury

    Institute of Scientific and Technical Information of China (English)

    Yulu Miao; Mingxia Zhang; Yulin Nie; Wan Zhao; Bin Huang; Zhengming Jiang; Shaoxiong Yu; Zhibin Huang; Hongjin Fu

    2007-01-01

    BACKGROUND: Besides local changes of cranial parenchymal cells, hemorrhage, etc., severe traumatic brain injuries also cause the changes of total body fluid and various functions, and the changes of lymphocytes and T lymphocyte subsets should be paid more attention to.OBJECTIVE: To reveal the changing laws of T lymphocyte subsets after severe traumatic brain injury, and compare with mild to moderate brain injury.DESIGN: A comparative observation.SETTINGS: Department of Neurosurgery, Longgang District Buji People's Hospital of Shenzhen City;Central Laboratory of Shenzhen Hospital of Prevention and Cure for Chronic Disease.PARTICIPANTS: All the subjects were selected from the Department of Neurosurgery, Longgang District Buji People's Hospital of Shenzhen City from August 2002 to August 2005. Thirty patients with severe brain injury, whose Glasgow coma score (GCS) was ≤ 8 points, were taken as the experimental group, including 21 males and 9 females, aging 16 - 62 years. Meanwhile, 30 patients with mild traumatic brain injury were taken as the control group (GCS ranged 14 - 15 points), including 18 males and 12 females, aging 15 - 58 years. All the subjects were in admission at 6 hours after injury, without disease of major organs before injury.Informed consents were obtained from all the patients or their relatives.conditions of pulmonaryinfections were observed at 4 days after injury. The differences of measurement data were compared with the t test.MAIN OUTCOME MEASURES: Changes of T lymphocytes subsets at 1 - 14 days after severe and mild or moderate traumatic injury.RESULTS: Finally, 28 and 25 patients with mild to moderate traumatic brain injury, whereas 25 and 21 patients with severe traumatic brain injury were analyzed at 7 and 14 days respectively, and the missed ones CD3, CD4, CD8, CD4/CD8 began to decrease, whereas CD8 increased in the experimental group, which were very significantly different from those in the control group (t =2.77 - 3.26, P < 0

  10. All astrocytes are not created equal—the role of astroglia in brain injury

    OpenAIRE

    Moore, Darcie L; Jessberger, Sebastian

    2013-01-01

    In two recent papers published in Nature Neuroscience and Cell Stem Cells, Magdalena Götz and colleagues shed new light on the in vivo response of glial cells to brain injury and characterize a highly heterogeneous behavior of astrocytes to chronic and acute brain injury.

  11. Cognitive impairments in patients with brain injury

    OpenAIRE

    Vladimir Vladimirovich Zakharov; E. A. Drozdova

    2013-01-01

    The paper gives the data of Russian and foreign authors and the results of this paper authors’ investigation of higher cerebral functions in patients who have sustained brain injury (BI). It shows their high prevalence, the predominance of cognitive impairments (CI) over neurological disorders in patients with mild and moderate injury, presents their quantitative and qualitative features (a preponderance of focal symptoms in severe injury and neurodynamic disorders in mild injury), describes ...

  12. Effects of a rapid-resisted elliptical training program on motor, cognitive and neurobehavioral functioning in adults with chronic traumatic brain injury.

    Science.gov (United States)

    Damiano, Diane L; Zampieri, Cristiane; Ge, Jie; Acevedo, Ana; Dsurney, John

    2016-08-01

    This small clinical trial utilized a novel rehabilitation strategy, rapid-resisted elliptical training, in an effort to increase motor, and thereby cognitive, processing speed in ambulatory individuals with traumatic brain injury (TBI). As an initial step, multimodal functional abilities were quantified and compared in 12 ambulatory adults with and 12 without TBI. After the baseline assessment, the group with TBI participated in an intensive 8-week daily exercise program using an elliptical trainer and was reassessed after completion and at an 8-week follow-up. The focus of training was on achieving a fast movement speed, and once the target was reached, resistance to motion was increased in small increments to increase intensity of muscle activation. Primary outcomes were: High-Level Mobility Assessment Tool (HiMAT), instrumented balance tests, dual-task (DT) performance and neurobehavioral questionnaires. The group with TBI had poorer movement excursion during balance tests and poorer dual-task (DT) performance. After training, balance reaction times improved and were correlated with gains in the HiMAT and DT. Sleep quality also improved and was correlated with improved depression and learning. This study illustrates how brain injury can affect multiple linked aspects of functioning and provides preliminary evidence that intensive rapid-resisted training has specific positive effects on dynamic balance and more generalized effects on sleep quality in TBI. PMID:27025506

  13. 45 CFR 1308.16 - Eligibility criteria: Traumatic brain injury.

    Science.gov (United States)

    2010-10-01

    ... 45 Public Welfare 4 2010-10-01 2010-10-01 false Eligibility criteria: Traumatic brain injury. 1308... DISABILITIES Health Services Performance Standards § 1308.16 Eligibility criteria: Traumatic brain injury. A child is classified as having traumatic brain injury whose brain injuries are caused by an...

  14. Aquaporin 9 in rat brain after severe traumatic brain injury

    OpenAIRE

    Hui Liu; Mei Yang; Guo-ping Qiu; Fei Zhuo; Wei-hua Yu; Shan-quan Sun; Yun Xiu

    2012-01-01

    OBJECTIVE: To reveal the expression and possible roles of aquaporin 9 (AQP9) in rat brain, after severe traumatic brain injury (TBI). METHODS: Brain water content (BWC), tetrazolium chloride staining, Evans blue staining, immunohistochemistry (IHC), immunofluorescence (IF), western blot, and real-time polymerase chain reaction were used. RESULTS: The BWC reached the first and second (highest) peaks at 6 and 72 hours, and the blood brain barrier (BBB) was severely destroyed at six hours after ...

  15. Cognitive impairments in patients with brain injury

    Directory of Open Access Journals (Sweden)

    Vladimir Vladimirovich Zakharov

    2013-01-01

    Full Text Available The paper gives the data of Russian and foreign authors and the results of this paper authors’ investigation of higher cerebral functions in patients who have sustained brain injury (BI. It shows their high prevalence, the predominance of cognitive impairments (CI over neurological disorders in patients with mild and moderate injury, presents their quantitative and qualitative features (a preponderance of focal symptoms in severe injury and neurodynamic disorders in mild injury, describes the predictors of their course and prognosis (the degree of injury is one of the most important predictors, and discusses current trends in the medical correction of detected abnormalities.

  16. Nonsurgical interventions after mild traumatic brain injury

    DEFF Research Database (Denmark)

    Nygren-de Boussard, Catharina; Holm, Lena W; Cancelliere, Carol;

    2014-01-01

    OBJECTIVE: To synthesize the best available evidence regarding the impact of nonsurgical interventions on persistent symptoms after mild traumatic brain injury (MTBI). DATA SOURCES: MEDLINE and other databases were searched (2001-2012) with terms including "rehabilitation." Inclusion criteria were...

  17. Traumatic brain injury and forensic neuropsychology.

    Science.gov (United States)

    Bigler, Erin D; Brooks, Michael

    2009-01-01

    As part of a special issue of The Journal of Head Trauma Rehabilitation, forensic neuropsychology is reviewed as it applies to traumatic brain injury (TBI) and other types of acquired brain injury in which clinical neuropsychologists and rehabilitation psychologists may be asked to render professional opinions about the neurobehavioral effects and outcome of a brain injury. The article introduces and overviews the topic focusing on the process of forensic neuropsychological consultation and practice as it applies to patients with TBI or other types of acquired brain injury. The emphasis is on the application of scientist-practitioner standards as they apply to legal questions about the status of a TBI patient and how best that may be achieved. This article introduces each topic area covered in this special edition. PMID:19333063

  18. Health psychology in brain injury rehabilitation services

    OpenAIRE

    Eldred, C.E.

    2006-01-01

    The work carried out in this portfolio was completed while working as a Health Psychologist in Training within a vocational rehabilitation service for adults with acquired brain injury All pieces of work were carried out within this setting expect for the consultancy unit which was carried out within a pilot service delivered by an Adult Disability Team ofa local Social Services. Individuals with acquired brain injury often do not have full understanding of the nature. degree or impact of the...

  19. Gender and environmental effects on regional brain-derived neurotrophic factor expression after experimental traumatic brain injury.

    Science.gov (United States)

    Chen, X; Li, Y; Kline, A E; Dixon, C E; Zafonte, R D; Wagner, A K

    2005-01-01

    Alterations in brain-derived neurotrophic factor expression have been reported in multiple brain regions acutely after traumatic brain injury, however neither injury nor post-injury environmental enrichment has been shown to affect hippocampal brain-derived neurotrophic factor gene expression in male rats chronically post-injury. Studies have demonstrated hormone-related neuroprotection for female rats after traumatic brain injury, and estrogen and exercise both influence brain-derived neurotrophic factor levels. Despite recent studies suggesting that exposure post-traumatic brain injury to environmental enrichment improves cognitive recovery in male rats, we have shown that environmental enrichment mediated improvements with spatial learning are gender specific and only positively affect males. Therefore the purpose of this study was to evaluate the effect of gender and environmental enrichment on chronic post-injury cortical and hippocampal brain-derived neurotrophic factor protein expression. Sprague-Dawley male and cycling female rats were placed into environmental enrichment or standard housing after controlled cortical impact or sham surgery. Four weeks post-surgery, hippocampal and frontal cortex brain-derived neurotrophic factor expression were examined using Western blot. Results revealed significant increases in brain-derived neurotrophic factor expression in the frontal cortex ipsilateral to injury for males (P=0.03). Environmental enrichment did not augment this effect. Neither environmental enrichment nor injury significantly affected cortical brain-derived neurotrophic factor expression for females. In the hippocampus ipsilateral to injury brain-derived neurotrophic factor expression for both males and females was half (49% and 51% respectively) of that observed in shams housed in the standard environment. For injured males, there was a trend in this region for environmental enrichment to restore brain-derived neurotrophic factor levels to sham values

  20. Traumatic Brain Injury: Looking Back, Looking Forward

    Science.gov (United States)

    Bartlett, Sue; Lorenz, Laura; Rankin, Theresa; Elias, Eileen; Weider, Katie

    2011-01-01

    This article is the eighth of a multi-part series on traumatic brain injury (TBI). Historically, TBI has received limited national attention and support. However, since it is the signature injury of the military conflicts in Iraq and Afghanistan, TBI has gained attention of elected officials, military leaders, policymakers, and the public. The…

  1. Plasticity and Inflammation following Traumatic Brain Injury

    OpenAIRE

    Hånell, Anders

    2011-01-01

    Traumatic Brain Injury (TBI) mainly affects young persons in traffic accidents and the elderly in fall accidents. Improvements in the clinical management have significantly improved the outcome following TBI but survivors still suffer from depression, memory problems, personality changes, epilepsy and fatigue. The initial injury starts a series of events that give rise to a secondary injury process and despite several clinical trials there is no drug available for clinical use that targets se...

  2. Functional level after Traumatic Brain Injury

    OpenAIRE

    Sandhaug, Maria

    2012-01-01

    Objectives: The objectives of the thesis were to describe the functional level (papers I and II) and self awareness of functional deficits (paper III) after moderate and severe Traumatic Brain Injury (TBI), and to evaluate the predictive impact of pre-injury and injury-related factors on functional level (papers I, II) and awareness of functional deficits (paper III). Material and methods: Papers I-II were cohort studies of 55 TBI patients (moderate = 21, severe = 34) and 65...

  3. 'Hidden' Brain Injury a Challenge for Military Doctors

    Science.gov (United States)

    ... nih.gov/medlineplus/news/fullstory_159316.html 'Hidden' Brain Injury a Challenge for Military Doctors Potentially fatal ... may suffer from a distinctive pattern of "hidden" brain injury, a small study finds. "Blast-related brain ...

  4. Traumatic brain injuries: Forensic and expertise aspects

    Directory of Open Access Journals (Sweden)

    Vuleković Petar

    2008-01-01

    Full Text Available Introduction. Traumatic brain injuries have major socio-economic importance due to their frequency, high mortality and serious consequences. According to their nature the consequences of these injuries may be classified as neurological, psychiatric and esthetic. Various lesions of brain structures cause neurological consequences such as disturbance of motor functions, sensibility, coordination or involuntary movements, speech disturbances and other deviations, as well as epilepsy. Psychiatric consequences include cognitive deficit, emotional disturbances and behavior disturbances. Criminal-legal aspect of traumatic brain injuries and litigation. Criminal-legal aspect of traumatic brain injuries expertise understands the qualification of these injuries as mild, serious and qualified serious body injuries as well as the expertise about the mechanisms of their occurrence. Litigation expertise includes the estimation of pain, fear, diminished, i.e. lost vital activity and disability, esthetic marring, and psychological suffer based on the diminished general vital activity and esthetic marring. Competence and timing of expertise. Evaluation of consequences of traumatic brain injuries should be performed only when it can be positively confirmed that they are permanent, i.e. at least one year after the injury. Expertise of these injuries is interdisciplinary. Among clinical doctors the most competent medical expert is the one who is in charge for diagnostics and injury treatment, with the recommendation to avoid, if possible, the doctor who conducted treatment. For the estimation of general vital activity, the neurological consequences, pain and esthetic marring expertise, the most competent doctors are neurosurgeon and neurologist. Psychological psychiatric consequences and fear expertise have to be performed by the psychiatrist. Specialists of forensic medicine contribute with knowledge of criminal low and legal expertise.

  5. Centralized rehabilitation after servere traumatic brain injury

    DEFF Research Database (Denmark)

    Engberg, Aase Worså; Liebach, Annette; Nordenbo, Annette Mosbæk

    2006-01-01

    OBJECTIVES: To present results from the first 3 years of centralized subacute rehabilitation after very severe traumatic brain injury (TBI), and to compare results of centralized versus decentralized rehabilitation. MATERIAL AND METHODS: Prospectively, the most severely injured group of adults from...... an uptake area of 2.4 million in Denmark were included at admission to a regional brain injury unit (BIU), on average 19 days after injury. Patients in the retrospective study used for comparison were randomly chosen from the national hospital register. RESULTS AND CONCLUSIONS: Out of 117 patients in...

  6. Reduced heart rate variability in chronic severe traumatic brain injury: Association with impaired emotional and social functioning, and potential for treatment using biofeedback.

    Science.gov (United States)

    Francis, Heather M; Fisher, Alana; Rushby, Jacqueline A; McDonald, Skye

    2016-01-01

    Heart rate variability (HRV) may provide an index of capacity for social functioning and may be remediated by HRV biofeedback. Given reductions in HRV are found following traumatic brain injury (TBI), the present study aimed to determine whether lower HRV in TBI is associated with social function, and whether HRV biofeedback might be a useful remediation technique in this population. Resting state HRV and measures of social and emotional processing were collected in 30 individuals with severe TBI (3-34 years post-injury) and 30 controls. This was followed by a single session of HRV biofeedback. HRV was positively associated with social cognition and empathy, and negatively associated with alexithymia for the TBI group. Both TBI and control groups showed significantly increased HRV on both time-domain (i.e., SDNN, rMSSD) and frequency-domain measures (LF, HF, LF:HF ratio) during biofeedback compared to baseline. These results suggest that decreased HRV is linked to social and emotional function following severe TBI, and may be a novel target for therapy using HRV biofeedback techniques. PMID:25627984

  7. Chronic injuries of the cruciate ligaments

    International Nuclear Information System (INIS)

    The high incidence of cruciate ligament injuries as a result of acute knee trauma with hemartrosis and abuse of diagnostic arthroscopies call for a suitable radiological imaging of the central pivot. Computed Arthrotomography (CAT) was used to examine the knee joint in 20 cases of clinically suspected chronic cruciate ligament injury. The images were correlated with arthroscopic and/or arthrotomic findings. Thirteen lesions of the anterior cruciate ligament (ACL) (65%) were found, plus 1 lesion of the posterior cruciate ligament (PCL) (5%), 2 associated lesions of ACL + PCL (10%), and 4 normal cases. Confirmation of pathology was available in all cases but one by arthroscopy and/or surgery. The central pivot diseases were classified as follows: absence, detachement, partial or complete tear. CAT findings of cruciate ligament injuries are emphasized and the role of the technique as compared to arthroscopy is discussed. CAT is useful in 3-D evaluation of central pivot and detection of different cruciate ligament injuries, with high sensitivity-specifity for ACL and high specifity-moderate sensitivity for PCL. In the evaluation of the chronic unstable knee, CAT is highly accurate and gives the surgeon useful information towards the planning of therapeutic procedures. CAT is almost non-invasive, well tolerated and easy to perform in out-patients, which make it a first-choice procedure in the screening of chronic ligament injuries

  8. Recovery after Brain Injury: Mechanisms and Principles

    Directory of Open Access Journals (Sweden)

    Randolph J. Nudo

    2013-12-01

    Full Text Available The past 20 years have represented an important period in the development of principles underlying neuroplasticity, especially as they apply to recovery from neurological injury. It is now generally accepted that acquired brain injuries, such as occur in stroke or trauma, initiate a cascade of regenerative events that last for at least several weeks, if not months. Many investigators have pointed out striking parallels between post-injury plasticity and the molecular and cellular events that take place during normal brain development. As evidence for the principles and mechanisms underlying post-injury neuroplasticity has been gleaned from both animal models and human populations, novel approaches to therapeutic intervention have been proposed. One important theme has persisted as the sophistication of clinicians and scientists in their knowledge of neuroplasticity mechanisms has grown: Behavioral experience is the most potent modulator of brain plasticity. While there is substantial evidence for this principle in normal, healthy brains, the injured brain is particularly malleable. Based on the quantity and quality of motor experience, the brain can be reshaped after injury in either adaptive or maladaptive ways. This paper reviews selected studies that have demonstrated the neurophysiological and neuroanatomical changes that are triggered by motor experience, by injury, and the interaction of these processes. In addition, recent studies using new and elegant techniques are providing novel perspectives on the events that take place in the injured brain, providing a real-time window into post-injury plasticity. These new approaches are likely to accelerate the pace of basic research, and provide a wealth of opportunities to translate basic principles into therapeutic methodologies.

  9. Manganese: Brain Species and Mechanisms of Brain Injury

    OpenAIRE

    Neth, Katharina

    2016-01-01

    Manganism is a Parkinson-related disease, which can arise by accumulation of the essential trace element manganese (Mn) in the brain by overexposure. Versatile Mn-species and imbalances of trace elements in serum and brain tissue of Mn-exposed rats were analyzed by methods of metallomics. Additionally, non-targeted metabolomics of brain tissue served for analysis of the multilateral mechanisms, which can lead to the neuronal injury. Finally, results from metallomics were correlated to the fin...

  10. Molecular Mechanisms of Cognitive Dysfunction following Traumatic Brain Injury

    Directory of Open Access Journals (Sweden)

    Kendall Rae Walker

    2013-07-01

    Full Text Available Traumatic brain injury (TBI results in significant disability due to cognitive deficits particularly in attention, learning and memory and higher-order executive functions. The role of TBI in chronic neurodegeneration and the development of neurodegenerative diseases including Alzheimer’s disease (AD, Parkinson’s disease (PD, Amyotrophic Lateral Sclerosis (ALS and most recently chronic traumatic encephalopathy (CTE is of particular importance. However, despite significant effort very few therapeutic options exist to prevent or reverse cognitive impairment following TBI. In this review we present experimental evidence of the known secondary injury mechanisms which contribute to neuronal cell loss, axonal injury and synaptic dysfunction and hence cognitive impairment both acutely and chronically following TBI. In particular we focus on the mechanisms linking TBI to the development of two forms of dementia: AD and CTE. We provide evidence of potential molecular mechanisms involved in modulating Aβ and Tau following TBI and provide evidence of the role of these mechanisms in AD pathology. Additionally we propose a mechanism by which Aβ generated as a direct result of TBI is capable of exacerbating secondary injury mechanisms thereby establishing a neurotoxic cascade that leads to chronic neurodegeneration.

  11. Dementia Resulting From Traumatic Brain Injury

    Science.gov (United States)

    Shively, Sharon; Scher, Ann I.; Perl, Daniel P.; Diaz-Arrastia, Ramon

    2013-01-01

    Traumatic brain injury (TBI) is among the earliest illnesses described in human history and remains a major source of morbidity and mortality in the modern era. It is estimated that 2% of the US population lives with long-term disabilities due to a prior TBI, and incidence and prevalence rates are even higher in developing countries. One of the most feared long-term consequences of TBIs is dementia, as multiple epidemiologic studies show that experiencing a TBI in early or midlife is associated with an increased risk of dementia in late life. The best data indicate that moderate and severe TBIs increase risk of dementia between 2-and 4-fold. It is less clear whether mild TBIs such as brief concussions result in increased dementia risk, in part because mild head injuries are often not well documented and retrospective studies have recall bias. However, it has been observed for many years that multiple mild TBIs as experienced by professional boxers are associated with a high risk of chronic traumatic encephalopathy (CTE), a type of dementia with distinctive clinical and pathologic features. The recent recognition that CTE is common in retired professional football and hockey players has rekindled interest in this condition, as has the recognition that military personnel also experience high rates of mild TBIs and may have a similar syndrome. It is presently unknown whether dementia in TBI survivors is pathophysiologically similar to Alzheimer disease, CTE, or some other entity. Such information is critical for developing preventive and treatment strategies for a common cause of acquired dementia. Herein, we will review the epidemiologic data linking TBI and dementia, existing clinical and pathologic data, and will identify areas where future research is needed. PMID:22776913

  12. Minocycline Attenuates Iron-Induced Brain Injury.

    Science.gov (United States)

    Zhao, Fan; Xi, Guohua; Liu, Wenqaun; Keep, Richard F; Hua, Ya

    2016-01-01

    Iron plays an important role in brain injury after intracerebral hemorrhage (ICH). Our previous study found minocycline reduces iron overload after ICH. The present study examined the effects of minocycline on the subacute brain injury induced by iron. Rats had an intracaudate injection of 50 μl of saline, iron, or iron + minocycline. All the animals were euthanized at day 3. Rat brains were used for immunohistochemistry (n = 5-6 per each group) and Western blotting assay (n = 4). Brain swelling, blood-brain barrier (BBB) disruption, and iron-handling proteins were measured. We found that intracerebral injection of iron resulted in brain swelling, BBB disruption, and brain iron-handling protein upregulation (p < 0.05). The co-injection of minocycline with iron significantly reduced iron-induced brain swelling (n = 5, p < 0.01). Albumin, a marker of BBB disruption, was measured by Western blot analysis. Minocycline significantly decreased albumin protein levels in the ipsilateral basal ganglia (p < 0.01). Iron-handling protein levels in the brain, including ceruloplasmin and transferrin, were reduced in the minocycline co-injected animals. In conclusion, the present study suggests that minocycline attenuates brain swelling and BBB disruption via an iron-chelation mechanism. PMID:26463975

  13. Epileptogenesis after traumatic brain injury in Plau-deficient mice.

    Science.gov (United States)

    Bolkvadze, Tamuna; Rantala, Jukka; Puhakka, Noora; Andrade, Pedro; Pitkänen, Asla

    2015-10-01

    Several components of the urokinase-type plasminogen activator receptor (uPAR)-interactome, including uPAR and its ligand sushi-repeat protein 2, X-linked (SRPX2), are linked to susceptibility to epileptogenesis in animal models and/or humans. Recent evidence indicates that urokinase-type plasminogen activator (uPA), a uPAR ligand with focal proteinase activity in the extracellular matrix, contributes to recovery-enhancing brain plasticity after various epileptogenic insults such as traumatic brain injury (TBI) and status epilepticus. Here, we examined whether deficiency of the uPA-encoding gene Plau augments epileptogenesis after TBI. Traumatic brain injury was induced by controlled cortical impact in the somatosensory cortex of adult male wild-type and Plau-deficient mice. Development of epilepsy and seizure susceptibility were assessed with a 3-week continuous video-electroencephalography monitoring and a pentylenetetrazol test, respectively. Traumatic brain injury-induced cortical or hippocampal pathology did not differ between genotypes. The pentylenetetrazol test revealed increased seizure susceptibility after TBI (p<0.05) in injured mice. Epileptogenesis was not exacerbated, however, in Plau-deficient mice. Taken together, Plau deficiency did not worsen controlled cortical impact-induced brain pathology or epileptogenesis caused by TBI when assessed at chronic timepoints. These data expand previous observations on Plau deficiency in models of status epilepticus and suggest that inhibition of focal extracellular proteinase activity resulting from uPA-uPAR interactions does not modify epileptogenesis after TBI. PMID:26253597

  14. Managing traumatic brain injury secondary to explosions

    Directory of Open Access Journals (Sweden)

    Burgess Paula

    2010-01-01

    Full Text Available Explosions and bombings are the most common deliberate cause of disasters with large numbers of casualties. Despite this fact, disaster medical response training has traditionally focused on the management of injuries following natural disasters and terrorist attacks with biological, chemical, and nuclear agents. The following article is a clinical primer for physicians regarding traumatic brain injury (TBI caused by explosions and bombings. The history, physics, and treatment of TBI are outlined.

  15. Time dysperception perspective for acquired brain injury

    Directory of Open Access Journals (Sweden)

    Federica ePiras

    2014-01-01

    Full Text Available Distortions of time perception are presented by a number of neuropsychiatric disorders. Here we survey timing abilities in clinical populations with acquired brain injuries in key cerebral areas recently implicated in human studies of timing. We purposely analyzed the complex relationship between cognitive and contextual factors involved in time estimation, as to characterize the correlation between timed and other cognitive behaviors in each group. We assume that interval timing is a solid construct to study cognitive dysfunctions following brain injury, as timing performance is a sensitive metric of information processing, while temporal cognition has the potential of influencing a wide range of cognitive processes. Moreover, temporal performance is a sensitive assay of damage to the underlying neural substrate after a brain insult. Further research in neurological and psychiatric patients will definitively answer the question of whether time distortions are manifestations of cognitive and behavioral symptoms of brain damage and definitively clarify their mechanisms.

  16. Prehospital Care of Traumatic Brain Injury

    Directory of Open Access Journals (Sweden)

    TVSP Murthy

    2008-01-01

    Full Text Available Traumatic brain injury (TBI occurs when a sudden trauma causes brain damage. Depending on the severity, outcome can be anything from complete recovery to permanent disability or death. Emergency medical services play a dominant role in provision of primary care at the site of injury. Since little can be done to reverse the initial brain damage due to trauma, attempts to prevent further brain damage and stabilize the patient before he can be brought to a specialized trauma care centre play a pivotal role in the final outcome. Recognition and early treatment of hypoten-sion, hypoxemia, and hypoglycemia, objective neurological assessment based on GCS and pupils, and safe transport to an optimal care centre are the key elements of prehospital care of a TBI patient.

  17. Brain SPECT in severs traumatic head injury

    International Nuclear Information System (INIS)

    The aim of this work was to compare the results of the early brain scintigraphy in traumatic brain injury to the long term neuropsychological behavior. Twenty four patients had an ECD-Tc99m SPECT, within one month after the trauma; scintigraphic abnormalities were evaluated according to a semi-quantitative analysis. The neuropsychological clinical investigation was interpreted by a synthetic approach to evaluate abnormalities related to residual motor deficit, frontal behavior, memory and language disorders. Fourteen patients (58%) had sequela symptoms. SPECT revealed 80 abnormalities and CT scan only 31. Statistical analysis of uptake values showed significantly lower uptake in left basal ganglia and brain stem in patients with sequela memory disorders. We conclude that the brain perfusion scintigraphy is able to detect more lesions than CT and that it could really help to predict the neuropsychological behavior after severe head injury. Traumatology could become in the future a widely accepted indication of perfusion SPECT. (authors)

  18. Chronic complications of spinal cord injury

    OpenAIRE

    Sezer, Nebahat; Akkuş, Selami; Uğurlu, Fatma Gülçin

    2015-01-01

    Spinal cord injury (SCI) is a serious medical condition that causes functional, psychological and socioeconomic disorder. Therefore, patients with SCI experience significant impairments in various aspects of their life. The goals of rehabilitation and other treatment approaches in SCI are to improve functional level, decrease secondary morbidity and enhance health-related quality of life. Acute and long-term secondary medical complications are common in patients with SCI. However, chronic com...

  19. Progress in imaging of brain radiation injury

    International Nuclear Information System (INIS)

    The mechanisms of brain radiation injury mainly include three hypotheses: vascular injury, glial cells damage and immune response. Most scholars' studies have recently supported the former two ones. Vascular injury plays a major role in the effect of delayed radiation injury. Focal brain injury and diffuse white matter injury can be definitely diagnosed by CT and MRI. T2-weighted imaging (T2WI) in MRI shows high sensitivity in water contents, and is not affected by the beam hardening artifacts from the cranial base. Compared with CT, the sensitivity of MR for detecting white matter lesions is two to threefold higher. When lesions occurs at the site of an irradiated cerebral tumor, tumor recurrence and focal cerebral necrosis cannot be differentiated by CT or MR, PET and MRS now present a certain advantage of differential diagnosis. Tumor presents high metabolism and necrosis demonstrates low metabolism by utilizing PET scanning, however PET's sensitivity and specificity are far from satisfactory. The amount or ratio of metabolic products in the region of interest measured by MRS contributes to the deferential diagnosis. In addition, PET functional imaging and MRS can also predict the early asymptomatic reversible radiation injury so as to allow the early therapy of steroids and possibly other drugs, prior to the development of irreversible changes

  20. Resting Network Plasticity Following Brain Injury

    OpenAIRE

    Toru Nakamura; Hillary, Frank G.; Biswal, Bharat B.

    2009-01-01

    The purpose of this study was to examine neural network properties at separate time-points during recovery from traumatic brain injury (TBI) using graph theory. Whole-brain analyses of the topological properties of the fMRI signal were conducted in 6 participants at 3 months and 6 months following severe TBI. Results revealed alterations of network properties including a change in the degree distribution, reduced overall strength in connectivity, and increased "small-worldness" from 3 months ...

  1. Plasticity and Injury in the Developing Brain

    OpenAIRE

    Johnston, Michael V.; Ishida, Akira; ISHIDA, Wako Nakajima; MATSUSHITA, Hiroko Baber; NISHIMURA, Akira; Tsuji, Masahiro

    2008-01-01

    The child’s brain is more malleable or plastic than that of adults and this accounts for the ability of children to learn new skills quickly or recovery from brain injuries. Several mechanisms contribute to this ability including overproduction and deletion of neurons and synapses, and activity-dependent stabilization of synapses. The molecular mechanisms for activity dependent synaptic plasticity are being discovered and this is leading to a better understanding of the pathogenesis of severa...

  2. Modeling premature brain injury and recovery

    OpenAIRE

    Scafidi, Joey; Fagel, Devon M.; Ment, Laura R.; Vaccarino, Flora M.

    2009-01-01

    Premature birth is a growing and significant public health problem because of the large number of infants that survive with neurodevelopmental sequelae from brain injury. Recent advances in neuroimaging have shown that although some neuroanatomical structures are altered, others improve over time. This review outlines recent insights into brain structure and function in these preterm infants at school age and relevant animal models. These animal models have provided scientists with an opportu...

  3. Interleukin-1 and acute brain injury

    Directory of Open Access Journals (Sweden)

    Katie N Murray

    2015-02-01

    Full Text Available Inflammation is the key host-defense response to infection and injury, yet also a major contributor to a diverse range of diseases, both peripheral and central in origin. Brain injury as a result of stroke or trauma is a leading cause of death and disability worldwide, yet there are no effective treatments, resulting in enormous social and economic costs. Increasing evidence, both preclinical and clinical, highlights inflammation as an important factor in stroke, both in determining outcome and as a contributor to risk. A number of inflammatory mediators have been proposed as key targets for intervention to reduce the burden of stroke, several reaching clinical trial, but as yet yielding no success. Many factors could explain these failures, including the lack of robust preclinical evidence and poorly designed clinical trials, in addition to the complex nature of the clinical condition. Lack of consideration in preclinical studies of associated co-morbidities prevalent in the clinical stroke population is now seen as an important omission in previous work. These co-morbidities (atherosclerosis, hypertension, diabetes, infection have a strong inflammatory component, supporting the need for greater understanding of how inflammation contributes to acute brain injury. Interleukin (IL-1 is the prototypical pro-inflammatory cytokine, first identified many years ago as the endogenous pyrogen. Research over the last 20 years or so reveals that IL-1 is an important mediator of neuronal injury and blocking the actions of IL-1 is beneficial in a number of experimental models of brain damage. Mechanisms underlying the actions of IL-1 in brain injury remain unclear, though increasing evidence indicates the cerebrovasculature as a key target. Recent literature supporting this and other aspects of how IL-1 and systemic inflammation in general contribute to acute brain injury are discussed in this review.

  4. Functional brain imaging to investigate the higher brain dysfunction induced by diffuse brain injury

    International Nuclear Information System (INIS)

    Higher brain dysfunction is the major problem of patients who recover from neurotrauma the prevents them from returning to their previous social life. Many such patients do not have focal brain damage detected with morphological imaging. We focused on studying the focal brain dysfunction that can be detected only with functional imaging with positron emission tomography (PET) in relation to the score of various cognition batteries. Patients who complain of higher brain dysfunction without apparent morphological cortical damage were recruited for this study. Thirteen patients with diffuse axonal injury (DAI) or cerebral concussion was included. They underwent a PET study to image glucose metabolism by 18F-fluorodeoxyglucose (FDG), and central benodiazepine receptor (cBZD-R) (marker of neuronal body) by 11C-flumazenil, together with cognition measurement by WAIS-R, WMS-R, and WCST etc. PET data were compared with age matched normal controls using statistical parametric mapping (SPM)2. DAI patients had a significant decrease in glucose matabolism and cBZD-R distribution in the cingulated cortex than normal controls. Patients diagnosed with concussion because of shorter consciousness disturbance also had abnormal FDG uptake and cBZD-R distribution. Cognition test scores were variable among patients. Degree of decreased glucose metabolism and cBZD-R distribution in the dominant hemishphere corresponded well to the severity of cognitive disturbance. PET molecular imaging was useful to depict focal cortical dysfunction of neurotrauma patients even when morphological change was not apparent. This method may be promising to clarify the pathophysiology of higher brain dysfunction of patients with diffuse axonal injury or chronic traumatic encephalopathy. (author)

  5. Organic brain syndrome

    Science.gov (United States)

    OBS; Organic mental disorder (OMS); Chronic organic brain syndrome ... Listed below are disorders associated with OBS. Brain injury caused by ... the brain ( subarachnoid hemorrhage ) Blood clot inside the ...

  6. Brain injury biomechanics in closed-head impact : Studies on injury epidemiology, tolerance criteria, biomechanics and traffic injury prevention

    OpenAIRE

    Viano, David

    1997-01-01

    Permanent disability from traumatic brain injury is a devastating consequence of traffic crashes. Injury prevention is a fruitful approach to reduce the incidence and severity of disabling brain injury. However, the development of effective prevention techniques requires better knowledge on the mechanisms and biomechanics of brain injury in closed-head impact. The overall aim of this study is focused on brain injury mechanisms, biomechanics, and tolerances in closed-head ...

  7. Chronic Treatment with a Water-Soluble Extract from the Culture Medium of Ganoderma lucidum Mycelia Prevents Apoptosis and Necroptosis in Hypoxia/Ischemia-Induced Injury of Type 2 Diabetic Mouse Brain

    Directory of Open Access Journals (Sweden)

    Meiyan Xuan

    2015-01-01

    Full Text Available Type 2 diabetes mellitus has been known to increase systemic oxidative stress by chronic hyperglycemia and visceral obesity and aggravate cerebral ischemic injury. On the basis of our previous study regarding a water-soluble extract from the culture medium of Ganoderma lucidum mycelia (designed as MAK, which exerts antioxidative and neuroprotective effects, the present study was conducted to evaluate the preventive effects of MAK on apoptosis and necroptosis (a programmed necrosis induced by hypoxia/ischemia (H/I in type 2 diabetic KKAy mice. H/I was induced by a combination of unilateral common carotid artery ligation with hypoxia (8% O2 for 20 min and subsequent reoxygenation. Pretreatment with MAK (1 g/kg, p.o. for a week significantly reduced H/I-induced neurological deficits and brain infarction volume assessed at 24 h of reoxygenation. Histochemical analysis showed that MAK significantly suppressed superoxide production, neuronal cell death, and vacuolation in the ischemic penumbra, which was accompanied by a decrease in the numbers of TUNEL- or cleaved caspase-3-positive cells. Furthermore, MAK decreased the expression of receptor-interacting protein kinase 3 mRNA and protein, a key molecule for necroptosis. These results suggest that MAK confers resistance to apoptotic and necroptotic cell death and relieves H/I-induced cerebral ischemic injury in type 2 diabetic mice.

  8. Chronic Treatment with a Water-Soluble Extract from the Culture Medium of Ganoderma lucidum Mycelia Prevents Apoptosis and Necroptosis in Hypoxia/Ischemia-Induced Injury of Type 2 Diabetic Mouse Brain.

    Science.gov (United States)

    Xuan, Meiyan; Okazaki, Mari; Iwata, Naohiro; Asano, Satoshi; Kamiuchi, Shinya; Matsuzaki, Hirokazu; Sakamoto, Takeshi; Miyano, Yoshiyuki; Iizuka, Hiroshi; Hibino, Yasuhide

    2015-01-01

    Type 2 diabetes mellitus has been known to increase systemic oxidative stress by chronic hyperglycemia and visceral obesity and aggravate cerebral ischemic injury. On the basis of our previous study regarding a water-soluble extract from the culture medium of Ganoderma lucidum mycelia (designed as MAK), which exerts antioxidative and neuroprotective effects, the present study was conducted to evaluate the preventive effects of MAK on apoptosis and necroptosis (a programmed necrosis) induced by hypoxia/ischemia (H/I) in type 2 diabetic KKAy mice. H/I was induced by a combination of unilateral common carotid artery ligation with hypoxia (8% O2 for 20 min) and subsequent reoxygenation. Pretreatment with MAK (1 g/kg, p.o.) for a week significantly reduced H/I-induced neurological deficits and brain infarction volume assessed at 24 h of reoxygenation. Histochemical analysis showed that MAK significantly suppressed superoxide production, neuronal cell death, and vacuolation in the ischemic penumbra, which was accompanied by a decrease in the numbers of TUNEL- or cleaved caspase-3-positive cells. Furthermore, MAK decreased the expression of receptor-interacting protein kinase 3 mRNA and protein, a key molecule for necroptosis. These results suggest that MAK confers resistance to apoptotic and necroptotic cell death and relieves H/I-induced cerebral ischemic injury in type 2 diabetic mice. PMID:25945116

  9. Recovery of resting brain connectivity ensuing mild traumatic brain injury

    Directory of Open Access Journals (Sweden)

    Rose Dawn Bharath

    2015-09-01

    Full Text Available Brains reveal amplified plasticity as they recover from an injury. We aimed to define time dependent plasticity changes in patients recovering from mild traumatic brain injury (mTBI. 25 subjects with mild head injury were longitudinally evaluated within 36 hours, 3 and 6 months using resting state functional connectivity (RSFC. Region of interest (ROI based connectivity differences over time within the patient group and in comparison with a healthy control group were analyzed at p<0.005. We found 33 distinct ROI pairs that revealed significant changes in their connectivity strength with time. Within three months, the majority of the ROI pairs had decreased connectivity in mTBI population, which increased and became comparable to healthy controls at 6 months. Initial imaging within 36 hours of injury revealed hyper connectivity predominantly involving the salience network and default mode network, which reduced at 3 months when lingual, inferior frontal and fronto-parietal networks revealed hyper connectivity. At six months all the evaluated networks revealed hyper connectivity and became comparable to the healthy controls. Our findings in a fairly homogenous group of patients with mTBI evaluated during the 6 month window of recovery defines time varying brain connectivity changes as the brain recovers from an injury. A majority of these changes were seen in the frontal and parietal lobes between 3-6 months after injury. Hyper connectivity of several networks supported normal recovery in the first six months and it remains to be seen in future studies whether this can predict an early and efficient recovery of brain function.

  10. Cerebral Blood Flow and Autoregulation after Pediatric Traumatic Brain Injury

    OpenAIRE

    Udomphorn, Yuthana; Armstead, William M.; Vavilala, Monica S.

    2008-01-01

    Traumatic brain injury is a global health concern and is the leading cause of traumatic morbidity and mortality in children. Despite a lower overall mortality than in adult traumatic brain injury, the cost to society from the sequelae of pediatric traumatic brain injury is very high. Predictors of poor outcome after traumatic brain injury include altered systemic and cerebral physiology, including altered cerebral hemodynamics. Cerebral autoregulation is often impaired following traumatic bra...

  11. Working with Students with Traumatic Brain Injury

    Science.gov (United States)

    Lucas, Matthew D.

    2010-01-01

    The participation of a student with Traumatic Brain Injury (TBI) in general physical education can often be challenging and rewarding for the student and physical education teacher. This article addresses common characteristics of students with TBI and presents basic solutions to improve the education of students with TBI in the general physical…

  12. Mild Traumatic Brain Injury: Facilitating School Success.

    Science.gov (United States)

    Hux, Karen; Hacksley, Carolyn

    1996-01-01

    A case study is used to demonstrate the effects of mild traumatic brain injury on educational efforts. Discussion covers factors complicating school reintegration, ways to facilitate school reintegration, identification of cognitive and behavioral consequences, minimization of educators' discomfort, reintegration program design, and family…

  13. Group Treatment in Acquired Brain Injury Rehabilitation

    Science.gov (United States)

    Bertisch, Hilary; Rath, Joseph F.; Langenbahn, Donna M.; Sherr, Rose Lynn; Diller, Leonard

    2011-01-01

    The current article describes critical issues in adapting traditional group-treatment methods for working with individuals with reduced cognitive capacity secondary to acquired brain injury. Using the classification system based on functional ability developed at the NYU Rusk Institute of Rehabilitation Medicine (RIRM), we delineate the cognitive…

  14. New Antioxidant Drugs for Neonatal Brain Injury

    Directory of Open Access Journals (Sweden)

    Maria Luisa Tataranno

    2015-01-01

    Full Text Available The brain injury concept covers a lot of heterogeneity in terms of aetiology involving multiple factors, genetic, hemodynamic, metabolic, nutritional, endocrinological, toxic, and infectious mechanisms, acting in antenatal or postnatal period. Increased vulnerability of the immature brain to oxidative stress is documented because of the limited capacity of antioxidant enzymes and the high free radicals (FRs generation in rapidly growing tissue. FRs impair transmembrane enzyme Na+/K+-ATPase activity resulting in persistent membrane depolarization and excessive release of FR and excitatory aminoacid glutamate. Besides being neurotoxic, glutamate is also toxic to oligodendroglia, via FR effects. Neuronal cells die of oxidative stress. Excess of free iron and deficient iron/binding metabolising capacity are additional features favouring oxidative stress in newborn. Each step in the oxidative injury cascade has become a potential target for neuroprotective intervention. The administration of antioxidants for suspected or proven brain injury is still not accepted for clinical use due to uncertain beneficial effects when treatments are started after resuscitation of an asphyxiated newborn. The challenge for the future is the early identification of high-risk babies to target a safe and not toxic antioxidant therapy in combination with standard therapies to prevent brain injury and long-term neurodevelopmental impairment.

  15. Traumatic Brain Injury: Nuclear Medicine Neuroimaging

    NARCIS (Netherlands)

    Sánchez-Catasús, Carlos A; Vállez Garcia, David; Le Riverend Morales, Eloísa; Galvizu Sánchez, Reinaldo; Dierckx, Rudi; Dierckx, Rudi AJO; Otte, Andreas; de Vries, Erik FJ; van Waarde, Aren; Leenders, Klaus L

    2014-01-01

    This chapter provides an up-to-date review of nuclear medicine neuroimaging in traumatic brain injury (TBI). 18F-FDG PET will remain a valuable tool in researching complex mechanisms associated with early metabolic dysfunction in TBI. Although evidence-based imaging studies are needed, 18F-FDG PET i

  16. Narrative Language in Traumatic Brain Injury

    Science.gov (United States)

    Marini, Andrea; Galetto, Valentina; Zampieri, Elisa; Vorano, Lorenza; Zettin, Marina; Carlomagno, Sergio

    2011-01-01

    Persons with traumatic brain injury (TBI) often show impaired linguistic and/or narrative abilities. The present study aimed to document the features of narrative discourse impairment in a group of adults with TBI. 14 severe TBI non-aphasic speakers (GCS less than 8) in the phase of neurological stability and 14 neurologically intact participants…

  17. Traumatic Brain Injury and Personality Change

    Science.gov (United States)

    Fowler, Marc; McCabe, Paul C.

    2011-01-01

    Traumatic brain injury (TBI) is the leading cause of death and lifelong disability in the United States for individuals below the age of 45. Current estimates from the Center for Disease Control (CDC) indicate that at least 1.4 million Americans sustain a TBI annually. TBI affects 475,000 children under age 14 each year in the United States alone.…

  18. Interviewing Children with Acquired Brain Injury (ABI)

    Science.gov (United States)

    Boylan, Anne-Marie; Linden, Mark; Alderdice, Fiona

    2009-01-01

    Research into the lives of children with acquired brain injury (ABI) often neglects to incorporate children as participants, preferring to obtain the opinions of the adult carer (e.g. McKinlay et al., 2002). There has been a concerted attempt to move away from this position by those working in children's research with current etiquette…

  19. Monitoring Agitated Behavior After acquired Brain Injury

    DEFF Research Database (Denmark)

    Aadal, Lena; Mortensen, Jesper; Nielsen, Jørgen Feldbaek

    2015-01-01

    Purpose: To describe the onset, duration, intensity, and nursing shift variation of agitated behavior in patients with acquired brain injury (ABI) at a rehabilitation hospital. Design: Prospective descriptive study. Methods: A total of 11 patients with agitated behavior were included. Agitated...

  20. Relatives of patients with severe brain injury

    DEFF Research Database (Denmark)

    Norup, Anne; Petersen, Janne; Lykke Mortensen, Erik

    2015-01-01

    PRIMARY OBJECTIVE: To investigate trajectories and predictors of trajectories of anxiety and depression in relatives of patients with a severe brain injury during the first year after injury. RESEARCH DESIGN: A prospective longitudinal study with four repeated measurements. SUBJECTS: Ninety...... relatives of patients with severe brain injury. METHODS: The relatives were assessed on the anxiety and depression scales from the Symptom Checklist-90-Revised and latent variable growth curve models were used to model the trajectories. The effects of patient's age, patient's Glasgow Coma Score, level of...... function and consciousness, gender and relationship of the relatives were modelled. RESULTS: Improvement was found in both symptoms of anxiety and depression during the 12-month study period. The analysis revealed different trajectories for symptoms of anxiety and depression, as anxiety had a more rapid...

  1. Resting network plasticity following brain injury.

    Directory of Open Access Journals (Sweden)

    Toru Nakamura

    Full Text Available The purpose of this study was to examine neural network properties at separate time-points during recovery from traumatic brain injury (TBI using graph theory. Whole-brain analyses of the topological properties of the fMRI signal were conducted in 6 participants at 3 months and 6 months following severe TBI. Results revealed alterations of network properties including a change in the degree distribution, reduced overall strength in connectivity, and increased "small-worldness" from 3 months to 6 months post injury. The findings here indicate that, during recovery from injury, the strength but not the number of network connections diminishes, so that over the course of recovery, the network begins to approximate what is observed in healthy adults. These are the first data examining functional connectivity in a disrupted neural system during recovery.

  2. Clinics in diagnostic imaging (153). Severe hypoxic ischaemic brain injury.

    OpenAIRE

    Chua, Wynne; Lim, Boon Keat; Lim, Tchoyoson Choie Cheio

    2014-01-01

    A 58-year-old Indian woman presented with asystole after an episode of haemetemesis, with a patient downtime of 20 mins. After initial resuscitation efforts, computed tomography of the brain, obtained to evaluate neurological injury, demonstrated evidence of severe hypoxic ischaemic brain injury. The imaging features of hypoxic ischaemic brain injury and the potential pitfalls with regard to image interpretation are herein discussed.

  3. Defense Centers of Excellence for Psychological Health & Traumatic Brain Injury

    Science.gov (United States)

    ... Defense Centers of Excellence For Psychological Health & Traumatic Brain Injury U.S. Department of Defense About DCoE Centers Leadership ... PTSD Suicide Prevention Provider Resources DCoE Resources Traumatic Brain Injury About Traumatic Brain Injury Tips for Treating mTBI ...

  4. Clinical Outcomes after Traumatic Brain Injury.

    Science.gov (United States)

    Sandsmark, Danielle K

    2016-06-01

    Traumatic brain injury (TBI) is a major cause of death and disability that often affects young people. After injury, the degree of recovery can be highly variable, with some people regaining near complete function while others remain severely disabled. Understanding what factors influence recovery is important for counseling patients and families in the acute period after injury and can help guide therapeutic decisions in the acute period following injury. In this review, prognostic algorithms useful for clinicians are discussed. Tools for grading patient outcomes, their role in clinical care and research studies, and their limitations are reviewed. Ongoing work focusing on the development of biomarkers to track TBI recovery and the refinement of clinical outcome metrics is summarized. PMID:27072952

  5. Forensic Pathology of Traumatic Brain Injury.

    Science.gov (United States)

    Finnie, J W

    2016-09-01

    Traumatic brain injury constitutes a significant proportion of cases requiring forensic examination, and it encompasses (1) blunt, nonmissile head injury, especially involving motor vehicle accidents, and (2) penetrating, missile injury produced by a range of high- and lower-velocity projectiles. This review examines the complex pathophysiology and biomechanics of both types of neurotrauma and assesses the macroscopic and histologic features of component lesions, which may be used to determine the cause and manner of death resulting from an intentional assault or accident. Estimation of the survival time postinjury by pathologic examination is also important where malicious head injury is suspected, in an attempt to ascertain a time at which the traumatic event might have been committed, thereby evaluating the authenticity of statements made by the alleged perpetrator. PMID:26578643

  6. Simvastatin Treatment in Traumatic Brain Injury: Operation Brain Trauma Therapy.

    Science.gov (United States)

    Mountney, Andrea; Bramlett, Helen M; Dixon, C Edward; Mondello, Stefania; Dietrich, W Dalton; Wang, Kevin K W; Caudle, Krista; Empey, Philip E; Poloyac, Samuel M; Hayes, Ronald L; Povlishock, John T; Tortella, Frank C; Kochanek, Patrick M; Shear, Deborah A

    2016-03-15

    Simvastatin, the fourth drug selected for testing by Operation Brain Trauma Therapy (OBTT), is a 3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitor used clinically to reduce serum cholesterol. In addition, simvastatin has demonstrated potent antineuroinflammatory and brain edema reducing effects and has shown promise in promoting functional recovery in pre-clinical models of traumatic brain injury (TBI). The purpose of this study was to assess the potential neuroprotective effects of oral administration of simvastatin on neurobehavioral, biomarker, and histopathological outcome measures compared across three pre-clinical TBI animal models. Adult male Sprague-Dawley rats were exposed to either moderate fluid percussion injury (FPI), controlled cortical impact injury (CCI), or penetrating ballistic-like brain injury (PBBI). Simvastatin (1 or 5 mg/kg) was delivered via oral gavage at 3 h post-injury and continued once daily out to 14 days post-injury. Results indicated an intermediate beneficial effect of simvastatin on motor performance on the gridwalk (FPI), balance beam (CCI), and rotarod tasks (PBBI). No significant therapeutic benefit was detected, however, on cognitive outcome across the OBTT TBI models. In fact, Morris water maze (MWM) performance was actually worsened by treatment in the FPI model and scored full negative points for low dose in the MWM latency and swim distance to locate the hidden platform. A detrimental effect on cortical tissue loss was also seen in the FPI model, and there were no benefits on histology across the other models. Simvastatin also produced negative effects on circulating glial fibrillary acidic protein biomarker outcomes that were evident in the FPI and PBBI models. Overall, the current findings do not support the beneficial effects of simvastatin administration over 2 weeks post-TBI using the oral route of administration and, as such, it will not be further pursued by OBTT. PMID:26541177

  7. Update of Endocrine Dysfunction following Pediatric Traumatic Brain Injury

    Directory of Open Access Journals (Sweden)

    Kent Reifschneider

    2015-07-01

    Full Text Available Traumatic brain injuries (TBI are common occurrences in childhood, often resulting in long term, life altering consequences. Research into endocrine sequelae following injury has gained attention; however, there are few studies in children. This paper reviews the pathophysiology and current literature documenting risk for endocrine dysfunction in children suffering from TBI. Primary injury following TBI often results in disruption of the hypothalamic-pituitary-adrenal axis and antidiuretic hormone production and release, with implications for both acute management and survival. Secondary injuries, occurring hours to weeks after TBI, result in both temporary and permanent alterations in pituitary function. At five years after moderate to severe TBI, nearly 30% of children suffer from hypopituitarism. Growth hormone deficiency and disturbances in puberty are the most common; however, any part of the hypothalamic-pituitary axis can be affected. In addition, endocrine abnormalities can improve or worsen with time, having a significant impact on children’s quality of life both acutely and chronically. Since primary and secondary injuries from TBI commonly result in transient or permanent hypopituitarism, we conclude that survivors should undergo serial screening for possible endocrine disturbances. High indices of suspicion for life threatening endocrine deficiencies should be maintained during acute care. Additionally, survivors of TBI should undergo endocrine surveillance by 6–12 months after injury, and then yearly, to ensure early detection of deficiencies in hormonal production that can substantially influence growth, puberty and quality of life.

  8. Respiratory mechanics in brain injury: A review.

    Science.gov (United States)

    Koutsoukou, Antonia; Katsiari, Maria; Orfanos, Stylianos E; Kotanidou, Anastasia; Daganou, Maria; Kyriakopoulou, Magdalini; Koulouris, Nikolaos G; Rovina, Nikoletta

    2016-02-01

    Several clinical and experimental studies have shown that lung injury occurs shortly after brain damage. The responsible mechanisms involve neurogenic pulmonary edema, inflammation, the harmful action of neurotransmitters, or autonomic system dysfunction. Mechanical ventilation, an essential component of life support in brain-damaged patients (BD), may be an additional traumatic factor to the already injured or susceptible to injury lungs of these patients thus worsening lung injury, in case that non lung protective ventilator settings are applied. Measurement of respiratory mechanics in BD patients, as well as assessment of their evolution during mechanical ventilation, may lead to preclinical lung injury detection early enough, allowing thus the selection of the appropriate ventilator settings to avoid ventilator-induced lung injury. The aim of this review is to explore the mechanical properties of the respiratory system in BD patients along with the underlying mechanisms, and to translate the evidence of animal and clinical studies into therapeutic implications regarding the mechanical ventilation of these critically ill patients. PMID:26855895

  9. Magnetic resonance imaging in diffuse brain injury

    International Nuclear Information System (INIS)

    Forty cases diagnosed as diffuse brain injury (DBI) were studied by magnetic resonance imaging (MRI) performed within 3 days after injury. These cases were divided into two groups, which were the concussion group and diffuse axonal injury (DAI) group established by Gennarelli. There were no findings on computerized tomography (CT) in the concussion group except for two cases which had a brain edema or subarachnoid hemorrhage. But on MRI, high intensity areas on T2 weighted imaging were demonstrated in the cerebral white matter in this group. Many lesions in this group were thought to be edemas of the cerebral white matter, because of the fact that on serial MRI, they were isointense. In mild types of DAI, the lesions on MRI were located only in the cerebral white matter, whereas, in the severe types of DAI, lesions were located in the basal ganglia, the corpus callosum, the dorsal part of the brain stem as well as in the cerebral white matter. As for CT findings, parenchymal lesions were not visualized especially in mild DAI. Our results suggested that the lesions in cerebral concussion were edemas in cerebral white matter. In mild DAI they were non-hemorrhagic contusion; and in severe DAI they were hemorrhagic contusions in the cerebral white matter, the basal ganglia, the corpus callosum or the dorsal part of the brain stem. (author)

  10. Magnetic resonance imaging in diffuse brain injury

    Energy Technology Data Exchange (ETDEWEB)

    Yokota, Hiroyuki; Yasuda, Kazuhiro; Mashiko, Kunihiro; Henmi, Hiroshi; Otsuka, Toshibumi; Kobayashi, Shiro; Nakazawa, Shozo (Nippon Medical School, Tokyo (Japan))

    1992-01-01

    Forty cases diagnosed as diffuse brain injury (DBI) were studied by magnetic resonance imaging (MRI) performed within 3 days after injury. These cases were divided into two groups, which were the concussion group and diffuse axonal injury (DAI) group established by Gennarelli. There were no findings on computerized tomography (CT) in the concussion group except for two cases which had a brain edema or subarachnoid hemorrhage. But on MRI, high intensity areas on T2 weighted imaging were demonstrated in the cerebral white matter in this group. Many lesions in this group were thought to be edemas of the cerebral white matter, because of the fact that on serial MRI, they were isointense. In mild types of DAI, the lesions on MRI were located only in the cerebral white matter, whereas, in the severe types of DAI, lesions were located in the basal ganglia, the corpus callosum, the dorsal part of the brain stem as well as in the cerebral white matter. As for CT findings, parenchymal lesions were not visualized especially in mild DAI. Our results suggested that the lesions in cerebral concussion were edemas in cerebral white matter. In mild DAI they were non-hemorrhagic contusion; and in severe DAI they were hemorrhagic contusions in the cerebral white matter, the basal ganglia, the corpus callosum or the dorsal part of the brain stem. (author).

  11. Traumatic brain injury and olfactory deficits

    DEFF Research Database (Denmark)

    Fortin, Audrey; Lefebvre, Mathilde Beaulieu; Ptito, Maurice

    2010-01-01

    PRIMARY OBJECTIVE: Olfactory functions are not systematically evaluated following traumatic brain injury (TBI). This study aimed at comparing two smell tests that are used in a clinical setting. RESEARCH DESIGN: The University of Pennsylvania Smell Identification Test (UPSIT) and the Alberta Smell....... RESULTS: The scores of the two smell tests were significantly correlated. Both tests indicated that patients with frontal lesion performed significantly worse than patients with other types of lesion. Mood and injury severity were not associated with olfactory impairment when age was taken into account...... Alberta Smell test. To refine their diagnosis, the UPSIT can also be used....

  12. Surviving severe traumatic brain injury in Denmark

    DEFF Research Database (Denmark)

    Odgaard, Lene; Poulsen, Ingrid; Kammersgaard, Lars Peter;

    2015-01-01

    PURPOSE: To identify all hospitalized patients surviving severe traumatic brain injury (TBI) in Denmark and to compare these patients to TBI patients admitted to highly specialized rehabilitation (HS-rehabilitation). PATIENTS AND METHODS: Patients surviving severe TBI were identified from The...... severe TBI were admitted to HS-rehabilitation. Female sex, older age, and non-working status pre-injury were independent predictors of no HS-rehabilitation among patients surviving severe TBI. CONCLUSION: The incidence rate of hospitalized patients surviving severe TBI was stable in Denmark and the...

  13. Imaging Brain Mechanisms in Chronic Visceral Pain

    OpenAIRE

    Mayer, Emeran A.; Gupta, Arpana; Kilpatrick, Lisa A.; Hong, Jui-Yang

    2015-01-01

    Chronic visceral pain syndromes are important clinical problems with largely unmet medical needs. Based on the common overlap with other chronic disorders of visceral or somatic pain, mood and affect, and their responsiveness to centrally targeted treatments, an important role of central nervous system in their pathophysiology is likely. A growing number of brain imaging studies in irritable bowel syndrome, functional dyspepsia and bladder pain syndrome/interstitial cystitis has identified ab...

  14. Fatigue in adults with traumatic brain injury

    DEFF Research Database (Denmark)

    Mollayeva, Tatyana; Kendzerska, Tetyana; Mollayeva, Shirin;

    2013-01-01

    BACKGROUND: Despite strong indications that fatigue is the most common and debilitating symptom after traumatic brain injury, little is known about its frequency, natural history, or relation to other factors. The current protocol outlines a strategy for a systematic review that will identify......, assess, and critically appraise studies that assessed predictors for fatigue and the consequences of fatigue on at least two separate time points following traumatic brain injury. METHODS/DESIGN: MEDLINE, EMBASE, the Cochrane Database of Systematic Reviews, CINAHL, and PsycINFO will be systematically...... quality appraisal. Randomized control trial data will be treated as a cohort. The quality will be assessed using the criteria defined by Hayden and colleagues. The review will be conducted and reported in compliance with the Preferred Reporting Items for Systematic Reviews and Meta-Analyses guidelines...

  15. Standardizing Data Collection in Traumatic Brain Injury

    OpenAIRE

    Maas, Andrew I.R.; Harrison-Felix, Cynthia L.; Menon, David; Adelson, P. David; Balkin, Tom; Bullock, Ross; Engel, Doortje C.; Gordon, Wayne; Langlois-Orman, Jean; Lew, Henry L.; Robertson, Claudia; Temkin, Nancy; Valadka, Alex; VERFAELLIE, MIEKE; Wainwright, Mark

    2011-01-01

    Collaboration among investigators, centers, countries, and disciplines is essential to advancing the care for traumatic brain injury (TBI). It is thus important that we “speak the same language.” Great variability, however, exists in data collection and coding of variables in TBI studies, confounding comparisons between and analysis across different studies. Randomized controlled trials can never address the many uncertainties concerning treatment approaches in TBI. Pooling data from differen...

  16. Traumatic Brain Injury, Boredom and Depression

    OpenAIRE

    James Danckert; Yael Goldberg

    2013-01-01

    Traumatic brain injury (TBI) often presents with co-morbid depression and elevated levels of boredom. We explored the relationship between boredom and depression in a group of mild (n = 38), moderate-to-severe TBI patients (n = 14) and healthy controls (n = 88), who completed the Beck Depression Inventory and Boredom Proneness Scales as part of a larger study. Results showed that the relationship between boredom and depression was strongest in moderate-to-severe TBI patients. We explored two ...

  17. Cooking breakfast after a brain injury

    OpenAIRE

    Tanguay, Annick N.; Davidson, Patrick S. R.; K. Vanessa eGuerrero Nuñez; Ferland, Mark B.

    2014-01-01

    Acquired brain injury (ABI) often compromises the ability to carry out instrumental activities of daily living such as cooking. ABI patients' difficulties with executive functions and memory result in less independent and efficient meal preparation. Accurately assessing safety and proficiency in cooking is essential for successful community reintegration following ABI, but in vivo assessment of cooking by clinicians is time-consuming, costly, and difficult to standardize. Accordingly, we exam...

  18. Anemia and brain oxygen after severe traumatic brain injury

    OpenAIRE

    Oddo, Mauro; Levine, Joshua M.; Kumar, Monisha; Iglesias, Katia; Frangos, Suzanne; Maloney-Wilensky, Eileen; Le Roux, Peter D.

    2016-01-01

    Purpose To investigate the relationship between hemoglobin (Hgb) and brain tissue oxygen tension (PbtO2) after severe traumatic brain injury (TBI) and to examine its impact on outcome. Methods This was a retrospective analysis of a prospective cohort of severe TBI patients whose PbtO2 was monitored. The relationship between Hgb—categorized into four quartiles (≤9; 9–10; 10.1–11; >11 g/dl)—and PbtO2 was analyzed using mixed-effects models. Anemia with compromised PbtO2 was defined as episodes...

  19. Inflammatory neuroprotection following traumatic brain injury.

    Science.gov (United States)

    Russo, Matthew V; McGavern, Dorian B

    2016-08-19

    Traumatic brain injury (TBI) elicits an inflammatory response in the central nervous system (CNS) that involves both resident and peripheral immune cells. Neuroinflammation can persist for years following a single TBI and may contribute to neurodegeneration. However, administration of anti-inflammatory drugs shortly after injury was not effective in the treatment of TBI patients. Some components of the neuroinflammatory response seem to play a beneficial role in the acute phase of TBI. Indeed, following CNS injury, early inflammation can set the stage for proper tissue regeneration and recovery, which can, perhaps, explain why general immunosuppression in TBI patients is disadvantageous. Here, we discuss some positive attributes of neuroinflammation and propose that inflammation be therapeutically guided in TBI patients rather than globally suppressed. PMID:27540166

  20. Traumatic brain injury in modern war

    Science.gov (United States)

    Ling, Geoffrey S. F.; Hawley, Jason; Grimes, Jamie; Macedonia, Christian; Hancock, James; Jaffee, Michael; Dombroski, Todd; Ecklund, James M.

    2013-05-01

    Traumatic brain injury (TBI) is common and especially with military service. In Iraq and Afghanistan, explosive blast related TBI has become prominent and is mainly from improvised explosive devices (IED). Civilian standard of care clinical practice guidelines (CPG) were appropriate has been applied to the combat setting. When such CPGs do not exist or are not applicable, new practice standards for the military are created, as for TBI. Thus, CPGs for prehospital care of combat TBI CPG [1] and mild TBI/concussion [2] were introduced as was a DoD system-wide clinical care program, the first large scale system wide effort to address all severities of TBI in a comprehensive organized way. As TBI remains incompletely understood, substantial research is underway. For the DoD, leading this effort are The Defense and Veterans Brain Injury Center, National Intrepid Center of Excellence and the Defense Centers of Excellence for Psychological Health and Traumatic Brain Injury. This program is a beginning, a work in progress ready to leverage advances made scientifically and always with the intent of providing the best care to its military beneficiaries.

  1. Neonatal ischemic brain injury: what every radiologist needs to know

    International Nuclear Information System (INIS)

    We present a pictorial review of neonatal ischemic brain injury and look at its pathophysiology, imaging features and differential diagnoses from a radiologist's perspective. The concept of perinatal stroke is defined and its distinction from hypoxic-ischemic injury is emphasized. A brief review of recent imaging advances is included and a diagnostic approach to neonatal ischemic brain injury is suggested. (orig.)

  2. Secondary Damage after Traumatic Brain Injury: Epidemiology, Pathophysiology and Therapy

    NARCIS (Netherlands)

    D.C. Engel (Doortje Caroline)

    2008-01-01

    textabstractTraumatic brain injury (TBI) is defined as a microscopic or macroscopic injury to the brain caused by external physical forces. Road traffic accidents, falls, sports injuries (i.e. boxing), recreational accidents (i.e. parachute jumping), the use of firearms, assault, child abuse, and se

  3. Caregiver burden in Danish family members of patients with severe brain injury

    DEFF Research Database (Denmark)

    Doser, Karoline; Norup, Anne

    more severe injuries, who spent more time on caregiving and reported more unmet needs. Overall, spouses spent significantly more time taking care of their family member than parents and reported higher levels of burden. CONCLUSIONS: The findings emphasized the continuing consequences of brain injury on......OBJECTIVE: To investigate caregiver burden and factors associated with caregiver burden among family members of patients with severe brain injury in the chronic phase. Additionally, the study aimed at investigating differences in burden between parents and spouses. METHODS: Forty-four Danish...... caregivers of patients with severe brain injury were contacted 3-6 years post-injury and asked to complete a measure of caregiver burden. RESULTS: Medium, high and low levels of burden were observed in 45%, 16% and 39% of family members, respectively. Higher burden was seen in caregivers of patients with...

  4. [Community-based rehabilitation and outpatient care for patients with acquired brain injury and chronic neurological disability in Germany: continuing support for social participation and re-integration in the neurological care system?].

    Science.gov (United States)

    Reuther, P; Hendrich, A; Kringler, W; Vespo, E

    2012-12-01

    In Germany a number of patients who are suffering from acquired brain injury and chronic neurological disability are either undersupplied or exposed to inappropriate care in their social environment. The number of these patients is increasing due to the changes in the procedures of care and due to demographic factors. While acute medical care and early rehabilitative treatment is accessible throughout the German health care system the necessary multimodal and competent care is rare or absent in the social participative sites such as life and occupational environments of the patients. The complex impairment of the brain, the central organ for sensorial, executive and other cognitive functions of human beings, renders the affected patient an exception in the system of medical and social care - this has only inadequately been considered in the past. The authors explain the necessity to disclose the status of a "human-with acquired-brain damage (Mensch-mit-erworbener-Hirnschädigung, MeH)" explicitly as severely disabled. The paper recommends a number of structural and procedural elements that have proven to overcome the insufficient or inappropriate support in integrating the patients suffering from acquired brain injury and chronic neurological disability in their social environment as well as for a demand-focused support with sustainable rehabilitative and ambulant follow-up procedures. Comparisons with other developed health care systems and international guidelines show that with organizing of early-supported-discharge, community-ambulation, shared-care and community-based-rehabilitation these problems have long since been identified elsewhere. Community-based and resident-oriented concepts have already been systematically implemented. In order to achieve the necessary support for the individual patient, a nation-wide development is necessary in Germany to perform the principles of the German social code and the principles of the Convention on the Rights of

  5. Imaging assessment of traumatic brain injury.

    Science.gov (United States)

    Currie, Stuart; Saleem, Nayyar; Straiton, John A; Macmullen-Price, Jeremy; Warren, Daniel J; Craven, Ian J

    2016-01-01

    Traumatic brain injury (TBI) constitutes injury that occurs to the brain as a result of trauma. It should be appreciated as a heterogeneous, dynamic pathophysiological process that starts from the moment of impact and continues over time with sequelae potentially seen many years after the initial event. Primary traumatic brain lesions that may occur at the moment of impact include contusions, haematomas, parenchymal fractures and diffuse axonal injury. The presence of extra-axial intracranial lesions such as epidural and subdural haematomas and subarachnoid haemorrhage must be anticipated as they may contribute greatly to secondary brain insult by provoking brain herniation syndromes, cranial nerve deficits, oedema and ischaemia and infarction. Imaging is fundamental to the management of patients with TBI. CT remains the imaging modality of choice for initial assessment due to its ease of access, rapid acquisition and for its sensitivity for detection of acute haemorrhagic lesions for surgical intervention. MRI is typically reserved for the detection of lesions that may explain clinical symptoms that remain unresolved despite initial CT. This is especially apparent in the setting of diffuse axonal injury, which is poorly discerned on CT. Use of particular MRI sequences may increase the sensitivity of detecting such lesions: diffusion-weighted imaging defining acute infarction, susceptibility-weighted imaging affording exquisite data on microhaemorrhage. Additional advanced MRI techniques such as diffusion tensor imaging and functional MRI may provide important information regarding coexistent structural and functional brain damage. Gaining robust prognostic information for patients following TBI remains a challenge. Advanced MRI sequences are showing potential for biomarkers of disease, but this largely remains at the research level. Various global collaborative research groups have been established in an effort to combine imaging data with clinical and

  6. In vivo characterization of chronic traumatic encephalopathy using [F-18]FDDNP PET brain imaging

    OpenAIRE

    Barrio, Jorge R.; Small, Gary W.; Wong, Koon-Pong; Huang, Sung-Cheng; Liu, Jie; Merrill, David A.; Giza, Christopher C.; Fitzsimmons, Robert P.; Omalu, Bennet; Bailes, Julian; Kepe, Vladimir

    2015-01-01

    Mild traumatic brain injuries are frequent events in the general population and are associated with a severe neurodegenerative disease, chronic traumatic encephalopathy (CTE). This disease is characterized by abnormal accumulation of protein aggregates, primarily tau proteins, which accumulate in brain areas responsible for mood, fear, stress, and cognition. There is no definitive clinical diagnosis of CTE at the present time, and this new work shows how a tau-sensitive brain imaging agent, [...

  7. Cerebral perfusion changes in traumatic diffuse brain injury. IMP SPECT studies

    International Nuclear Information System (INIS)

    Diffuse brain injury (DBI) is characterized by axonal degeneration and neuronal damage which cause diffuse brain atrophy. We have investigated the time course of abnormalities in cerebral perfusion distribution in cases of DBI by using Iodine-123-IMP SPECT, and the relationship to the appearance of diffuse brain atrophy. SPECT scans were performed on eight patients with diffuse brain injury due to closed cranial trauma in acute and chronic stages. All patients showed abnormalities in cerebral perfusion with decreases in perfusion, even in non-depicted regions on MRI, and the affected areas varied throughout the period of observation. Diffuse brain atrophy appeared in all patients. In some patients, diffuse brain atrophy was observed at or just after the time when the maximum number of lesions on SPECT were seen. The abnormalities in cerebral perfusion in cases of DBI might therefore be related to axonal degeneration and neuronal damage which causes diffuse brain atrophy. (author)

  8. Aquaporin 9 in rat brain after severe traumatic brain injury

    Directory of Open Access Journals (Sweden)

    Hui Liu

    2012-03-01

    Full Text Available OBJECTIVE: To reveal the expression and possible roles of aquaporin 9 (AQP9 in rat brain, after severe traumatic brain injury (TBI. METHODS: Brain water content (BWC, tetrazolium chloride staining, Evans blue staining, immunohistochemistry (IHC, immunofluorescence (IF, western blot, and real-time polymerase chain reaction were used. RESULTS: The BWC reached the first and second (highest peaks at 6 and 72 hours, and the blood brain barrier (BBB was severely destroyed at six hours after the TBI. The worst brain ischemia occurred at 72 hours after TBI. Widespread AQP9-positive astrocytes and neurons in the hypothalamus were detected by means of IHC and IF after TBI. The abundance of AQP9 and its mRNA increased after TBI and reached two peaks at 6 and 72 hours, respectively, after TBI. CONCLUSIONS: Increased AQP9 might contribute to clearance of excess water and lactate in the early stage of TBI. Widespread AQP9-positive astrocytes might help lactate move into neurons and result in cellular brain edema in the later stage of TBI. AQP9-positive neurons suggest that AQP9 plays a role in energy balance after TBI.

  9. Cushing's ulcer in traumatic brain injury

    Institute of Scientific and Technical Information of China (English)

    Biteghe-bi-Nzeng Alain; WANG Yun-jie

    2008-01-01

    Traumatic brain injury(TBI)remains a complicated and urgent disease in our modernized cities. It becomes now a public health disease. We have got more and more patients in Neurosurgery Intensive Care Unit following motor vehicle accidents and others causes. TBI brings multiple disorders,from the primary injury to secondary injury. The body received the disturbances in the brain,in the hypothalamo-pituitary-adrenocortical(HPA)axis,in the gastric mucosa,in the immune and neuroendocrine systems.The mortality of TBI is more than 50 000 deaths/year, the third of the mortality of all iniuries. Cushing ulcer is one of the severe complications of TBI and its mortality rate is more than 50%. Many studies have improved the management of TBI and the associated complications to give patients a better outcome. Furthers studies need to be done based on the similar methodology to clarify the different steps of the HPA axis and the neuroendocrine change associated. The aim of the present review is to assess the clinical and endocrinal features of hypopituitarism and stress ulcer following TBI.

  10. Astrocytes mediate the neuroprotective effects of Tibolone following brain injury

    Directory of Open Access Journals (Sweden)

    Luis Miguel Garcia-Segura

    2015-04-01

    Full Text Available Recently, astrocytes have become a key central player in mediating important functions in the brain. These physiological processes include neurotransmitter recycling, energy management, metabolic shuttle, immune sensing, K+ buffer, antioxidant supply and release of neurotrophic factors and gliotransmitters. These astrocytic roles are somehow altered upon brain injury, therefore strategies aimed at better protecting astrocytes are an essential asset to maintain brain homeostasis. In this context, estrogenic compounds, such as Tibolone, have attracted attention for their beneficial effects in acute and chronic degenerative diseases. Tibolone may act through binding to estrogen, androgen or progesterone receptors and exert protective effects by reducing astrocytes cell death and oxidative stress signaling mechanisms. Although Tibolone has a multifactorial effect in the brain, its mechanisms of action are not completely understood. In this work, we highlight the role of Tibolone in brain protection upon damage, how astrocytes might mediate part of its neuroprotective actions and discuss the effects of Tibolone in diminishing the harmful consequences of a metabolic insult and energy failure in the setting of a pathological event.

  11. Electrophysiologic monitoring in acute brain injury.

    Science.gov (United States)

    Claassen, Jan; Vespa, Paul

    2014-12-01

    To determine the optimal use and indications of electroencephalography (EEG) in critical care management of acute brain injury (ABI). An electronic literature search was conducted for articles in English describing electrophysiological monitoring in ABI from January 1990 to August 2013. A total of 165 studies were included. EEG is a useful monitor for seizure and ischemia detection. There is a well-described role for EEG in convulsive status epilepticus and cardiac arrest (CA). Data suggest EEG should be considered in all patients with ABI and unexplained and persistent altered consciousness and in comatose intensive care unit (ICU) patients without an acute primary brain condition who have an unexplained impairment of mental status. There remain uncertainties about certain technical details, e.g., the minimum duration of EEG studies, the montage, and electrodes. Data obtained from both EEG and EP studies may help estimate prognosis in ABI patients, particularly following CA and traumatic brain injury. Data supporting these recommendations is sparse, and high quality studies are needed. EEG is used to monitor and detect seizures and ischemia in ICU patients and indications for EEG are clear for certain disease states, however, uncertainty remains on other applications. PMID:25208668

  12. Mild Traumatic Brain Injuries : A 10-year follow-up

    OpenAIRE

    Elgmark Andersson, Elisabeth; Bedics, Beate Kärrdahl; Falkmer, Torbjörn

    2011-01-01

    Objective and design: Long-term consequences of mild traumatic brain injuries were investigated based on a 10-year follow-up of patients from a previously published randomized controlled study of mild traumatic brain injuries. One aim was to describe changes over time after mild traumatic brain injuries in terms of the extent of persisting post-concussion symptoms, life satisfaction, perceived health, activities of daily living, changes in life roles and sick leave. Another aim was to identif...

  13. Accelerated recovery from acute brain injuries: clinical efficacy of neurotrophic treatment in stroke and traumatic brain injuries.

    Science.gov (United States)

    Bornstein, N; Poon, W S

    2012-04-01

    Stroke is one of the most devastating vascular diseases in the world as it is responsible for almost five million deaths per year. Almost 90% of all strokes are ischemic and mainly due to atherosclerosis, cardiac embolism and small-vessel disease. Intracerebral or subarachnoid hemorrhage can lead to hemorrhagic stroke, which usually has the poorest prognosis. Cerebrolysin is a peptide preparation which mimics the action of a neurotrophic factor, protecting stroke-injured neurons and promoting neuroplasticity and neurogenesis. Cerebrolysin has been widely studied as a therapeutic tool for both ischemic and hemorrhagic stroke, as well as traumatic brain injury. In ischemic stroke, Cerebrolysin given as an adjuvant therapy to antiplatelet and rheologically active medication resulted in accelerated improvement in global, neurological and motor functions, cognitive performance and activities of daily living. Cerebrolysin was also safe and well tolerated when administered in patients suffering from hemorrhagic stroke. Traumatic brain injury leads to transient or chronic impairments in physical, cognitive, emotional and behavioral functions. This is associated with deficits in the recognition of basic emotions, the capacity to interpret the mental states of others, and executive functioning. Pilot clinical studies with adjuvant Cerebrolysin in the acute and postacute phases of the injury have shown faster recovery, which translates into an earlier onset of rehabilitation and shortened hospitalization time. PMID:22514794

  14. Imaging brain mechanisms in chronic visceral pain.

    Science.gov (United States)

    Mayer, Emeran A; Gupta, Arpana; Kilpatrick, Lisa A; Hong, Jui-Yang

    2015-04-01

    Chronic visceral pain syndromes are important clinical problems with largely unmet medical needs. Based on the common overlap with other chronic disorders of visceral or somatic pain, mood and affect, and their responsiveness to centrally targeted treatments, an important role of central nervous system in their pathophysiology is likely. A growing number of brain imaging studies in irritable bowel syndrome, functional dyspepsia, and bladder pain syndrome/interstitial cystitis has identified abnormalities in evoked brain responses, resting state activity, and connectivity, as well as in gray and white matter properties. Structural and functional alterations in brain regions of the salience, emotional arousal, and sensorimotor networks, as well as in prefrontal regions, are the most consistently reported findings. Some of these changes show moderate correlations with behavioral and clinical measures. Most recently, data-driven machine-learning approaches to larger data sets have been able to classify visceral pain syndromes from healthy control subjects. Future studies need to identify the mechanisms underlying the altered brain signatures of chronic visceral pain and identify targets for therapeutic interventions. PMID:25789437

  15. Clinical utility of brain stimulation modalities following traumatic brain injury: current evidence

    Directory of Open Access Journals (Sweden)

    Li S

    2015-06-01

    Full Text Available Shasha Li,1,2 Ana Luiza Zaninotto,2,3 Iuri Santana Neville,4 Wellingson Silva Paiva,4 Danuza Nunn,2 Felipe Fregni21Department of Rehabilitation Medicine, West China Hospital, Sichuan University, Chengdu, Sichuan, People’s Republic of China; 2Spaulding Neuromodulation Center, Harvard Medical School, Boston, MA, USA; 3Division of Psychology, Hospital das Clínicas, University of São Paulo, São Paulo, Brazil; 4Division of Neurosurgery, University of São Paulo Medical School, São Paulo, São Paulo, BrazilAbstract: Traumatic brain injury (TBI remains the main cause of disability and a major public health problem worldwide. This review focuses on the neurophysiology of TBI, and the rationale and current state of evidence of clinical application of brain stimulation to promote TBI recovery, particularly on consciousness, cognitive function, motor impairments, and psychiatric conditions. We discuss the mechanisms of different brain stimulation techniques including major noninvasive and invasive stimulations. Thus far, most noninvasive brain stimulation interventions have been nontargeted and focused on the chronic phase of recovery after TBI. In the acute stages, there is limited available evidence of the efficacy and safety of brain stimulation to improve functional outcomes. Comparing the studies across different techniques, transcranial direct current stimulation is the intervention that currently has the higher number of properly designed clinical trials, though total number is still small. We recognize the need for larger studies with target neuroplasticity modulation to fully explore the benefits of brain stimulation to effect TBI recovery during different stages of recovery.Keywords: traumatic brain injury, brain stimulation, neuroplasticity

  16. Long-term effects of mild traumatic brain injury on cognitive performance

    OpenAIRE

    Dean, Philip J. A.; Sterr, Annette

    2013-01-01

    Although a proportion of individuals report chronic cognitive difficulties after mild traumatic brain injury (mTBI), results from behavioral testing have been inconsistent. In fact, the variability inherent to the mTBI population may be masking subtle cognitive deficits. We hypothesized that this variability could be reduced by accounting for post-concussion syndrome (PCS) in the sample. Thirty-six participants with mTBI (>1 year post-injury) and 36 non-head injured controls performed informa...

  17. A study of rotational brain injury.

    Science.gov (United States)

    Misra, J C; Chakravarty, S

    1984-01-01

    Of concern in the paper is an investigation on brain injuries which may occur owing to an input angular acceleration of the head. The study is based on the use of an improved mathematical model for the cranium. The eccentricity of the braincase is incorporated through the consideration of a prolate spheroidal shell as the representative of the skull. Also the dissipative mechanical behaviour of the brain material (as per the observations of experimenters) has been accounted for by considering the material contained in the shell as viscoelastic. The problem is formulated in terms of prolate spheroidal coordinates. The singularities of the governing equations of motion (when expressed in the prolate coordinate system) are removed by a suitable transformation of the concerned dependent variable, viz. the one that stands for the angular displacement of a representative point of the system. In the first place the solution of the boundary value problem is sought in the Laplace transform space, by employing a finite difference technique. Use of the alternating-direction-implicit method together with Thomas algorithm was made for obtaining the angular acceleration in the transformed space. The Laplace inversion is also carried out with the help of numerical procedures (Gauss quadrature formula is used for this purpose). The results of the parametric study are presented through graphs. The plots illustrate the shear stresses and strains in the brain medium. A meaningful comparison of the computational results with those of previous investigations indicate that the eccentricity of the braincase plays a significant role in causing injury to the brain. PMID:6480621

  18. Cyclosporine Treatment in Traumatic Brain Injury: Operation Brain Trauma Therapy.

    Science.gov (United States)

    Dixon, C Edward; Bramlett, Helen M; Dietrich, W Dalton; Shear, Deborah A; Yan, Hong Q; Deng-Bryant, Ying; Mondello, Stefania; Wang, Kevin K W; Hayes, Ronald L; Empey, Philip E; Povlishock, John T; Tortella, Frank C; Kochanek, Patrick M

    2016-03-15

    Operation Brain Trauma Therapy (OBTT) is a consortium of investigators using multiple pre-clinical models of traumatic brain injury (TBI) to bring acute therapies to clinical trials. To screen therapies, we used three rat models (parasagittal fluid percussion injury [FPI], controlled cortical impact [CCI], and penetrating ballistic-like brain injury [PBBI]). We report results of the third therapy (cyclosporin-A; cyclosporine; [CsA]) tested by OBTT. At each site, rats were randomized to treatment with an identical regimen (TBI + vehicle, TBI + CsA [10 mg/kg], or TBI + CsA [20 mg/kg] given intravenously at 15 min and 24 h after injury, and sham). We assessed motor and Morris water maze (MWM) tasks over 3 weeks after TBI and lesion volume and hemispheric tissue loss at 21 days. In FPI, CsA (10 mg/kg) produced histological protection, but 20 mg/kg worsened working memory. In CCI, CsA (20 mg/kg) impaired MWM performance; surprisingly, neither dose showed benefit on any outcome. After PBBI, neither dose produced benefit on any outcome, and mortality was increased (20 mg/kg) partly caused by the solvent vehicle. In OBTT, CsA produced complex effects with histological protection at the lowest dose in the least severe model (FPI), but only deleterious effects as model severity increased (CCI and PBBI). Biomarker assessments included measurements of glial fibrillary acidic protein (GFAP) and ubiquitin C-terminal hydrolase-L1 (UCH-L1) in blood at 4 or 24 h after injury. No positive treatment effects were seen on biomarker levels in any of the models, whereas significant increases in 24 h UCH-L1 levels were seen with CsA (20 mg/kg) after CCI and 24 h GFAP levels in both CsA treated groups in the PBBI model. Lack of behavioral protection in any model, indicators of toxicity, and a narrow therapeutic index reduce enthusiasm for clinical translation. PMID:26671075

  19. Erythropoietin Treatment in Traumatic Brain Injury: Operation Brain Trauma Therapy.

    Science.gov (United States)

    Bramlett, Helen M; Dietrich, W Dalton; Dixon, C Edward; Shear, Deborah A; Schmid, Kara E; Mondello, Stefania; Wang, Kevin K W; Hayes, Ronald L; Povlishock, John T; Tortella, Frank C; Kochanek, Patrick M

    2016-03-15

    Experimental studies targeting traumatic brain injury (TBI) have reported that erythropoietin (EPO) is an endogenous neuroprotectant in multiple models. In addition to its neuroprotective effects, it has also been shown to enhance reparative processes including angiogenesis and neurogenesis. Based on compelling pre-clinical data, EPO was tested by the Operation Brain Trauma Therapy (OBTT) consortium to evaluate therapeutic potential in multiple TBI models along with biomarker assessments. Based on the pre-clinical TBI literature, two doses of EPO (5000 and 10,000 IU/kg) were tested given at 15 min after moderate fluid percussion brain injury (FPI), controlled cortical impact (CCI), or penetrating ballistic-like brain injury (PBBI) with subsequent behavioral, histopathological, and biomarker outcome assessments. There was a significant benefit on beam walk with the 5000 IU dose in CCI, but no benefit on any other motor task across models in OBTT. Also, no benefit of EPO treatment across the three TBI models was noted using the Morris water maze to assess cognitive deficits. Lesion volume analysis showed no treatment effects after either FPI or CCI; however, with the 5000 IU/kg dose of EPO, a paradoxical increase in lesion volume and percent hemispheric tissue loss was seen after PBBI. Biomarker assessments included measurements of glial fibrillary acidic protein (GFAP) and ubiquitin C-terminal hydrolase-L1 (UCH-L1) in blood at 4 or 24 h after injury. No treatment effects were seen on biomarker levels after FPI, whereas treatment at either dose exacerbated the increase in GFAP at 24 h in PBBI but attenuated 24-4 h delta UCH-L1 levels at high dose in CCI. Our data indicate a surprising lack of efficacy of EPO across three established TBI models in terms of behavioral, histopathological, and biomarker assessments. Although we cannot rule out the possibility that other doses or more prolonged treatment could show different effects, the lack of efficacy of EPO

  20. The History and Evolution of Experimental Traumatic Brain Injury Models.

    Science.gov (United States)

    Povlishock, John

    2016-01-01

    This narrative provides a brief history of experimental animal model development for the study of traumatic brain injury. It draws upon a relatively rich history of early animal modeling that employed higher order animals to assess concussive brain injury while exploring the importance of head movement versus stabilization in evaluating the animal's response to injury. These themes are extended to the development of angular/rotational acceleration/deceleration models that also exploited brain movement to generate both the morbidity and pathology typically associated with human traumatic brain injury. Despite the significance of these early model systems, their limitations and overall practicality are discussed. Consideration is given to more contemporary rodent animal models that replicate individual/specific features of human injury, while via various transgenic technologies permitting the evaluation of injury-mediated pathways. The narrative closes on a reconsideration of higher order, porcine animal models of injury and their implication for preclinical/translational research. PMID:27604709

  1. Robust whole-brain segmentation: application to traumatic brain injury.

    Science.gov (United States)

    Ledig, Christian; Heckemann, Rolf A; Hammers, Alexander; Lopez, Juan Carlos; Newcombe, Virginia F J; Makropoulos, Antonios; Lötjönen, Jyrki; Menon, David K; Rueckert, Daniel

    2015-04-01

    We propose a framework for the robust and fully-automatic segmentation of magnetic resonance (MR) brain images called "Multi-Atlas Label Propagation with Expectation-Maximisation based refinement" (MALP-EM). The presented approach is based on a robust registration approach (MAPER), highly performant label fusion (joint label fusion) and intensity-based label refinement using EM. We further adapt this framework to be applicable for the segmentation of brain images with gross changes in anatomy. We propose to account for consistent registration errors by relaxing anatomical priors obtained by multi-atlas propagation and a weighting scheme to locally combine anatomical atlas priors and intensity-refined posterior probabilities. The method is evaluated on a benchmark dataset used in a recent MICCAI segmentation challenge. In this context we show that MALP-EM is competitive for the segmentation of MR brain scans of healthy adults when compared to state-of-the-art automatic labelling techniques. To demonstrate the versatility of the proposed approach, we employed MALP-EM to segment 125 MR brain images into 134 regions from subjects who had sustained traumatic brain injury (TBI). We employ a protocol to assess segmentation quality if no manual reference labels are available. Based on this protocol, three independent, blinded raters confirmed on 13 MR brain scans with pathology that MALP-EM is superior to established label fusion techniques. We visually confirm the robustness of our segmentation approach on the full cohort and investigate the potential of derived symmetry-based imaging biomarkers that correlate with and predict clinically relevant variables in TBI such as the Marshall Classification (MC) or Glasgow Outcome Score (GOS). Specifically, we show that we are able to stratify TBI patients with favourable outcomes from non-favourable outcomes with 64.7% accuracy using acute-phase MR images and 66.8% accuracy using follow-up MR images. Furthermore, we are able to

  2. Increased expression of aquaporin-4 in human traumatic brain injury and brain tumors

    Institute of Scientific and Technical Information of China (English)

    HU Hua; YAO Hong-tian; ZHANG Wei-ping; ZHANG LEI; DING Wei; ZHANG Shi-hong; CHEN Zhong; WEI Er-qing

    2005-01-01

    Objective: To characterize the expression of aquaporin-4 (AQP4), one of the aquaporins (AQPs), in human brain specimens from patients with traumatic brain injury or brain tumors. Methods: Nineteen human brain specimens were obtained from the patients with traumatic brain injury, brain tumors, benign meningioma or early stage hemorrhagic stroke. MRI or CT imaging was used to assess brain edema. Hematoxylin and eosin staining were used to evaluate cell damage. Immunohistochemistry was used to detect the AQP4 expression. Results: AQP4 expression was increased from 15h to at least 8 d after injury. AQP4immunoreactivity was strong around astrocytomas, ganglioglioma and metastatic adenocarcinoma. However, AQP4 immunoreactivity was only found in the centers of astrocytomas and ganglioglioma, but not in metastatic adenocarcinoma derived from lung.Conclusion: AQP4 expression increases in human brains after traumatic brain injury, within brain-derived tumors, and around brain tumors.

  3. Neuropsychological rehabilitation for traumatic brain injury patients

    Directory of Open Access Journals (Sweden)

    Marzena Chantsoulis

    2015-05-01

    Full Text Available The aim of this review is to discuss the basic forms of neuropsychological rehabilitation for patients with traumatic brain injury (TBI. More broadly, we discussed cognitive rehabilitation therapy (CRT which constitutes a fundamental component in therapeutic interaction at many centres worldwide. Equally presented is a comprehensive model of rehabilitation, the fundamental component of which is CRT. It should be noted that the principles of this approach first arose in Poland in the 1970s, in other words, several decades before their appearance in other programmemes. Taken into consideration are four factors conditioning the effectiveness of such a process: comprehensiveness, earlier interaction, universality and its individualized character. A comprehensive programmeme of rehabilitation covers: cognitive rehabilitation, individual and group rehabilitation with the application of a therapeutic environment, specialist vocational rehabilitation, as well as family psychotherapy. These training programmemes are conducted within the scope of the ‘Academy of Life,’ which provides support for the patients in their efforts and shows them the means by which they can overcome existing difficulties. Equally emphasized is the close cooperation of the whole team of specialists, as well as the active participation of the family as an essential condition for the effectiveness of rehabilitation and, in effect, a return of the patient to a relatively normal life. Also presented are newly developing neurothechnologies and the neuromarkers of brain injuries. This enables a correct diagnosis to be made and, as a result, the selection of appropriate methods for neuropsychological rehabilitation, including neurotherapy.

  4. Psychiatric disorders and traumatic brain injury

    Directory of Open Access Journals (Sweden)

    Marcelo Schwarzbold

    2008-09-01

    Full Text Available Marcelo Schwarzbold1, Alexandre Diaz1, Evandro Tostes Martins2, Armanda Rufino1, Lúcia Nazareth Amante1,3, Maria Emília Thais1, João Quevedo4, Alexandre Hohl1, Marcelo Neves Linhares1,5,6, Roger Walz1,61Núcleo de Pesquisas em Neurologia Clínica e Experimental (NUPNEC, Departamento de Clínica Médica, Hospital Universitário, UFSC, Florianópolis, SC, Brazil; 2Unidade de Terapia Intensiva, Hospital Governador Celso Ramos, Florianópolis, SC, Brazil; 3Departamento de Enfermagem, UFSC, Florianópolis, SC, Brazil; 4Laboratório de Neurociências, UNESC, Criciúma, SC, Brazil; 5Departamento de Cirurgia, Hospital Universitário, UFSC, Florianópolis, SC, Brazil; 6Centro de Cirurgia de Epilepsia de Santa Catarina (CEPESC, Hospital Governador Celso Ramos, Florianópolis, SC, BrazilAbstract: Psychiatric disorders after traumatic brain injury (TBI are frequent. Researches in this area are important for the patients’ care and they may provide hints for the comprehension of primary psychiatric disorders. Here we approach epidemiology, diagnosis, associated factors and treatment of the main psychiatric disorders after TBI. Finally, the present situation of the knowledge in this field is discussed.Keywords: psychiatric disorders, traumatic brain injury, neuropsychiatry, diagnostic, epidemiology, pathophysiology

  5. Windows to the Brain (WttB): Transparent Nanocrystalline Yttria Stabilized Zirconia Cranial Implants for Non-Invasive, Chronic Access to the Brain for Optical Diagnostics and Therapeutics

    OpenAIRE

    Damestani, Yasaman

    2015-01-01

    Windows to the Brain (WttB) platform can improve patient care by enabling the delivery and/or collection of light into/from the brain, on demand, over large areas, and on a chronically-recurring basis without the need for repeated craniotomies. WttB holds the transformative potential for facilitating diagnosis and treatment of a wide variety of brain pathologies and neurological disorders including cerebral edema, traumatic brain injury, stroke, glioma, and neurodegenerative diseases.We have ...

  6. Graph Analysis of Functional Brain Networks for Cognitive Control of Action in Traumatic Brain Injury

    Science.gov (United States)

    Caeyenberghs, Karen; Leemans, Alexander; Heitger, Marcus H.; Leunissen, Inge; Dhollander, Thijs; Sunaert, Stefan; Dupont, Patrick; Swinnen, Stephan P.

    2012-01-01

    Patients with traumatic brain injury show clear impairments in behavioural flexibility and inhibition that often persist beyond the time of injury, affecting independent living and psychosocial functioning. Functional magnetic resonance imaging studies have shown that patients with traumatic brain injury typically show increased and more broadly…

  7. Peripheral nerve injury is associated with chronic, reversible changes in global DNA methylation in the mouse prefrontal cortex.

    Directory of Open Access Journals (Sweden)

    Maral Tajerian

    Full Text Available Changes in brain structure and cortical function are associated with many chronic pain conditions including low back pain and fibromyalgia. The magnitude of these changes correlates with the duration and/or the intensity of chronic pain. Most studies report changes in common areas involved in pain modulation, including the prefrontal cortex (PFC, and pain-related pathological changes in the PFC can be reversed with effective treatment. While the mechanisms underlying these changes are unknown, they must be dynamically regulated. Epigenetic modulation of gene expression in response to experience and environment is reversible and dynamic. Epigenetic modulation by DNA methylation is associated with abnormal behavior and pathological gene expression in the central nervous system. DNA methylation might also be involved in mediating the pathologies associated with chronic pain in the brain. We therefore tested a whether alterations in DNA methylation are found in the brain long after chronic neuropathic pain is induced in the periphery using the spared nerve injury modal and b whether these injury-associated changes are reversible by interventions that reverse the pathologies associated with chronic pain. Six months following peripheral nerve injury, abnormal sensory thresholds and increased anxiety were accompanied by decreased global methylation in the PFC and the amygdala but not in the visual cortex or the thalamus. Environmental enrichment attenuated nerve injury-induced hypersensitivity and reversed the changes in global PFC methylation. Furthermore, global PFC methylation correlated with mechanical and thermal sensitivity in neuropathic mice. In summary, induction of chronic pain by peripheral nerve injury is associated with epigenetic changes in the brain. These changes are detected long after the original injury, at a long distance from the site of injury and are reversible with environmental manipulation. Changes in brain structure and

  8. White Matter Damage and Cognitive Impairment after Traumatic Brain Injury

    Science.gov (United States)

    Kinnunen, Kirsi Maria; Greenwood, Richard; Powell, Jane Hilary; Leech, Robert; Hawkins, Peter Charlie; Bonnelle, Valerie; Patel, Maneesh Chandrakant; Counsell, Serena Jane; Sharp, David James

    2011-01-01

    White matter disruption is an important determinant of cognitive impairment after brain injury, but conventional neuroimaging underestimates its extent. In contrast, diffusion tensor imaging provides a validated and sensitive way of identifying the impact of axonal injury. The relationship between cognitive impairment after traumatic brain injury…

  9. Referral decision support in patients with subacute brain injury

    DEFF Research Database (Denmark)

    Pedersen, Asger R; Nielsen, Jørgen F; Jensen, Jim;

    2016-01-01

    support in the RCS-E and the item specific threshold model, when patients with acquired brain injury are to be referred to CSS or DSS as their primary rehabilitation. Implications for Rehabilitation Efficient rehabilitation after acquired brain injury requires rehabilitation settings that meet patient...

  10. Magnetic susceptibility artifacts in a diffuse brain injury and their pathological significance

    International Nuclear Information System (INIS)

    In our study, FLAIR images and multishot echo planar imaging T2-weighted images (EPI T2-WI) were used in addition to conventional T1-weighted images, T2-weighted images and T2-weighted sagittal images. In this series we focused our attention on small parenchymatous lesions of a mild or moderate form of diffuse brain injury. These injuries are shown as high intensity areas on T2-weighted images (T2-high intensity lesions) but are not visualized in CT images. This series consisted of 29 patients who were diagnosed with diffuse brain injury and whose CT scans showed a Diffuse Injury I or II. Nineteen patients were studied in an acute or subacute stage. In all but 3 patients, small T2-high intensity lesions were found in the brain parenchyma. In the follow-up study brain edema was suggested because the lesions tended to be absent within 3 months in T2-weighted images and FLAIR. In 10 patients examined during a chronic stage. Small hemorrhages in patients with Diffuse Injury II were shown with variable intensities on the conventional T1- and T2-weighted images, but were visualized with low intensity in an EPI T2-WI. In diffuse brain injuries, small T2-high intensity lesions have been considered to be brain edema or ischemic insults. Our data however, suggested that microhemorrhages associated with brain edema were resent in most of the supratentorial lesions, and in more than a half of the lesions in the corpus callosum and the brain stem. These findings appear similar to contusions, which are defined as traumatic bruises of the neural parenchyma. The use of MRI has increased our understanding of in vivo pathological changes in mild or moderate forms of diffuse brain injury. (K.H.)

  11. Ventilator-Associated Pneumonia in Pediatric Traumatic Brain Injury.

    Science.gov (United States)

    Hamele, Mitchell; Stockmann, Chris; Cirulis, Meghan; Riva-Cambrin, Jay; Metzger, Ryan; Bennett, Tellen D; Bratton, Susan L

    2016-05-01

    Ventilator-associated pneumonia (VAP) is a common occurrence among intubated pediatric traumatic brain injury (TBI) patients. However, little is known about the epidemiology, risk factors, and microbiology of VAP in pediatric TBI. We reviewed a cohort of 119 pediatric moderate-to-severe TBI patients and identified 42 with VAP by positive protected bronchial brush specimens. Location of intubation, severity of injury, and antibiotic administration within 2 days after injury were not associated with VAP. Most treatments for elevated intracranial pressure were associated with increased risk of VAP; however, in a multi-variable analysis barbiturate coma (hazard ratio [HR], 3.2; 95% confidence interval [CI] 1.4-7.3), neuromuscular blockade (NMBA; HR, 3.4; 95% CI 1.6-7.3), and use of a cooling blanket for euthermia (HR 2.4; 95% CI 1.1-5.5) remained independently associated with VAP. Most VAP (55%) occurred prior to hospital Day 4 and only 7% developed VAP after Day 7. Methicillin-sensitive Staphylococcus aureus (34%), Haemophilus influenzae (22%), and Streptococcus pneumoniae (15%) were the most common organisms, comprising 71% of isolated pathogens (36% of infections were polymicrobial). Patients with VAP had significantly longer intensive care unit and hospital stays, as well as increased risk of chronic care needs after discharge, but not mortality. VAP is a common occurrence in pediatric TBI patients, and early empiric therapy for patients requiring barbiturate infusion, NMBA, or use of a cooling blanket could mitigate morbidity. PMID:26203702

  12. Increased expression of aquaporin-4 in human traumatic brain injury and brain tumors

    Institute of Scientific and Technical Information of China (English)

    HuaHu; Wei-PingZhang; LeiZhang; ZhongChen; Er-QingWei

    2004-01-01

    Aquaporin-4 (AQP4) is one of the aquaporins (AQPs), a water channel family. In the brain, AQP4 is expressed in astroeyte foot processes, and plays an important role in water homeostasis and in the formation of brain edema. In our study, AQP4 expression in human brain specimens from patients with traumatic brain injury or different brain tumors was detected

  13. Serious brain injury coexisting with multiple injuries caused by traffic accidents in 69 cases

    Institute of Scientific and Technical Information of China (English)

    张浚; 张鹤飞; 等

    1999-01-01

    Objective To explore the speciality,diagnosis,cure principle of serious brain injury coexisting with nultiple injuries caused by traffic accidents.Methods To analyze the clinic data of 69 cases of serious rain injury combined by oter parts of injuries caused by traffic accidents received from January 1998 to April 1999.Results This type of injury took up 11.5 percent of brain injuries in the same term and 33.6 percent of serious brain injuries.The specialities of the injury are that most of them were pedestrians crashed by vehicles.Coesisting injuries including chest injury and limb fractures accounted for a large part.The brain injury usally presented profound disturbance of consciousness,being dangerous and complicated,and a high ISS value.After treatment 13 cases died,9 cases was heavily crippled,11 cases lightly crippled,and 36 cases recovered.The death was usually caused by brain injury.Conclusions Road traffic accidents increased substantially every year.Most of them are related with violating drive rules and regulations.It is important to decrease the road traffic accidents by strengthening propaganda on traffic safety and traffic management.The main principles for salvage should emphasize the importance of pre-hospital emergency rescue and the accurate diagnosis rate,especially the distinction between coma and shock.The priority should be put on those injuries threatening to life.

  14. Brain and head injury in infancy and childhood

    International Nuclear Information System (INIS)

    This article describes typical head injuries in infants and children. In comparison with adults there are distinct differences in the etiology of trauma and in the kind of reaction of the skull and brain. In infants and children there are three different types of trauma: birth trauma, accidental and non-accidental injury. The typical injuries in these three groups are described. (orig.)

  15. Astrocytes as therapeutic targets of estrogenic compounds following brain injuries

    Directory of Open Access Journals (Sweden)

    George E. Barreto

    2015-03-01

    Full Text Available For decades, astrocytes have been considered to be non-excitable support cells that are relatively resistant to brain injury. This view has changed radically during the past twenty years. Multiple essential functions are performed by astrocytes in normal brain. Astrocytes are dynamically involved in synaptic transmission, metabolic and ionic homeostasis, and inflammatory maintenance of the blood brain barrier. Advances in our understanding of astrocytes include new observations about their structure, organization, and function. Astrocytes play an active and important role in the pathophysiology of brain damage. Brain injury impairs mitochondrial function and this is accompanied by increased oxidative stress, leading to prominent astrogliosis, which involves changes in gene expression and morphology, and therefore glial scar formation. Recent works have demonstrated a protective role of reactive astrocytes after brain injury. Nevertheless, others have pointed to an inhibitory role of astrocytes in axonal regeneration after injury. Reactive astrogliosis is a complex phenomenon that includes a mixture of positive and negative responses for neuronal survival and regeneration. Reactive astroglia maintains the integrity of the blood-brain barrier and the survival of the perilesional tissue, but may prevent axonal and damaged tissue regeneration. Neuroprotective strategies aiming at reducing gliosis and enhance brain plasticity are of potential interest for translational neuroscience research in brain injuries. In this context, neurosteroids have shown to be a promising strategy to protect brain against injury, as their effects may rely on reducing gliosis, brain inflammation and potentially modulating recovery from brain injury by engaging mechanisms of neural plasticity. In conclusion, in this work we will consider particularly the two-edged sword role of reactive astrocytes, which is an experimental paradigm helpful in discriminating destructive

  16. Patterns of Brain Injury in Inborn Errors of Metabolism

    OpenAIRE

    Gropman, Andrea L.

    2012-01-01

    Many inborn errors of metabolism (IEMs) are associated with irreversible brain injury. For many, it is unclear how metabolite intoxication or substrate depletion accounts for the specific neurologic findings observed. IEM-associated brain injury patterns are characterized by whether the process involves gray matter, white matter, or both, and beyond that, whether subcortical or cortical gray matter nuclei are involved. Despite global insults, IEMs may result in selective injury to deep gray m...

  17. Neonatal ischemic brain injury: what every radiologist needs to know

    Energy Technology Data Exchange (ETDEWEB)

    Badve, Chaitra A.; Khanna, Paritosh C.; Ishak, Gisele E. [Seattle Children' s Hospital, University of Washington Medical Center, Department of Radiology, Seattle, WA (United States)

    2012-05-15

    We present a pictorial review of neonatal ischemic brain injury and look at its pathophysiology, imaging features and differential diagnoses from a radiologist's perspective. The concept of perinatal stroke is defined and its distinction from hypoxic-ischemic injury is emphasized. A brief review of recent imaging advances is included and a diagnostic approach to neonatal ischemic brain injury is suggested. (orig.)

  18. Genetic susceptibility to traumatic brain injury and apolipoprotein E gene

    Institute of Scientific and Technical Information of China (English)

    SUN Xiao-chuan; JIANG Yong

    2008-01-01

    @@ Traumatic brain injury (TBI) is defined as an injury caused by a blow or jolt to the head or a penetrating head injury that disrupts the normal function of the brain. It is a common emergency and severe case in neurosurgery field. Nowadays, there are more and more evidences showing that TBI, which is apparently similar in pathology and severity in the acute stage, may have different outcomes.

  19. Secondary Damage after Traumatic Brain Injury: Epidemiology, Pathophysiology and Therapy

    OpenAIRE

    Engel, Doortje Caroline

    2008-01-01

    textabstractTraumatic brain injury (TBI) is defined as a microscopic or macroscopic injury to the brain caused by external physical forces. Road traffic accidents, falls, sports injuries (i.e. boxing), recreational accidents (i.e. parachute jumping), the use of firearms, assault, child abuse, and several rare causes e.g. the use of nail guns or lawn mowers have all been described as causes of TBI. The pathology of TBI can be classified by mechanism (closed versus penetrating); clinical severi...

  20. Chronic alcohol ingestion delays skeletal muscle regeneration following injury

    OpenAIRE

    Dekeyser, Graham J; Clary, Caroline R; OTIS, JEFFREY S.

    2013-01-01

    Background Chronic alcohol ingestion may cause severe biochemical and pathophysiological derangements to skeletal muscle. Unfortunately, these alcohol-induced events may also prime skeletal muscle for worsened, delayed, or possibly incomplete repair following acute injury. As alcoholics may be at increased risk for skeletal muscle injury, our goals were to identify the effects of chronic alcohol ingestion on components of skeletal muscle regeneration. To accomplish this, age- and gender-match...

  1. Routine and quantitative EEG in mild traumatic brain injury.

    Science.gov (United States)

    Nuwer, Marc R; Hovda, David A; Schrader, Lara M; Vespa, Paul M

    2005-09-01

    This article reviews the pathophysiology of mild traumatic brain injury, and the findings from EEG and quantitative EEG (QEEG) testing after such an injury. Research on the clinical presentation and pathophysiology of mild traumatic brain injury is reviewed with an emphasis on details that may pertain to EEG or QEEG and their interpretation. Research reports on EEG and QEEG in mild traumatic brain injury are reviewed in this setting, and conclusions are drawn about general diagnostic results that can be determined using these tests. QEEG strengths and weaknesses are reviewed in the context of factors used to determine the clinical usefulness of proposed diagnostic tests. Clinical signs, symptoms, and the pathophysiologic axonal injury and cytotoxicity tend to clear over weeks or months after a mild head injury. Loss of consciousness might be similar to a non-convulsive seizure and accompanied subsequently by postictal-like symptoms. EEG shows slowing of the posterior dominant rhythm and increased diffuse theta slowing, which may revert to normal within hours or may clear more slowly over many weeks. There are no clear EEG or QEEG features unique to mild traumatic brain injury. Late after head injury, the correspondence is poor between electrophysiologic findings and clinical symptoms. Complicating factors are reviewed for the proposed commercial uses of QEEG as a diagnostic test for brain injury after concussion or mild traumatic brain injury. The pathophysiology, clinical symptoms and electrophysiological features tend to clear over time after mild traumatic brain injury. There are no proven pathognomonic signatures useful for identifying head injury as the cause of signs and symptoms, especially late after the injury. PMID:16029958

  2. The potential of neural transplantation for brain repair and regeneration following traumatic brain injury

    Institute of Scientific and Technical Information of China (English)

    Dong Sun

    2016-01-01

    Traumatic brain injury is a major health problem worldwide. Currently, there is no effective treatment to improve neural structural repair and functional recovery of patients in the clinic. Cell transplantation is a potential strategy to repair and regenerate the injured brain. This review article summarized recent de-velopment in cell transplantation studies for post-traumatic brain injury brain repair with varying types of cell sources. It also discussed the potential of neural transplantation to repair/promote recovery of the injured brain following traumatic brain injury.

  3. 78 FR 37834 - Submission for OMB review; 30-Day Comment Request; Federal Interagency Traumatic Brain Injury...

    Science.gov (United States)

    2013-06-24

    ... Interagency Traumatic Brain Injury Research (FITBIR) Informatics System Data Access Request SUMMARY: Under the... Collection: Federal Interagency Traumatic Brain Injury Research (FITBIR) Informatics System Data...

  4. Metallic gold reduces TNFalpha expression, oxidative DNA damage and pro-apoptotic signals after experimental brain injury

    DEFF Research Database (Denmark)

    Pedersen, Mie Ostergaard; Larsen, Agnete; Pedersen, Dan Sonne;

    2009-01-01

    Brain injury represents a major health problem and may result in chronic inflammation and neurodegeneration. Due to antiinflammatory effects of gold, we have investigated the cerebral effects of metallic gold particles following a focal brain injury (freeze-lesion) in mice. Gold particles 20......-45 microm in size or the vehicle (placebo) were implanted in the cortical tissue followed by a cortical freeze-lesioning. At 1-2 weeks post-injury, brains were analyzed by using immunohistochemistry and markers of inflammation, oxidative stress and apoptosis. This study shows that gold treatment...

  5. Levetiracetam Treatment in Traumatic Brain Injury: Operation Brain Trauma Therapy.

    Science.gov (United States)

    Browning, Megan; Shear, Deborah A; Bramlett, Helen M; Dixon, C Edward; Mondello, Stefania; Schmid, Kara E; Poloyac, Samuel M; Dietrich, W Dalton; Hayes, Ronald L; Wang, Kevin K W; Povlishock, John T; Tortella, Frank C; Kochanek, Patrick M

    2016-03-15

    Levetiracetam (LEV) is an antiepileptic agent targeting novel pathways. Coupled with a favorable safety profile and increasing empirical clinical use, it was the fifth drug tested by Operation Brain Trauma Therapy (OBTT). We assessed the efficacy of a single 15 min post-injury intravenous (IV) dose (54 or 170 mg/kg) on behavioral, histopathological, and biomarker outcomes after parasagittal fluid percussion brain injury (FPI), controlled cortical impact (CCI), and penetrating ballistic-like brain injury (PBBI) in rats. In FPI, there was no benefit on motor function, but on Morris water maze (MWM), both doses improved latencies and path lengths versus vehicle (p < 0.05). On probe trial, the vehicle group was impaired versus sham, but both LEV treated groups did not differ versus sham, and the 54 mg/kg group was improved versus vehicle (p < 0.05). No histological benefit was seen. In CCI, there was a benefit on beam balance at 170 mg/kg (p < 0.05 vs. vehicle). On MWM, the 54 mg/kg dose was improved and not different from sham. Probe trial did not differ between groups for either dose. There was a reduction in hemispheric tissue loss (p < 0.05 vs. vehicle) with 170 mg/kg. In PBBI, there was no motor, cognitive, or histological benefit from either dose. Regarding biomarkers, in CCI, 24 h glial fibrillary acidic protein (GFAP) blood levels were lower in the 170 mg/kg group versus vehicle (p < 0.05). In PBBI, GFAP blood levels were increased in vehicle and 170 mg/kg groups versus sham (p < 0.05) but not in the 54 mg/kg group. No treatment effects were seen for ubiquitin C-terminal hydrolase-L1 across models. Early single IV LEV produced multiple benefits in CCI and FPI and reduced GFAP levels in PBBI. LEV achieved 10 points at each dose, is the most promising drug tested thus far by OBTT, and the only drug to improve cognitive outcome in any model. LEV has been advanced to testing in the micropig model in OBTT. PMID:26671550

  6. Surgical management of traumatic brain injury

    DEFF Research Database (Denmark)

    Hartings, Jed A; Vidgeon, Steven; Strong, Anthony J;

    2014-01-01

    for TBI were enrolled in the Co-Operative Studies on Brain Injury Depolarizations (COSBID) at King's College Hospital (KCH, n = 27) and Virginia Commonwealth University (VCU, n = 24) from July 2004 to March 2010. Subdural electrode strips were placed at the time of surgery for subsequent...... contusions: 48%-52%), signs of mass effect (midline shift ≥ 5 mm: 43%-52%), and preoperative intracranial pressure (ICP). At VCU, however, surgeries were performed earlier (median 0.51 vs 0.83 days posttrauma, p < 0.05), bone flaps were larger (mean 82 vs 53 cm(2), p < 0.001), and craniectomies were more......-effectiveness study provides evidence for major practice variation in surgical management of severe TBI. Although ages differed between the 2 cohorts, the results suggest that a more aggressive approach, including earlier surgery, larger craniotomy, and removal of bone flap, may reduce ICP, prevent cortical spreading...

  7. Accommodation in mild traumatic brain injury

    Directory of Open Access Journals (Sweden)

    Wesley Green, MS

    2010-05-01

    Full Text Available Accommodative dysfunction in individuals with mild traumatic brain injury (mTBI can have a negative impact on quality of life, functional abilities, and rehabilitative progress. In this study, we used a range of dynamic and static objective laboratory and clinical measurements of accommodation to assess 12 adult patients (ages 18-40 years with mTBI. The results were compared with either 10 control subjects with no visual impairment or normative literature values where available. Regarding the dynamic parameters, responses in those with mTBI were slowed and exhibited fatigue effects. With respect to static parameters, reduced accommodative amplitude and abnormal accommodative interactions were found in those with mTBI. These results provide further evidence for the substantial impact of mTBI on accommodative function. These findings suggest that a range of accommodative tests should be included in the comprehensive vision examination of individuals with mTBI.

  8. Investigation of blast-induced traumatic brain injury

    OpenAIRE

    Taylor, Paul A.; Ludwigsen, John S.; Ford, Corey C.

    2014-01-01

    Objective Many troops deployed in Iraq and Afghanistan have sustained blast-related, closed-head injuries from being within non-lethal distance of detonated explosive devices. Little is known, however, about the mechanisms associated with blast exposure that give rise to traumatic brain injury (TBI). This study attempts to identify the precise conditions of focused stress wave energy within the brain, resulting from blast exposure, which will correlate with a threshold for persistent brain in...

  9. Traumatic Brain Injury and Delayed Sequelae: A Review - Traumatic Brain Injury and Mild Traumatic Brain Injury (Concussion) are Precursors to Later-Onset Brain Disorders, Including Early-Onset Dementia

    OpenAIRE

    Michael A. Kiraly; Kiraly, Stephen J.

    2007-01-01

    Brain injuries are too common. Most people are unaware of the incidence of and horrendous consequences of traumatic brain injury (TBI) and mild traumatic brain injury (MTBI). Research and the advent of sophisticated imaging have led to progression in the understanding of brain pathophysiology following TBI. Seminal evidence from animal and human experiments demonstrate links between TBI and the subsequent onset of premature, psychiatric syndromes and neurodegenerative diseases, including Alzh...

  10. Mild traumatic brain injuries in adults

    Directory of Open Access Journals (Sweden)

    Dhaval Shukla

    2010-01-01

    Full Text Available Mild traumatic brain injury (mTBI is the commonest form of TBI. Though the name implies, it may not be mild in certain cases. There is a lot of heterogeneity in nomenclature, classification, evaluation and outcome of mTBI. We have reviewed the relevant articles on mTBI in adults, particularly its definition, evaluation and outcome, published in the last decade. The aspects of mTBI like pediatric age group, sports concussion, and postconcussion syndrome were not reviewed. There is general agreement that Glasgow coma score (GCS of 13 should not be considered as mTBI as the risk of intracranial lesion is higher than in patients with GCS 14-15. All patients with GCS of <15 should be evaluated with a computed tomography (CT scan. Patients with GCS 15 and risk factors or neurological symptoms should also be evaluated with CT scan. The outcome of mTBI depends on the combination of preinjury, injury and postinjury factors. Overall outcome of mTBI is good with mortality around 0.1% and disability around 10%.

  11. Diabetes Insipidus after Traumatic Brain Injury

    Directory of Open Access Journals (Sweden)

    Cristina Capatina

    2015-07-01

    Full Text Available Traumatic brain injury (TBI is a significant cause of morbidity and mortality in many age groups. Neuroendocrine dysfunction has been recognized as a consequence of TBI and consists of both anterior and posterior pituitary insufficiency; water and electrolyte abnormalities (diabetes insipidus (DI and the syndrome of inappropriate antidiuretic hormone secretion (SIADH are amongst the most challenging sequelae. The acute head trauma can lead (directly or indirectly to dysfunction of the hypothalamic neurons secreting antidiuretic hormone (ADH or of the posterior pituitary gland causing post-traumatic DI (PTDI. PTDI is usually diagnosed in the first days after the trauma presenting with hypotonic polyuria. Frequently, the poor general status of most patients prevents adequate fluid intake to compensate the losses and severe dehydration and hypernatremia occur. Management consists of careful monitoring of fluid balance and hormonal replacement. PTDI is associated with high mortality, particularly when presenting very early following the injury. In many surviving patients, the PTDI is transient, lasting a few days to a few weeks and in a minority of cases, it is permanent requiring management similar to that offered to patients with non-traumatic central DI.

  12. Sexual changes associated with traumatic brain injury.

    Science.gov (United States)

    Ponsford, Jennie

    2003-01-01

    Findings from numerous outcome studies have suggested that people with traumatic brain injuries (TBI) experience relationship difficulties and changes in sexuality. However, there have been few investigations of these problems. This paper reports the results of a study of sexuality following TBI, which aimed to identify changes in sexual behaviour, affect, self-esteem, and relationship quality, and their inter-relationships. Two hundred and eight participants with moderate-to-severe TBI (69% males) completed a questionnaire 1-5 years post-injury. Their responses were compared with those of 150 controls, matched for age, gender, and education. Of TBI participants 36-54% reported: (1) A decrease in the importance of sexuality, opportunities, and frequency of engaging in sexual activities; (2) reduced sex drive; (3) a decline in their ability to give their partner sexual satisfaction and to engage in sexual intercourse; and (4) decreased enjoyment of sexual activity and ability to stay aroused and to climax. The frequencies of such negative changes were significantly higher than those reported by controls and far outweighed the frequency of increases on these dimensions. A significant proportion of TBI participants also reported decreased self-confidence, sex appeal, higher levels of depression, and decreased communication levels and relationship quality with their sexual partner. Factors associated with sexual problems in the TBI group are explored and implications of all findings discussed. PMID:21854338

  13. Effort test performance in clinical acute brain injury, community brain injury, and epilepsy populations.

    Science.gov (United States)

    Hampson, Natalie E; Kemp, Steven; Coughlan, Anthony K; Moulin, Chris J A; Bhakta, Bipin B

    2014-01-01

    Effort tests have become commonplace within medico-legal and forensic contexts and their use is rising within clinical settings. It is recognized that some patients may fail effort tests due to cognitive impairment and not because of poor effort. However, investigation of the base rate of failure among clinical populations other than dementia is limited. Forty-seven clinical participants were recruited and comprised three subgroups: acute brain injury (N = 11), community brain injury (N = 20), and intractable epilepsy (N = 16). Base rates of failure on the Word Memory Test (WMT; Green, 2003 ) and six other less well-validated measures were investigated. A significant minority of patients failed effort tests according to standard cutoff scores, particularly patients with severe traumatic brain injury and marked frontal-executive features. The WMT was able to identify failures associated with significant cognitive impairment through the application of profile analysis and/or lowered cutoff levels. Implications for clinical assessment, effort test interpretation, and future research are discussed. PMID:25084843

  14. Psychological effects of chronic injury in elite athletes.

    OpenAIRE

    Shuer, M L; Dietrich, M S

    1997-01-01

    Many athletes train in a constant state of pain or injury while meeting the demands of an elite level program. It is hypothesized that the emotional distress experienced by athletes with chronic injuries is not inconsequential. A self-report battery, the Impact of Event Scale, was administered to 280 inter-collegiate athletes at a division I institution in an attempt to examine their response to chronic injury. Of the 280, 134 (48%) had been injured by study definition, with 117 (42%) meeting...

  15. Clinical neurorestorative progress in traumatic brain injury

    Directory of Open Access Journals (Sweden)

    Huang H

    2015-03-01

    Full Text Available Huiling Huang,1 Lin Chen,2,3 Hongyun Huang4–61Tianjin Key Laboratory of Cerebral Vascular and Neurodegenerative Diseases, Tianjin Huanhu Hospital, Tianjin Neurosurgical Institute, Tianjin, People's Republic of China; 2Medical Center, Tsinghua University, Beijing, People's Republic of China; 3Tsinghua University Yuquan Hospital, Beijing, People's Republic of China; 4General Hospital of Chinese people's Armed Police Forces, 5Beijing Rehabilitation Hospital of Capital Medical University, Beijing, People's Republic of China; 6Beijing Hongtianji Neuroscience Academy, Beijing, People's Republic of ChinaAbstract: Traumatic brain injury (TBI is a leading cause of death and disability from trauma to the central nervous system. Besides the surgical interventions and symptomatic management, the conventional therapies for TBI and its sequelae are still limited. Recently emerging evidence suggests that some neurorestorative treatments appear to have a potential therapeutic role for TBI and improving the patient's quality of life. The current clinical neurorestorative strategies available in TBI include pharmacological treatments (recombinant human interleukin-1 receptor antagonist, amantadine, lithium, and valproate, the neuromodulation treatments (repetitive transcranial magnetic stimulation, transcranial direct current stimulation, and low-level laser therapy, cell transplantation (bone marrow stromal cells and umbilical cord stromal cells, and combined neurorehabilitation. In this review, we summarize the recent clinical neurorestorative progress in the management of neurodegeneration as well as cognitive and motor deficits after TBI; indeed further clinical trials are required to provide more robust evidence.Keywords: brain trauma, neurorestorative treatment, cell transplantation, clinical study

  16. Disability pensions in relation to traumatic brain injury: a population study

    DEFF Research Database (Denmark)

    Teasdale, T W; Engberg, A W

    2000-01-01

    award appeared to be independent of the injury itself. Rather, being awarded a disability pension appeared to be related to conditions which themselves are risk factors for a traumatic brain injury, e.g. chronic skeletomuscular disease and psychiatric disorders including alcoholism. Comparison with......From a Danish national register of hospitalizations, all patients were identified who had a discharge diagnosis of traumatic brain injury between the years 1979-1993 inclusive, at ages 18-66 years inclusive. These were classified as having suffered either a concussion (n = 74,398), a cranial....... Date of application, grounds for the application, and the pension level awarded were noted. Analysis of the date of application for the disability pension revealed that in all groups a high proportion of the pension applications had been made prior to the injury. Among the concussion group, the pension...

  17. Acute Blast Injury Reduces Brain Abeta in Two Rodent Species

    Directory of Open Access Journals (Sweden)

    GregoryAElder

    2012-12-01

    Full Text Available Blast-induced traumatic brain injury (TBI has been a major cause of morbidity and mortality in the conflicts in Iraq and Afghanistan. How the primary blast wave affects the brain is not well understood. In particular, it is unclear whether blast injures the brain through mechanisms similar to those found in non-blast closed impact injuries (nbTBI. The β-amyloid (Aβ peptide associated with the development of Alzheimer’s disease (AD is elevated acutely following TBI in humans as well as in experimental animal models of nbTBI. We examined levels of brain Aβ following experimental blast injury using enzyme-linked immunosorbent assays for Aβ 40 and 42. In both rat and mouse models of blast injury, rather than being increased, endogenous rodent brain Aβ levels were decreased acutely following injury. Levels of the amyloid precursor protein (APP were increased following blast exposure although there was no evidence of axonal pathology based on APP immunohistochemical staining. Unlike the findings in nbTBI animal models, levels of the β-secretase, BACE-1, and the γ-secretase component presenilin-1 were unchanged following blast exposure. These studies have implications for understanding the nature of blast injury to the brain. They also suggest that strategies aimed at lowering Aβ production may not be effective for treating acute blast injury to the brain.

  18. Traumatic Brain Injury and Delayed Sequelae: A Review - Traumatic Brain Injury and Mild Traumatic Brain Injury (Concussion are Precursors to Later-Onset Brain Disorders, Including Early-Onset Dementia

    Directory of Open Access Journals (Sweden)

    Michael A. Kiraly

    2007-01-01

    Full Text Available Brain injuries are too common. Most people are unaware of the incidence of and horrendous consequences of traumatic brain injury (TBI and mild traumatic brain injury (MTBI. Research and the advent of sophisticated imaging have led to progression in the understanding of brain pathophysiology following TBI. Seminal evidence from animal and human experiments demonstrate links between TBI and the subsequent onset of premature, psychiatric syndromes and neurodegenerative diseases, including Alzheimer's disease (AD and Parkinson's disease (PD. Objectives of this summary are, therefore, to instill appreciation regarding the importance of brain injury prevention, diagnosis, and treatment, and to increase awareness regarding the long-term delayed consequences following TBI.

  19. Delayed, post-injury treatment with aniracetam improves cognitive performance after traumatic brain injury in rats.

    Science.gov (United States)

    Baranova, Anna I; Whiting, Mark D; Hamm, Robert J

    2006-08-01

    Chronic cognitive impairment is an enduring aspect of traumatic brain injury (TBI) in both humans and animals. Treating cognitive impairment in the post-traumatic stages of injury often involves the delivery of pharmacologic agents aimed at specific neurotransmitter systems. The current investigation examined the effects of the nootropoic drug aniracetam on cognitive recovery following TBI in rats. Three experiments were performed to determine (1) the optimal dose of aniracetam for treating cognitive impairment, (2) the effect of delaying drug treatment for a period of days following TBI, and (3) the effect of terminating drug treatment before cognitive assessment. In experiment 1, rats were administered moderate fluid percussion injury and treated with vehicle, 25, or 50 mg/kg aniracetam for 15 days. Both doses of aniracetam effectively reduced injury-induced deficits in the Morris water maze (MWM) as measured on postinjury days 11-15. In experiment 2, injured rats were treated with 50 mg/kg aniracetam or vehicle beginning on day 11 postinjury and continuing for 15 days. MWM performance, assessed on days 26-30, indicates that aniracetam-treated animals performed as well as sham-injured controls. In experiment 3, animals were injured and treated with aniracetam for 15 days. Drug treatment was terminated during MWM testing on postinjury days 16-20. In this experiment, aniracetam-treated rats did not perform better than vehicle-treated rats. The results of these experiments indicate that aniracetam is an effective treatment for cognitive impairment induced by TBI, even when treatment is delayed for a period of days following injury. PMID:16928181

  20. DARPA challenge: developing new technologies for brain and spinal injuries

    Science.gov (United States)

    Macedonia, Christian; Zamisch, Monica; Judy, Jack; Ling, Geoffrey

    2012-06-01

    The repair of traumatic injuries to the central nervous system remains among the most challenging and exciting frontiers in medicine. In both traumatic brain injury and spinal cord injuries, the ultimate goals are to minimize damage and foster recovery. Numerous DARPA initiatives are in progress to meet these goals. The PREventing Violent Explosive Neurologic Trauma program focuses on the characterization of non-penetrating brain injuries resulting from explosive blast, devising predictive models and test platforms, and creating strategies for mitigation and treatment. To this end, animal models of blast induced brain injury are being established, including swine and non-human primates. Assessment of brain injury in blast injured humans will provide invaluable information on brain injury associated motor and cognitive dysfunctions. The Blast Gauge effort provided a device to measure warfighter's blast exposures which will contribute to diagnosing the level of brain injury. The program Cavitation as a Damage Mechanism for Traumatic Brain Injury from Explosive Blast developed mathematical models that predict stresses, strains, and cavitation induced from blast exposures, and is devising mitigation technologies to eliminate injuries resulting from cavitation. The Revolutionizing Prosthetics program is developing an avant-garde prosthetic arm that responds to direct neural control and provides sensory feedback through electrical stimulation. The Reliable Neural-Interface Technology effort will devise technologies to optimally extract information from the nervous system to control next generation prosthetic devices with high fidelity. The emerging knowledge and technologies arising from these DARPA programs will significantly improve the treatment of brain and spinal cord injured patients.

  1. Assessing neuro-systemic & behavioral components in the pathophysiology of blast-related brain injury.

    Science.gov (United States)

    Kobeissy, Firas; Mondello, Stefania; Tümer, Nihal; Toklu, Hale Z; Whidden, Melissa A; Kirichenko, Nataliya; Zhang, Zhiqun; Prima, Victor; Yassin, Walid; Anagli, John; Chandra, Namas; Svetlov, Stan; Wang, Kevin K W

    2013-01-01

    Among the U.S. military personnel, blast injury is among the leading causes of brain injury. During the past decade, it has become apparent that even blast injury as a form of mild traumatic brain injury (mTBI) may lead to multiple different adverse outcomes, such as neuropsychiatric symptoms and long-term cognitive disability. Blast injury is characterized by blast overpressure, blast duration, and blast impulse. While the blast injuries of a victim close to the explosion will be severe, majority of victims are usually at a distance leading to milder form described as mild blast TBI (mbTBI). A major feature of mbTBI is its complex manifestation occurring in concert at different organ levels involving systemic, cerebral, neuronal, and neuropsychiatric responses; some of which are shared with other forms of brain trauma such as acute brain injury and other neuropsychiatric disorders such as post-traumatic stress disorder. The pathophysiology of blast injury exposure involves complex cascades of chronic psychological stress, autonomic dysfunction, and neuro/systemic inflammation. These factors render blast injury as an arduous challenge in terms of diagnosis and treatment as well as identification of sensitive and specific biomarkers distinguishing mTBI from other non-TBI pathologies and from neuropsychiatric disorders with similar symptoms. This is due to the "distinct" but shared and partially identified biochemical pathways and neuro-histopathological changes that might be linked to behavioral deficits observed. Taken together, this article aims to provide an overview of the current status of the cellular and pathological mechanisms involved in blast overpressure injury and argues for the urgent need to identify potential biomarkers that can hint at the different mechanisms involved. PMID:24312074

  2. Assessing Neuro-Systemic & Behavioral Components in the Pathophysiology of Blast-Related Brain Injury

    Directory of Open Access Journals (Sweden)

    Firas H Kobeissy

    2013-11-01

    Full Text Available Among the U.S. military personnel, blast injury is among the leading causes of brain injury. During the past decade, it has become apparent that even blast injury as a form of mild traumatic brain injury (mTBI may lead to multiple different adverse outcomes, such as neuropsychiatric symptoms and long-term cognitive disability. Blast injury is characterized by blast overpressure (BOP, blast duration, and blast impulse. While the blast injuries of a victim close to the explosion will be severe, majority of victims are usually at a distance leading to milder form described as mild blast TBI (mbTBI. A major feature of mbTBI is its complex manifestation occurring in concert at different organ levels involving systemic, cerebral, neuronal and neuropsychiatric responses; some of which are shared with other forms of brain trauma such as acute brain injury and other neuropsychiatric disorders such as PTSD. The pathophysiology of blast injury exposure involves complex cascades of chronic psychological stress, autonomic dysfunction and neuro/systemic inflammation. These factors render blast injury as an arduous challenge in terms of diagnosis and treatment as well as identification of sensitive and specific biomarkers distinguishing mTBI from other non-TBI pathologies and from neuropsychiatric disorders with similar symptoms. This is due to the distinct but shared and partially identified biochemical pathways and neuro-histopathological changes that might be linked to behavioral deficits observed. Taken together, this article aims to provide an overview of the current status of the cellular and pathological mechanisms involved in blast overpressure injury and argues for the urgent need to identify potential biomarkers that can hint at the different mechanisms involved.

  3. BDNF Meditated trkB and Synapsin I Changes within the Hippocampus after Mild Traumatic Brain Injury in Rat:Reflections of Injury-induced Neuroplasticity

    Institute of Scientific and Technical Information of China (English)

    2005-01-01

    1 IntroductionTraumatic brain injury (TBI) can produce chronic cognitive learning/memory deficits that are thought to be mediated, in part, by impaired hippocampal function. Brain-derived neurotrophic factor (BDNF), its signal transduction receptor trkB and its downstream effector synapsin I are involved in this period. BDNF, trkB and the slope of field excitatory post-synaptic potential(fEPSP) were measured in the hippocampus of rat after fluid percussion brain injury (FPI). Isofluorane anaesthe- tizeed 50...

  4. Brain injury tolerance limit based on computation of axonal strain.

    Science.gov (United States)

    Sahoo, Debasis; Deck, Caroline; Willinger, Rémy

    2016-07-01

    Traumatic brain injury (TBI) is the leading cause of death and permanent impairment over the last decades. In both the severe and mild TBIs, diffuse axonal injury (DAI) is the most common pathology and leads to axonal degeneration. Computation of axonal strain by using finite element head model in numerical simulation can enlighten the DAI mechanism and help to establish advanced head injury criteria. The main objective of this study is to develop a brain injury criterion based on computation of axonal strain. To achieve the objective a state-of-the-art finite element head model with enhanced brain and skull material laws, was used for numerical computation of real world head trauma. The implementation of new medical imaging data such as, fractional anisotropy and axonal fiber orientation from Diffusion Tensor Imaging (DTI) of 12 healthy patients into the finite element brain model was performed to improve the brain constitutive material law with more efficient heterogeneous anisotropic visco hyper-elastic material law. The brain behavior has been validated in terms of brain deformation against Hardy et al. (2001), Hardy et al. (2007), and in terms of brain pressure against Nahum et al. (1977) and Trosseille et al. (1992) experiments. Verification of model stability has been conducted as well. Further, 109 well-documented TBI cases were simulated and axonal strain computed to derive brain injury tolerance curve. Based on an in-depth statistical analysis of different intra-cerebral parameters (brain axonal strain rate, axonal strain, first principal strain, Von Mises strain, first principal stress, Von Mises stress, CSDM (0.10), CSDM (0.15) and CSDM (0.25)), it was shown that axonal strain was the most appropriate candidate parameter to predict DAI. The proposed brain injury tolerance limit for a 50% risk of DAI has been established at 14.65% of axonal strain. This study provides a key step for a realistic novel injury metric for DAI. PMID:27038501

  5. Tensor-Based Morphometry Reveals Volumetric Deficits in Moderate=Severe Pediatric Traumatic Brain Injury.

    Science.gov (United States)

    Dennis, Emily L; Hua, Xue; Villalon-Reina, Julio; Moran, Lisa M; Kernan, Claudia; Babikian, Talin; Mink, Richard; Babbitt, Christopher; Johnson, Jeffrey; Giza, Christopher C; Thompson, Paul M; Asarnow, Robert F

    2016-05-01

    Traumatic brain injury (TBI) can cause widespread and prolonged brain degeneration. TBI can affect cognitive function and brain integrity for many years after injury, often with lasting effects in children, whose brains are still immature. Although TBI varies in how it affects different individuals, image analysis methods such as tensor-based morphometry (TBM) can reveal common areas of brain atrophy on magnetic resonance imaging (MRI), secondary effects of the initial injury, which will differ between subjects. Here we studied 36 pediatric moderate to severe TBI (msTBI) participants in the post-acute phase (1-6 months post-injury) and 18 msTBI participants who returned for their chronic assessment, along with well-matched controls at both time-points. Participants completed a battery of cognitive tests that we used to create a global cognitive performance score. Using TBM, we created three-dimensional (3D) maps of individual and group differences in regional brain volumes. At both the post-acute and chronic time-points, the greatest group differences were expansion of the lateral ventricles and reduction of the lingual gyrus in the TBI group. We found a number of smaller clusters of volume reduction in the cingulate gyrus, thalamus, and fusiform gyrus, and throughout the frontal, temporal, and parietal cortices. Additionally, we found extensive associations between our cognitive performance measure and regional brain volume. Our results indicate a pattern of atrophy still detectable 1-year post-injury, which may partially underlie the cognitive deficits frequently found in TBI. PMID:26393494

  6. Tensor-Based Morphometry Reveals Volumetric Deficits in Moderate=Severe Pediatric Traumatic Brain Injury

    Science.gov (United States)

    Hua, Xue; Villalon-Reina, Julio; Moran, Lisa M.; Kernan, Claudia; Babikian, Talin; Mink, Richard; Babbitt, Christopher; Johnson, Jeffrey; Giza, Christopher C.; Thompson, Paul M.; Asarnow, Robert F.

    2016-01-01

    Abstract Traumatic brain injury (TBI) can cause widespread and prolonged brain degeneration. TBI can affect cognitive function and brain integrity for many years after injury, often with lasting effects in children, whose brains are still immature. Although TBI varies in how it affects different individuals, image analysis methods such as tensor-based morphometry (TBM) can reveal common areas of brain atrophy on magnetic resonance imaging (MRI), secondary effects of the initial injury, which will differ between subjects. Here we studied 36 pediatric moderate to severe TBI (msTBI) participants in the post-acute phase (1–6 months post-injury) and 18 msTBI participants who returned for their chronic assessment, along with well-matched controls at both time-points. Participants completed a battery of cognitive tests that we used to create a global cognitive performance score. Using TBM, we created three-dimensional (3D) maps of individual and group differences in regional brain volumes. At both the post-acute and chronic time-points, the greatest group differences were expansion of the lateral ventricles and reduction of the lingual gyrus in the TBI group. We found a number of smaller clusters of volume reduction in the cingulate gyrus, thalamus, and fusiform gyrus, and throughout the frontal, temporal, and parietal cortices. Additionally, we found extensive associations between our cognitive performance measure and regional brain volume. Our results indicate a pattern of atrophy still detectable 1-year post-injury, which may partially underlie the cognitive deficits frequently found in TBI. PMID:26393494

  7. Proton spectroscopy of radiation-induced injury to the brain

    International Nuclear Information System (INIS)

    This paper reports on the role of hydrogen MR spectroscopy (HMRS) in differentiating radiation-injured brain from normal brain and neoplasm, the authors performed HMRS on five cat brains with iatrogenically produced radiation injury. Reductions in N-acetyl aspartate (NAA/choline, and NAA/creatine-phosphocreatine (CR)) resonances were demonstrated in voxels from the five irradiated hemispheres compared with normal hemispheres (P < .01). NAA/CR ratios below 1.21 were always associated with radiation injury; ratios above 1.30 demarcated normal hemispheres. Large unassigned amino acid resonances from 2.0 to 2.5 ppm were also present. Results of autopsy examination confirmed radiation-induced white matter injury. Using NAA/CR ratios, one can separate normal brain from radiation-injured brain. Differentiating residual tumor from radiation-injured and normal brain may be possible with HMRS

  8. Time Series Analysis of Spontaneous Upper-Extremity Movements of Premature Infants With Brain Injuries

    OpenAIRE

    Ohgi, Shohei; Morita, Satoru; Loo, Kek Khee; Mizuike, Chihiro

    2008-01-01

    Background and Purpose: Comparisons of spontaneous movements of premature infants with brain injuries and those without brain injuries can provide insights into normal and abnormal processes in the ontogeny of motor development. In this study, the characteristics of spontaneous upper-extremity movements of premature infants with brain injuries and those without brain injuries were examined with time series analysis.

  9. Pain Catastrophizing Correlates with Early Mild Traumatic Brain Injury Outcome.

    Science.gov (United States)

    Chaput, Geneviève; Lajoie, Susanne P; Naismith, Laura M; Lavigne, Gilles

    2016-01-01

    Background. Identifying which patients are most likely to be at risk of chronic pain and other postconcussion symptoms following mild traumatic brain injury (MTBI) is a difficult clinical challenge. Objectives. To examine the relationship between pain catastrophizing, defined as the exaggerated negative appraisal of a pain experience, and early MTBI outcome. Methods. This cross-sectional design included 58 patients diagnosed with a MTBI. In addition to medical chart review, postconcussion symptoms were assessed by self-report at 1 month (Time 1) and 8 weeks (Time 2) after MTBI. Pain severity, psychological distress, level of functionality, and pain catastrophizing were measured by self-report at Time 2. Results. The pain catastrophizing subscales of rumination, magnification, and helplessness were significantly correlated with pain severity (r = .31 to .44), number of postconcussion symptoms reported (r = .35 to .45), psychological distress (r = .57 to .67), and level of functionality (r = -.43 to -.29). Pain catastrophizing scores were significantly higher for patients deemed to be at high risk of postconcussion syndrome (6 or more symptoms reported at both Time 1 and Time 2). Conclusions. Higher levels of pain catastrophizing were related to adverse early MTBI outcomes. The early detection of pain catastrophizing may facilitate goal-oriented interventions to prevent or minimize the development of chronic pain and other postconcussion symptoms. PMID:27445604

  10. Pain Catastrophizing Correlates with Early Mild Traumatic Brain Injury Outcome

    Directory of Open Access Journals (Sweden)

    Geneviève Chaput

    2016-01-01

    Full Text Available Background. Identifying which patients are most likely to be at risk of chronic pain and other postconcussion symptoms following mild traumatic brain injury (MTBI is a difficult clinical challenge. Objectives. To examine the relationship between pain catastrophizing, defined as the exaggerated negative appraisal of a pain experience, and early MTBI outcome. Methods. This cross-sectional design included 58 patients diagnosed with a MTBI. In addition to medical chart review, postconcussion symptoms were assessed by self-report at 1 month (Time 1 and 8 weeks (Time 2 after MTBI. Pain severity, psychological distress, level of functionality, and pain catastrophizing were measured by self-report at Time 2. Results. The pain catastrophizing subscales of rumination, magnification, and helplessness were significantly correlated with pain severity (r=.31 to .44, number of postconcussion symptoms reported (r=.35 to .45, psychological distress (r=.57 to .67, and level of functionality (r=-.43 to -.29. Pain catastrophizing scores were significantly higher for patients deemed to be at high risk of postconcussion syndrome (6 or more symptoms reported at both Time 1 and Time 2. Conclusions. Higher levels of pain catastrophizing were related to adverse early MTBI outcomes. The early detection of pain catastrophizing may facilitate goal-oriented interventions to prevent or minimize the development of chronic pain and other postconcussion symptoms.

  11. Money, Language Barriers Can Affect Kids' Brain Injury Care

    Science.gov (United States)

    ... https://medlineplus.gov/news/fullstory_159124.html Money, Language Barriers Can Affect Kids' Brain Injury Care Those ... included providers of physical and occupational therapy; speech, language and cognitive therapy; and mental health services. The ...

  12. Money, Language Barriers Can Affect Kids' Brain Injury Care

    Science.gov (United States)

    ... nih.gov/medlineplus/news/fullstory_159124.html Money, Language Barriers Can Affect Kids' Brain Injury Care Those ... included providers of physical and occupational therapy; speech, language and cognitive therapy; and mental health services. The ...

  13. Spreading depolarizations and late secondary insults after traumatic brain injury

    DEFF Research Database (Denmark)

    Hartings, Jed A; Strong, Anthony J; Fabricius, Martin;

    2009-01-01

    Here we investigated the incidence of cortical spreading depolarizations (spreading depression and peri-infarct depolarization) after traumatic brain injury (TBI) and their relationship to systemic physiologic values during neurointensive care. Subdural electrode strips were placed on peri...

  14. Spreading depolarisations and outcome after traumatic brain injury

    DEFF Research Database (Denmark)

    Hartings, Jed A; Bullock, M Ross; Okonkwo, David O;

    2011-01-01

    Pathological waves of spreading mass neuronal depolarisation arise repeatedly in injured, but potentially salvageable, grey matter in 50-60% of patients after traumatic brain injury (TBI). We aimed to ascertain whether spreading depolarisations are independently associated with unfavourable...

  15. Federal Interagency Traumatic Brain Injury Research (FITBIR) Informatics System

    Data.gov (United States)

    U.S. Department of Health & Human Services — The Federal Interagency Traumatic Brain Injury Research (FITBIR) informatics system is an extensible, scalable informatics platform for TBI relevant imaging,...

  16. GH and Pituitary Hormone Alterations After Traumatic Brain Injury.

    Science.gov (United States)

    Karaca, Züleyha; Tanrıverdi, Fatih; Ünlühızarcı, Kürşad; Kelestimur, Fahrettin

    2016-01-01

    Traumatic brain injury (TBI) is a crucially important public health problem around the world, which gives rise to increased mortality and is the leading cause of physical and psychological disability in young adults, in particular. Pituitary dysfunction due to TBI was first described 95years ago. However, until recently, only a few papers have been published in the literature and for this reason, TBI-induced hypopituitarism has been neglected for a long time. Recent studies have revealed that TBI is one of the leading causes of hypopituitarism. TBI which causes hypopituitarism may be characterized by a single head injury such as from a traffic accident or by chronic repetitive head trauma as seen in combative sports including boxing, kickboxing, and football. Vascular damage, hypoxic insult, direct trauma, genetic predisposition, autoimmunity, and neuroinflammatory changes may have a role in the development of hypopituitarism after TBI. Because of the exceptional structure of the hypothalamo-pituitary vasculature and the special anatomic location of anterior pituitary cells, GH is the most commonly lost hormone after TBI, and the frequency of isolated GHD is considerably high. TBI-induced pituitary dysfunction remains undiagnosed and therefore untreated in most patients because of the nonspecific and subtle clinical manifestations of hypopituitarism. Treatment of TBI-induced hypopituitarism depends on the deficient anterior pituitary hormones. GH replacement therapy has some beneficial effects on metabolic parameters and neurocognitive dysfunction. Patients with TBI without neuroendocrine changes and those with TBI-induced hypopituitarism share the same clinical manifestations, such as attention deficits, impulsion impairment, depression, sleep abnormalities, and cognitive disorders. For this reason, TBI-induced hypopituitarism may be neglected in TBI victims and it would be expected that underlying hypopituitarism would aggravate the clinical picture of TBI itself

  17. Cooking breakfast after a brain injury

    Science.gov (United States)

    Tanguay, Annick N.; Davidson, Patrick S. R.; Guerrero Nuñez, Karla V.; Ferland, Mark B.

    2014-01-01

    Acquired brain injury (ABI) often compromises the ability to carry out instrumental activities of daily living such as cooking. ABI patients' difficulties with executive functions and memory result in less independent and efficient meal preparation. Accurately assessing safety and proficiency in cooking is essential for successful community reintegration following ABI, but in vivo assessment of cooking by clinicians is time-consuming, costly, and difficult to standardize. Accordingly, we examined the usefulness of a computerized meal preparation task (the Breakfast Task; Craik and Bialystok, 2006) as an indicator of real life meal preparation skills. Twenty-two ABI patients and 22 age-matched controls completed the Breakfast Task. Patients also completed the Rehabilitation Activities of Daily Living Survey (RADLS; Salmon, 2003) and prepared actual meals that were rated by members of the clinical team. As expected, the ABI patients had significant difficulty on all aspects of the Breakfast Task (failing to have all their foods ready at the same time, over- and under-cooking foods, setting fewer places at the table, and so on) relative to controls. Surprisingly, however, patients' Breakfast Task performance was not correlated with their in vivo meal preparation. These results indicate caution when endeavoring to replace traditional evaluation methods with computerized tasks for the sake of expediency. PMID:25228863

  18. Cooking breakfast after a brain injury

    Directory of Open Access Journals (Sweden)

    Annick N. Tanguay

    2014-09-01

    Full Text Available Acquired brain injury (ABI often compromises the ability to carry out instrumental activities of daily living such as cooking. ABI patients’ difficulties with executive functions and memory result in less independent and efficient meal preparation. Accurately assessing safety and proficiency in cooking is essential for successful community reintegration following ABI, but in vivo assessment of cooking by clinicians is time-consuming, costly, and difficult to standardize. Accordingly, we examined the usefulness of a computerized meal preparation task (the Breakfast Task; Craik & Bialystok, 2006 as an indicator of real life meal preparation skills. Twenty-two ABI patients and 22 age-matched controls completed the Breakfast Task and the Rehabilitation Activities of Daily Living Survey (RADLS; Salmon, 2003. Patients also prepared actual meals, and were rated by members of the clinical team. As expected, the ABI patients had significant difficulty on all aspects of the Breakfast Task (failing to have all their foods ready at the same time, over- and under-cooking foods, setting fewer places at the table, and so on relative to controls. Surprisingly, however, patients’ Breakfast Task performance was not correlated with their in vivo meal preparation. These results indicate caution when endeavoring to replace traditional evaluation methods with computerized tasks for the sake of expediency.

  19. Neuroprotective efficacy of a proneurogenic compound after traumatic brain injury.

    Science.gov (United States)

    Blaya, Meghan O; Bramlett, Helen M; Naidoo, Jacinth; Pieper, Andrew A; Dietrich, W Dalton

    2014-03-01

    Traumatic brain injury (TBI) is characterized by histopathological damage and long-term sensorimotor and cognitive dysfunction. Recent studies have reported the discovery of the P7C3 class of aminopropyl carbazole agents with potent neuroprotective properties for both newborn neural precursor cells in the adult hippocampus and mature neurons in other regions of the central nervous system. This study tested, for the first time, whether the highly active P7C3-A20 compound would be neuroprotective, promote hippocampal neurogenesis, and improve functional outcomes after experimental TBI. Sprague-Dawley rats subjected to moderate fluid percussion brain injury were evaluated for quantitative immunohistochemical and behavioral changes after trauma. P7C3-A20 (10 mg/kg) or vehicle was initiated intraperitoneally 30 min postsurgery and twice per day every day thereafter for 7 days. Administration of P7C3-A20 significantly reduced overall contusion volume, preserved vulnerable anti-neuronal nuclei (NeuN)-positive pericontusional cortical neurons, and improved sensorimotor function 1 week after trauma. P7C3-A20 treatment also significantly increased both bromodeoxyuridine (BrdU)- and doublecortin (DCX)-positive cells within the subgranular zone of the ipsilateral dentate gyrus 1 week after TBI. Five weeks after TBI, animals treated with P7C3-A20 showed significantly increased BrdU/NeuN double-labeled neurons and improved cognitive function in the Morris water maze, compared to TBI-control animals. These results suggest that P7C3-A20 is neuroprotective and promotes endogenous reparative strategies after TBI. We propose that the chemical scaffold represented by P7C3-A20 provides a basis for optimizing and advancing new pharmacological agents for protecting patients against the early and chronic consequences of TBI. PMID:24070637

  20. Cortical edema in moderate fluid percussion brain injury is attenuated by vagus nerve stimulation.

    Science.gov (United States)

    Clough, R W; Neese, S L; Sherill, L K; Tan, A A; Duke, A; Roosevelt, R W; Browning, R A; Smith, D C

    2007-06-29

    Development of cerebral edema (intracellular and/or extracellular water accumulation) following traumatic brain injury contributes to mortality and morbidity that accompanies brain injury. Chronic intermittent vagus nerve stimulation (VNS) initiated at either 2 h or 24 h (VNS: 30 s train of 0.5 mA, 20 Hz, biphasic pulses every 30 min) following traumatic brain injury enhances recovery of motor and cognitive function in rats in the weeks following brain injury; however, the mechanisms of facilitated recovery are unknown. The present study examines the effects of VNS on development of acute cerebral edema following unilateral fluid percussion brain injury (FPI) in rats, concomitant with assessment of their behavioral recovery. Two hours following FPI, VNS was initiated. Behavioral testing, using both beam walk and locomotor placing tasks, was conducted at 1 and 2 days following FPI. Edema was measured 48 h post-FPI by the customary method of region-specific brain weights before and after complete dehydration. Results of this study replicated that VNS initiated at 2 h after FPI: 1) effectively facilitated the recovery of vestibulomotor function at 2 days after FPI assessed by beam walk performance (P<0.01); and 2) tended to improve locomotor placing performance at the same time point (P=0.18). Most interestingly, results of this study showed that development of edema within the cerebral cortex ipsilateral to FPI was significantly attenuated at 48 h in FPI rats receiving VNS compared with non-VNS FPI rats (P<0.04). Finally, a correlation analysis between beam walk performance and cerebral edema following FPI revealed a significant inverse correlation between behavior performance and cerebral edema. Together, these results suggest that VNS facilitation of motor recovery following experimental brain injury in rats is associated with VNS-mediated attenuation of cerebral edema. PMID:17543463

  1. The psychosocial outcome of anoxic brain injury following cardiac arrest

    OpenAIRE

    Wilson, Michelle

    2012-01-01

    Aim of the study The psychosocial outcome of anoxic brain injury following cardiac arrest is a relatively under researched, but clinically important area. The aim of the current study was to add to the limited existing literature exploring the psychosocial outcome for cardiac arrest survivors, but specifically explore if there is a greater impact on psychosocial outcome in individuals experiencing anoxic brain injury as a result. Methods A range of self report measures were used to c...

  2. Psychotherapy after acquired brain injury: Is less more?

    Directory of Open Access Journals (Sweden)

    Rudi Coetzer

    2014-02-01

    Full Text Available This paper considers the challenges and dilemmas facing psychotherapists working with neurological patients, and in particular those who work in the context of under-resourced brain injury rehabilitation healthcare systems. Through the subjective process of reflective practice integral to clinical supervision, the author attempts to identify five core aspects of psychotherapy intended to augment post-acute long- term rehabilitation programmes and interventions after acquired brain injury.

  3. Cognitive functions in drivers with brain injury : Anticipation and adaption

    OpenAIRE

    Lundqvist, Anna

    2001-01-01

    The purpose of this thesis was to improve the understanding of what cognitive functions are important for driving performance, investigate the impact of impaired cognitive functions on drivers with brain injury, and study adaptation strategies relevant for driving performance after brain injury. Finally, the predictive value of a neuropsychological test battery was evaluated for driving performance. Main results can be summarized in the following conclusions: (a) Cognitive functions in terms ...

  4. Endogenous lipoid pneumonia in a cachectic patient after brain injury

    OpenAIRE

    Zhang, Ji; Mu, Jiao; Lin, Wei; Dong, Hongmei

    2015-01-01

    Endogenous lipoid pneumonia (EnLP) is an uncommon non-life-threatening inflammatory lung disease that usually occurs in patients with conditions such as lung cancers, primary sclerosing cholangitis, and undifferentiated connective tissue disease. Here we report a case of EnLP in a paralytic and cachectic patient with bronchopneumonia after brain injury. A 40-year-old man experienced a severe brain injury in an automobile accident. He was treated for 1 month and his status plateaued. However, ...

  5. Antagonism of purinergic signalling improves recovery from traumatic brain injury

    OpenAIRE

    Choo, Anthony M.; William J. Miller; Chen, Yung-Chia; Nibley, Philip; Patel, Tapan P.; Goletiani, Cezar; Morrison, Barclay; Kutzing, Melinda K.; Firestein, Bonnie L.; Sul, Jai-Yoon; Haydon, Philip G.; Meaney, David F.

    2013-01-01

    The recent public awareness of the incidence and possible long-term consequences of traumatic brain injury only heightens the need to develop effective approaches for treating this neurological disease. In this report, we identify a new therapeutic target for traumatic brain injury by studying the role of astrocytes, rather than neurons, after neurotrauma. We use in vivo multiphoton imaging and show that mechanical forces during trauma trigger intercellular calcium waves throughout the astroc...

  6. Optimizing sedation in patients with acute brain injury

    OpenAIRE

    Oddo, Mauro; Crippa, Ilaria Alice; Mehta, Sangeeta; Menon, David; Payen, Jean-Francois; Taccone, Fabio Silvio; Citerio, Giuseppe

    2016-01-01

    Daily interruption of sedative therapy and limitation of deep sedation have been shown in several randomized trials to reduce the duration of mechanical ventilation and hospital length of stay, and to improve the outcome of critically ill patients. However, patients with severe acute brain injury (ABI; including subjects with coma after traumatic brain injury, ischaemic/haemorrhagic stroke, cardiac arrest, status epilepticus) were excluded from these studies. Therefore, whether the new paradi...

  7. Injury to Allografts: innate immune pathways to acute and chronic rejection

    International Nuclear Information System (INIS)

    An emerging body of evidence suggests that innate immunity, as the first line of host defense against invading pathogens or their components [pathogen-associated molecular patterns, (PAMPs)], plays also a critical role in acute and chronic allograft rejection. Injury to the donor organ induces an inflammatory milieu in the allograft, which appears to be the initial key event for activation of the innate immune system. Injury-induced generation of putative endogenous molecular ligand, in terms of damaged/danger-associated molecular patterns (DAMPs) such as heat shock proteins, are recognized by Toll-like receptors (TLRs), a family of pattern recognition receptors on cells of innate immunity. Acute allograft injury (e.g. oxidative stress during donor brain-death condition, post-ischemic reperfusion injury in the recipient) includes DAMPs which may interact with, and activate, innate TLR-bearing dendritic cells (DCs) which, in turn, via direct allo-recognition through donor-derived DCs and indirect allo-recogntion through recipient-derived DCs, initiate the recipient's adaptive alloimmune response leading to acute allograft rejection. Chronic injurious events in the allograft (e.g. hypertension, hyperlipidemia, CMV infection, administration of cell-toxic drugs [calcineurin-inhibitors]) induce the generation of DAMPs, which may interact with and activate innate TLR-bearing vascular cells (endothelial cells, smooth muscle cells) which, in turn, contribute to the development of atherosclerosis of donor organ vessels (alloatherosclerosis), thus promoting chronic allograft rejection. (author)

  8. Transcranial amelioration of inflammation and cell death after brain injury

    Science.gov (United States)

    Roth, Theodore L.; Nayak, Debasis; Atanasijevic, Tatjana; Koretsky, Alan P.; Latour, Lawrence L.; McGavern, Dorian B.

    2014-01-01

    Traumatic brain injury (TBI) is increasingly appreciated to be highly prevalent and deleterious to neurological function. At present, no effective treatment options are available, and little is known about the complex cellular response to TBI during its acute phase. To gain insights into TBI pathogenesis, we developed a novel murine closed-skull brain injury model that mirrors some pathological features associated with mild TBI in humans and used long-term intravital microscopy to study the dynamics of the injury response from its inception. Here we demonstrate that acute brain injury induces vascular damage, meningeal cell death, and the generation of reactive oxygen species (ROS) that ultimately breach the glial limitans and promote spread of the injury into the parenchyma. In response, the brain elicits a neuroprotective, purinergic-receptor-dependent inflammatory response characterized by meningeal neutrophil swarming and microglial reconstitution of the damaged glial limitans. We also show that the skull bone is permeable to small-molecular-weight compounds, and use this delivery route to modulate inflammation and therapeutically ameliorate brain injury through transcranial administration of the ROS scavenger, glutathione. Our results shed light on the acute cellular response to TBI and provide a means to locally deliver therapeutic compounds to the site of injury.

  9. Retinochoroidal changes after severe brain impact injury in rabbits

    Institute of Scientific and Technical Information of China (English)

    2001-01-01

    Objective: To investigate retinochoroidal changes and establisheye damage model after brain impact injury.Methods: An eye damage model after brain impact injury was established by striking the frontoparietal zone in rabbits with BIM-Ⅱ bioimpact machine. Seventeen rabbits were killed at 4 different intervals after injury. The pathological characteristics of the retinal and choroid damages were observed.Results: All the rabbits had severe brain injury with subarachnoid hemorrhage and brain contusion. The eye damage occurred in all of the 17 rabbits. Hemorrhage in optic nerve sheaths was observed and retinal edema and bleeding was discovered with ophthalmoscope. Histopathologic study displayed subarachnoid hemorrhage in the retrobulbar portion of the retinal nerve, general choroid blood vessel dilatation, retinal nerve fibre swelling within 6 hours after injury, and flat retinal detachment with subretinal proteinoid exudation, and degeneration and disappearance of the outer segment of the optic cell over 6 hours after injury.Conclusions: The pathological characteristic of the eye damage at early stage following brain impact injury is local circulation disturbance. At late stage, it features in retinal detachment, and optic cellular degeneration and necrosis.

  10. Development of an Ontology for Rehabilitation: Traumatic Brain Injury

    Science.gov (United States)

    Grove, Michael J.

    2013-01-01

    Traumatic Brain Injury (TBI) rehabilitation interventions are very heterogeneous due to injury characteristics and pathology, patient demographics, healthcare settings, caregiver variability, and individualized, multi-discipline treatment plans. Consequently, comparing and generalizing the effectiveness of interventions is limited largely due to…

  11. Traumatic Brain Injury: Persistent Misconceptions and Knowledge Gaps among Educators

    Science.gov (United States)

    Ettel, Deborah; Glang, Ann E.; Todis, Bonnie; Davies, Susan C.

    2016-01-01

    Each year approximately 700,000 U.S. children aged 0-19 years sustain a traumatic brain injury (TBI) placing them at risk for academic, cognitive, and behavioural challenges. Although TBI has been a special education disability category for 25 years, prevalence studies show that of the 145,000 students each year who sustain long-term injury from…

  12. Neuroprotective effect of Pycnogenol® following traumatic brain injury

    OpenAIRE

    Scheff, Stephen W.; Ansari, Mubeen A.; Roberts, Kelly N.

    2012-01-01

    Traumatic brain injury (TBI) involves primary and secondary injury cascades that underlie delayed neuronal dysfunction and death. Oxidative stress is one of the most celebrated secondary injury mechanisms. A close relationship exists between levels of oxidative stress and the pathogenesis of TBI. However, other cascades, such as an increase in proinflammatory cytokines, also play important roles in the overall response to the trauma. Pharmacologic intervention, in order to be successful, requ...

  13. Head motions while riding roller coasters: Implications for brain injury

    OpenAIRE

    Pfister, Bryan J.; Chickola, Larry; Smith, Douglas H.

    2009-01-01

    The risk of traumatic brain injury (TBI) while riding roller coasters has received substantial attention. Case reports of TBI around the time of riding roller coasters have led many medical professionals to assert that the high gravitational forces (G-forces) induced by roller coasters pose a significant TBI risk. Head injury research, however, has shown that G-forces alone cannot predict TBI. Established head injury criterions and procedures were employed to compare the potential of TBI betw...

  14. Mental Trauma Experienced by Caregivers of patients with Diffuse Axonal Injury or Severe Traumatic Brain Injury

    Directory of Open Access Journals (Sweden)

    Syed Tajuddin Syed Hassan

    2013-09-01

    Full Text Available Context: As with care giving and rehabilitation in chronic illnesses, the concern with traumatic brain injury (TBI, particularly with diffuse axonal injury (DAI, is that the caregivers are so overwhelmingly involved in caring and rehabilitation of the victim that in the process they become traumatized themselves. This review intends to shed light on the hidden and silent trauma sustained by the caregivers of severe brain injury survivors. Motor vehicle accident (MVA is the highest contributor of TBI or DAI. The essence of trauma is the infliction of pain and suffering and having to bear the pain (i.e. by the TBI survivor and the burden of having to take care and manage and rehabilitate the TBI survivor (i.e. by the TBI caregiver. Moreover many caregivers are not trained for their care giving task, thus compounding the stress of care giving and rehabilitating patients. Most research on TBI including DAI, focus on the survivors and not on the caregivers. TBI injury and its effects and impacts remain the core question of most studies, which are largely based on the quantitative approach.Evidence Acquisition: Qualitative research can better assess human sufferings such as in the case of DAI trauma. While quantitative research can measure many psychometric parameters to assess some aspects of trauma conditions, qualitative research is able to fully reveal the meaning, ramification and experience of TBI trauma. Both care giving and rehabilitation are overwhelmingly demanding; hence , they may complicate the caregivers’ stress. However, some positive outcomes also exist.Results: Caregivers involved in caring and rehabilitation of TBI victims may become mentally traumatized. Posttraumatic recovery of the TBI survivor can enhance the entire family’s closeness and bonding as well as improve the mental status of the caregiver.Conclusions: A long-term longitudinal study encompassing integrated research is needed to fully understand the traumatic

  15. Low pressure hyperbaric oxygen therapy and SPECT brain imaging in the treatment of blast-induced chronic traumatic brain injury (post-concussion syndrome) and post traumatic stress disorder: a case report

    OpenAIRE

    Harch, Paul G.; Fogarty, Edward F; Staab, Paul K; Van Meter, Keith

    2009-01-01

    A 25-year-old male military veteran presented with diagnoses of post concussion syndrome and post traumatic stress disorder three years after loss of consciousness from an explosion in combat. The patient underwent single photon emission computed tomography brain blood flow imaging before and after a block of thirty-nine 1.5 atmospheres absolute hyperbaric oxygen treatments. The patient experienced a permanent marked improvement in his post-concussive symptoms, physical exam findings, and bra...

  16. Assessment of brain retraction injury from tumor operation with 99Tcm-ECD brain SPECT imaging

    International Nuclear Information System (INIS)

    Objective: To evaluate the rCBF of brain retraction injury by 99Tcm-ECD SPECT imaging. Methods: The 99Tcm-ECD SPECT brain imaging was performed in 21 patients with brain tumor before and after operation. To compare the rCBF of peripheral tumor region with that of retraction injury region by semi-quantitative analysis. The rCBF levels of the central and peripheral areas of brain retraction injury were also studied. Results: Both the peripheral tumor region before operation and retraction region after operation were ischemic, but the difference between them was significant (P99Tcm-ECD SPECT brain imaging is a useful technique in detecting retraction injury come from brain tumor operation

  17. Early endocrine alterations reflect prolonged stress and relate to one year functional outcome in patients with severe brain injury

    DEFF Research Database (Denmark)

    Marina, Djordje; Klose, Marianne; Nordenbo, Annette;

    2015-01-01

    OBJECTIVE: Severe brain injury poses a risk of developing acute and chronic hypopituitarism. Pituitary hormone alterations developed in the early recovery phase after brain injury may have implications for long-term functional recovery. The objective was to assess the pattern and prevalence of......-Extended. RESULTS: Three months after the injury, elevated stress hormones (i.e. 30 min. stimulated cortisol, prolactin and/or insulin-like growth factor 1) and/or suppressed gonadal- or thyroid hormones were recorded in 68% and 32% of the patients, respectively. At one year, lower functioning level (Functional...

  18. Is Progressive Chronic Kidney Disease a Slow Acute Kidney Injury?

    Science.gov (United States)

    Cowgill, Larry D; Polzin, David J; Elliott, Jonathan; Nabity, Mary B; Segev, Gilad; Grauer, Gregory F; Brown, Scott; Langston, Cathy; van Dongen, Astrid M

    2016-11-01

    International Renal Interest Society chronic kidney disease Stage 1 and acute kidney injury Grade I categorizations of kidney disease are often confused or ignored because patients are nonazotemic and generally asymptomatic. Recent evidence suggests these seemingly disparate conditions may be mechanistically linked and interrelated. Active kidney injury biomarkers have the potential to establish a new understanding for traditional views of chronic kidney disease, including its early identification and possible mediators of its progression, which, if validated, would establish a new and sophisticated paradigm for the understanding and approach to the diagnostic evaluation, and treatment of urinary disease in dogs and cats. PMID:27593574

  19. Neuronal regeneration in a zebrafish model of adult brain injury

    Directory of Open Access Journals (Sweden)

    Norihito Kishimoto

    2012-03-01

    Neural stem cells in the subventricular zone (SVZ of the adult mammalian forebrain are a potential source of neurons for neural tissue repair after brain insults such as ischemic stroke and traumatic brain injury (TBI. Recent studies show that neurogenesis in the ventricular zone (VZ of the adult zebrafish telencephalon has features in common with neurogenesis in the adult mammalian SVZ. Here, we established a zebrafish model to study injury-induced neurogenesis in the adult brain. We show that the adult zebrafish brain possesses a remarkable capacity for neuronal regeneration. Telencephalon injury prompted the proliferation of neuronal precursor cells (NPCs in the VZ of the injured hemisphere, compared with in the contralateral hemisphere. The distribution of NPCs, viewed by BrdU labeling and ngn1-promoter-driven GFP, suggested that they migrated laterally and reached the injury site via the subpallium and pallium. The number of NPCs reaching the injury site significantly decreased when the fish were treated with an inhibitor of γ-secretase, a component of the Notch signaling pathway, suggesting that injury-induced neurogenesis mechanisms are at least partly conserved between fish and mammals. The injury-induced NPCs differentiated into mature neurons in the regions surrounding the injury site within a week after the injury. Most of these cells expressed T-box brain protein (Tbr1, suggesting they had adopted the normal neuronal fate in this region. These results suggest that the telencephalic VZ contributes to neural tissue recovery following telencephalic injury in the adult zebrafish, and that the adult zebrafish is a useful model for regenerative medicine.

  20. Treatments for traumatic brain injury with emphasis on transcranial near-infrared laser phototherapy

    OpenAIRE

    Morries LD; Cassano P; Henderson TA

    2015-01-01

    Larry D Morries,1 Paolo Cassano,2 Theodore A Henderson1,3 1Neuro-Laser Foundation, Lakewood, CO, 2Harvard Medical School, Depression Clinical and Research Program, Massachusetts General Hospital, Boston, MA, 3The Synaptic Space, Centennial, CO, USA Abstract: Traumatic brain injury (TBI) is a growing health concern affecting civilians and military personnel. In this review, treatments for the chronic TBI patient are discussed, including pharmaceuticals, nutraceuticals, cognitive therapy, and...

  1. Modeling community integration in workers with delayed recovery from mild traumatic brain injury

    OpenAIRE

    Mollayeva, Tatyana; Shapiro, Colin M; Mollayeva, Shirin; Cassidy, J David; Colantonio, Angela

    2015-01-01

    Background Delayed recovery in persons after mild traumatic brain injury (mTBI) is poorly understood. Community integration (CI) is endorsed by persons with neurological disorders as an important outcome. We aimed to describe CI and its associated factors in insured Ontario workers with delayed recovery following mTBI. Methods A cross-sectional study of insured workers in the chronic phase following mTBI was performed at a rehabilitation hospital in Ontario, Canada. Sociodemographic, occupati...

  2. The impact of chronic stress on the rat brain lipidome

    OpenAIRE

    Oliveira, Tiago Gil; Chan, Robin B.; Bravo, Francisca Vaz; Miranda, André; Silva, Rita Ribeiro; Zhou, Bowen; Marques, Fernanda; Pinto, Vítor; Cerqueira, João José; Di Paolo, Gilbert; Sousa, Nuno

    2015-01-01

    Chronic stress is a major risk factor for several human disorders that affect modern societies. The brain is a key target of chronic stress. In fact, there is growing evidence indicating that exposure to stress affects learning and memory, decision making and emotional responses, and may even predispose for pathological processes, such as Alzheimer’s disease (AD) and depression. Lipids are a major constituent of the brain, and specifically signaling lipids have been shown to regulate brain fu...

  3. Treatment for delayed brain injury after pituitary irradiation

    International Nuclear Information System (INIS)

    Treatment for delayed brain injury after pituitary irradiation is discussed. Six cases with delayed brain injury were treated with a combination of dexamethasone or betamethasone, with heparin, glycerol, dextran 40 and some vasodilators. Two cases with temporal lobe syndrome were treated in the early stages of brain injury for a period of over 12 months were almost completely cured, another two cases with chiasma syndrome were treated in the relatively late stages, showed a partial improvement. One case which was irradiated 120 GY during 13 years did not improve. The final case treated with steroids for a short period also resulted in failure and the patient underwent an operation for the removal of the necrotic mass three years after the radiotherapy. Steroid therapy started in the early stages of brain injury after irradiation for over the 12 months is thought to be effective. Heparin therapy was also effective in one out of three cases, but in one of the cases subarachnoid hemorrhage from a traumatic aneurysm occurred during the therapy. In an acute phase, showing edematous change of the injured brain, the administration of glycerol is also thought to be useful. But the effectiveness of the other medicines containing some vasodilators was obscure or doubtful. We propose the following : (1) A meticulous observation is essential for the patients who received high doses of irradiation to diagnose brain injury in the early reversible stage. (2) Steroids should be given immediately in this reversible stage of brain injury before the irreversible ''necrosis'' occurs. (3) Steroids should be maintained for a long period over 12 months. (4) Heparin therapy is also thought to be effective, but careful precautions to avoid hemorrhagic complications before the therapy should be scheduled. This recommended plan may also be used for the treatment of brain injuries after cranial irradiation for other intracranial tumors. (author)

  4. Treatment for delayed brain injury after pituitary irradiation

    Energy Technology Data Exchange (ETDEWEB)

    Fujii, Takashi; Misumi, Shuzoh; Shibasaki, Takashi; Tamura, Masaru; Kunimine, Hideo; Hayakawa, Kazushige; Niibe, Hideo; Miyazaki, Mizuho; Miyagi, Osamu.

    1988-03-01

    Treatment for delayed brain injury after pituitary irradiation is discussed. Six cases with delayed brain injury were treated with a combination of dexamethasone or betamethasone, with heparin, glycerol, dextran 40 and some vasodilators. Two cases with temporal lobe syndrome were treated in the early stages of brain injury for a period of over 12 months were almost completely cured, another two cases with chiasma syndrome were treated in the relatively late stages, showed a partial improvement. One case which was irradiated 120 GY during 13 years did not improve. The final case treated with steroids for a short period also resulted in failure and the patient underwent an operation for the removal of the necrotic mass three years after the radiotherapy. Steroid therapy started in the early stages of brain injury after irradiation for over the 12 months is thought to be effective. Heparin therapy was also effective in one out of three cases, but in one of the cases subarachnoid hemorrhage from a traumatic aneurysm occurred during the therapy. In an acute phase, showing edematous change of the injured brain, the administration of glycerol is also thought to be useful. But the effectiveness of the other medicines containing some vasodilators was obscure or doubtful. We propose the following : (1) A meticulous observation is essential for the patients who received high doses of irradiation to diagnose brain injury in the early reversible stage. (2) Steroids should be given immediately in this reversible stage of brain injury before the irreversible ''necrosis'' occurs. (3) Steroids should be maintained for a long period over 12 months. (4) Heparin therapy is also thought to be effective, but careful precautions to avoid hemorrhagic complications before the therapy should be scheduled. This recommended plan may also be used for the treatment of brain injuries after cranial irradiation for other intracranial tumors.

  5. Bryostatin-1 Restores Blood Brain Barrier Integrity following Blast-Induced Traumatic Brain Injury.

    Science.gov (United States)

    Lucke-Wold, Brandon P; Logsdon, Aric F; Smith, Kelly E; Turner, Ryan C; Alkon, Daniel L; Tan, Zhenjun; Naser, Zachary J; Knotts, Chelsea M; Huber, Jason D; Rosen, Charles L

    2015-12-01

    Recent wars in Iraq and Afghanistan have accounted for an estimated 270,000 blast exposures among military personnel. Blast traumatic brain injury (TBI) is the 'signature injury' of modern warfare. Blood brain barrier (BBB) disruption following blast TBI can lead to long-term and diffuse neuroinflammation. In this study, we investigate for the first time the role of bryostatin-1, a specific protein kinase C (PKC) modulator, in ameliorating BBB breakdown. Thirty seven Sprague-Dawley rats were used for this study. We utilized a clinically relevant and validated blast model to expose animals to moderate blast exposure. Groups included: control, single blast exposure, and single blast exposure + bryostatin-1. Bryostatin-1 was administered i.p. 2.5 mg/kg after blast exposure. Evan's blue, immunohistochemistry, and western blot analysis were performed to assess injury. Evan's blue binds to albumin and is a marker for BBB disruption. The single blast exposure caused an increase in permeability compared to control (t = 4.808, p < 0.05), and a reduction back toward control levels when bryostatin-1 was administered (t = 5.113, p < 0.01). Three important PKC isozymes, PKCα, PKCδ, and PKCε, were co-localized primarily with endothelial cells but not astrocytes. Bryostatin-1 administration reduced toxic PKCα levels back toward control levels (t = 4.559, p < 0.01) and increased the neuroprotective isozyme PKCε (t = 6.102, p < 0.01). Bryostatin-1 caused a significant increase in the tight junction proteins VE-cadherin, ZO-1, and occludin through modulation of PKC activity. Bryostatin-1 ultimately decreased BBB breakdown potentially due to modulation of PKC isozymes. Future work will examine the role of bryostatin-1 in preventing chronic neurodegeneration following repetitive neurotrauma. PMID:25301233

  6. Chronic post-traumatic headache after mild head injury

    DEFF Research Database (Denmark)

    Kjeldgaard, Dorte; Forchhammer, Hysse; Teasdale, Tom;

    2014-01-01

    BACKGROUND: The aetiology behind chronic post-traumatic headache (CPTH) after mild head injury is unclear and management is complicated. In order to optimize treatment strategies we aimed to characterize a CPTH population. METHODS: Ninety patients with CPTH and 45 patients with chronic primary he...... levels of disability for the CPTH patients suggests directions for further research into what important factors are embedded in the patients' PTSD symptoms and might explain their prolonged illness....

  7. Measuring and Inducing Brain Plasticity in Chronic Aphasia

    Science.gov (United States)

    Fridriksson, Julius

    2011-01-01

    Brain plasticity associated with anomia recovery in aphasia is poorly understood. Here, I review four recent studies from my lab that focused on brain modulation associated with long-term anomia outcome, its behavioral treatment, and the use of transcranial brain stimulation to enhance anomia treatment success in individuals with chronic aphasia…

  8. Neuroprotective levels of IGF-1 exacerbate epileptogenesis after brain injury.

    Science.gov (United States)

    Song, Yu; Pimentel, Corrin; Walters, Katherine; Boller, Lauren; Ghiasvand, Shabnam; Liu, Jing; Staley, Kevin J; Berdichevsky, Yevgeny

    2016-01-01

    Exogenous Insulin-Like Growth Factor-1 (IGF-1) is neuroprotective in animal models of brain injury, and has been considered as a potential therapeutic. Akt-mTOR and MAPK are downstream targets of IGF-1 signaling that are activated after brain injury. However, both brain injury and mTOR are linked to epilepsy, raising the possibility that IGF-1 may be epileptogenic. Here, we considered the role of IGF-1 in development of epilepsy after brain injury, using the organotypic hippocampal culture model of post-traumatic epileptogenesis. We found that IGF-1 was neuroprotective within a few days of injury but that long-term IGF-1 treatment was pro-epileptic. Pro-epileptic effects of IGF-1 were mediated by Akt-mTOR signaling. We also found that IGF-1 - mediated increase in epileptic activity led to neurotoxicity. The dualistic nature of effects of IGF-1 treatment demonstrates that anabolic enhancement through IGF-1 activation of mTOR cascade can be beneficial or harmful depending on the stage of the disease. Our findings suggest that epilepsy risk may need to be considered in the design of neuroprotective treatments for brain injury. PMID:27561791

  9. Low Level Primary Blast Injury in Rodent Brain

    OpenAIRE

    Pun, Pamela B. L.; Kan, Enci Mary; Salim, Agus; Li, Zhaohui; Ng, Kian Chye; Moochhala, Shabbir M; Ling, Eng-Ang; Tan, Mui Hong; Lu, Jia

    2011-01-01

    The incidence of blast attacks and resulting traumatic brain injuries has been on the rise in recent years. Primary blast is one of the mechanisms in which the blast wave can cause injury to the brain. The aim of this study was to investigate the effects of a single sub-lethal blast over pressure (BOP) exposure of either 48.9 kPa (7.1 psi) or 77.3 kPa (11.3 psi) to rodents in an open-field setting. Brain tissue from these rats was harvested for microarray and histopathological analyses. Gross...

  10. Acute Blast Injury Reduces Brain Abeta in Two Rodent Species

    OpenAIRE

    GregoryAElder; MiguelA.Gama Sosa; RitaDe Gasperi; MichaelCShaughness; StevenTDeKosky; SamGandy; MadhusoodanaPNambiar; JohnWSteele

    2012-01-01

    Blast-induced traumatic brain injury (TBI) has been a major cause of morbidity and mortality in the conflicts in Iraq and Afghanistan. How the primary blast wave affects the brain is not well understood. In particular, it is unclear whether blast injures the brain through mechanisms similar to those found in non-blast closed impact injuries (nbTBI). The β-amyloid (Aβ) peptide associated with the development of Alzheimer’s disease (AD) is elevated acutely following TBI in humans as well as in ...

  11. Low level primary blast injury in rodent brain

    OpenAIRE

    Enci MaryKan; AgusSalim; Zhao HuiLi; Eng-AngLing

    2011-01-01

    The incidence of blast attacks and resulting traumatic brain injuries has been on the rise in recent years. Primary blast is one of the mechanisms in which the blast wave can cause injury to the brain. The aim of this study was to investigate the effects of a single sub-lethal blast over pressure exposure of either 48.9 kPa (7.1 psi) or 77.3 kPa (11.3 psi) to rodents in an open-field setting. Brain tissue from these rats was harvested for microarray and histopathological analyses. Gross histo...

  12. Acute Blast Injury Reduces Brain Abeta in Two Rodent Species

    OpenAIRE

    De Gasperi, Rita; Gama Sosa, Miguel A; Kim, Soong Ho; Steele, John W.; Shaughness, Michael C; Maudlin-Jeronimo, Eric; Hall, Aaron A.; DeKosky, Steven T.; McCarron, Richard M; Nambiar, Madhusoodana P.; Gandy, Sam; Ahlers, Stephen T.; Elder, Gregory A.

    2012-01-01

    Blast-induced traumatic brain injury (TBI) has been a major cause of morbidity and mortality in the conflicts in Iraq and Afghanistan. How the primary blast wave affects the brain is not well understood. In particular, it is unclear whether blast injures the brain through mechanisms similar to those found in non-blast closed impact injuries (nbTBI). The β-amyloid (Aβ) peptide associated with the development of Alzheimer’s disease is elevated acutely following TBI in humans as well as in exper...

  13. Emergency treatment options for pediatric traumatic brain injury

    OpenAIRE

    Exo, J; Smith, C.; Smith, R.; Bell, MJ

    2009-01-01

    Traumatic brain injury is a leading killer of children and is a major public health problem around the world. Using general principles of neurocritical care, various treatment strategies have been developed to attempt to restore homeostasis to the brain and allow brain healing, including mechanical factors, cerebrospinal fluid diversion, hyperventilation, hyperosmolar therapies, barbiturates and hypothermia. Careful application of these therapies, normally in a step-wise fashion as intracrani...

  14. Astrocytes mediate the neuroprotective effects of Tibolone following brain injury

    OpenAIRE

    Luis Miguel Garcia-Segura; Barreto, George E.

    2015-01-01

    Recently, astrocytes have become a key central player in mediating important functions in the brain. These physiological processes include neurotransmitter recycling, energy management, metabolic shuttle, immune sensing, K+ buffer, antioxidant supply and release of neurotrophic factors and gliotransmitters. These astrocytic roles are somehow altered upon brain injury, therefore strategies aimed at better protecting astrocytes are an essential asset to maintain brain homeostasis. In this cont...

  15. Enriched environment improves the cognitive effects from traumatic brain injury in mice.

    Science.gov (United States)

    Schreiber, S; Lin, R; Haim, L; Baratz-Goldstien, R; Rubovitch, V; Vaisman, N; Pick, C G

    2014-09-01

    To date, there is yet no established effective treatment (medication or cognitive intervention) for post-traumatic brain injury (TBI) patients with chronic sequelae. Enriched environment (EE) has been recognized of importance in brain regulation, behaviour and physiology. Rodents reared in, or pre-exposed to EE, recovered better from brain insults. Using the concussive head trauma model of minimal TBI in mice, we evaluated the effect of transition to EE following a weight-drop (30g or 50g) induced mTBI on behavioural and cognitive parameters in mice in the Novel Object Recognition task, the Y- and the Elevated Plus mazes. In all assays, both mTBI groups (30g, 50g) housed in normal conditions were equally and significantly impaired 6 weeks post injury in comparison with the no-mTBI (pjuggling training and intensive cognitive stimulation. PMID:24906196

  16. Acute decrease in alkaline phosphatase after brain injury: A potential mechanism for tauopathy.

    Science.gov (United States)

    Arun, Peethambaran; Oguntayo, Samuel; Albert, Stephen Van; Gist, Irene; Wang, Ying; Nambiar, Madhusoodana P; Long, Joseph B

    2015-11-16

    Dephosphorylation of phosphorylated Tau (pTau) protein, which is essential for the preservation of neuronal microtubule assemblies and for protection against trauma-induced tauopathy and chronic traumatic encephalopathy (CTE), is primarily achieved in brain by tissue non-specific alkaline phosphatase (TNAP). Paired helical filaments (PHFs) and Tau isolated from Alzheimer's disease (AD) patients' brains have been shown to form microtubule assemblies with tubulin only after treatment with TNAP or protein phosphatase-2A, 2B and -1, suggesting that Tau protein in the PHFs of neurons in AD brain is hyperphosphorylated, which prevents microtubule assembly. Using blast or weight drop models of traumatic brain injury (TBI) in rats, we observed pTau accumulation in the brain as early as 6h post-injury and further accumulation which varied regionally by 24h post-injury. The pTau accumulation was accompanied by reduced TNAP expression and activity in these brain regions and a significantly decreased plasma total alkaline phosphatase activity after the weight drop. These results reveal that both blast- and impact acceleration-induced head injuries cause an acute decrease in the level/activity of TNAP in the brain, which potentially contributes to trauma-induced accumulation of pTau and the resultant tauopathy. The regional changes in the level/activity of TNAP or accumulation of pTau after these injuries did not correlate with the accumulation of amyloid precursor protein, suggesting that the basic mechanism underlying tauopathy in TBI might be distinct from that associated with AD. PMID:26483321

  17. Therapeutic effect of nimodipine on experimental brain injury

    Institute of Scientific and Technical Information of China (English)

    杨树源; 王增光

    2003-01-01

    Objective: To study the therapeutic effect of nimodipine on experimental brain injury.Methods: Experimental and control rabbits were subjected to a closed head injury. In one group nimodipine was given intravenously and the effect evaluated by electron microscopy, brain water content, calcium levels, transcranial Doppler, and intracranial pressure monitoring.Results: In rabbits treated with nimodipine the level of neuronal cytosolic free calcium was markedly decreased. There were less cellular damage and less spasm of the middle cerebral artery seen on electron microscopy. No difference regarding intracranial pressure changes between the two groups was noted. Conclusions: Nimodipine has a protective action on brain injury by blocking a series of pathological reactions induced by neuronal calcium overload, and by reducing the spasm of brain vessels and improving cerebral blood flow.

  18. Translational Research for Blast-Induced Traumatic Brain Injury: Injury Mechanism to Development of Medical Instruments

    Science.gov (United States)

    Nakagawa, A.; Ohtani, K.; Arafune, T.; Washio, T.; Iwasaki, M.; Endo, T.; Ogawa, Y.; Kumabe, T.; Takayama, K.; Tominaga, T.

    1. Investigation of shock wave-induced phenomenon: blast-induced traumatic brain injury Blast wave (BW) is generated by explosion and is comprised of lead shock wave (SE) followed by subsequent supersonic flow.

  19. Chronic traumatic encephalopathy pathology in a neurodegenerative disorders brain bank.

    Science.gov (United States)

    Bieniek, Kevin F; Ross, Owen A; Cormier, Kerry A; Walton, Ronald L; Soto-Ortolaza, Alexandra; Johnston, Amelia E; DeSaro, Pamela; Boylan, Kevin B; Graff-Radford, Neill R; Wszolek, Zbigniew K; Rademakers, Rosa; Boeve, Bradley F; McKee, Ann C; Dickson, Dennis W

    2015-12-01

    Chronic traumatic encephalopathy (CTE) is a progressive neurodegenerative disorder linked to repetitive traumatic brain injury (TBI) and characterized by deposition of hyperphosphorylated tau at the depths of sulci. We sought to determine the presence of CTE pathology in a brain bank for neurodegenerative disorders for individuals with and without a history of contact sports participation. Available medical records of 1721 men were reviewed for evidence of past history of injury or participation in contact sports. Subsequently, cerebral cortical samples were processed for tau immunohistochemistry in cases with a documented history of sports exposure as well as age- and disease-matched men and women without such exposure. For cases with available frozen tissue, genetic analysis was performed for variants in APOE, MAPT, and TMEM106B. Immunohistochemistry revealed 21 of 66 former athletes had cortical tau pathology consistent with CTE. CTE pathology was not detected in 198 individuals without exposure to contact sports, including 33 individuals with documented single-incident TBI sustained from falls, motor vehicle accidents, domestic violence, or assaults. Among those exposed to contact sports, those with CTE pathology did not differ from those without CTE pathology with respect to noted clinicopathologic features. There were no significant differences in genetic variants for those with CTE pathology, but we observed a slight increase in MAPT H1 haplotype, and there tended to be fewer homozygous carriers of the protective TMEM106B rs3173615 minor allele in those with sports exposure and CTE pathology compared to those without CTE pathology. In conclusion, this study has identified a small, yet significant, subset of individuals with neurodegenerative disorders and concomitant CTE pathology. CTE pathology was only detected in individuals with documented participation in contact sports. Exposure to contact sports was the greatest risk factor for CTE pathology. Future

  20. Proton MR spectroscopy in mild traumatic brain injury

    International Nuclear Information System (INIS)

    To assess the role of 1H MRS in the detection of changes in cerebral metabolite levels in pyramidal tracts after mild traumatic brain injury (MTBI) and to compare metabolite alterations to the clinical status (Glasgow Coma Scale). Study group consisted of 25 patients after mild traumatic brain injury, with a score of 11 to 15 in GCS. The MR studies were performed with a 1.5 T scanner. The results of spectra approximation (presented as metabolite ratios: NAA/Cr, NAA/Cho, Cho/Cr, lac/Cr, lip/Cr, Glx/Cr) were subjected to statistical analysis. MR spectra were recorded from a normal-appearing brain region: internal capsules and cerebral peduncles. Spectra from traumatic patients were compared with a control group including 34 healthy volunteers recorded with the same techniques. The statistical analysis revealed significant differences between the data obtained from various brain regions of the same patients after an MTBI and between the study and the control group. Proton MR spectroscopy detects changes in cerebral metabolite levels in apparently normal regions. In pyramidal tracts (internal capsules, cerebral peduncles), we noticed a significant reduction of NAA /Cho, lip/Cr, lac/Cr and Glx/Cr. In patients with mild brain injury, we can detect some metabolite abnormalities in normal-appearing brain structures. Proton MRS is a very useful tool for evaluation of major changes in metabolite levels in pyramidal tracts after mild traumatic brain injury

  1. Peripheral nervous system involvement in chronic spinal cord injury

    DEFF Research Database (Denmark)

    Tankisi, Hatice; Pugdahl, Kirsten; Rasmussen, Mikkel Mylius;

    2015-01-01

    Introduction: Upper motor neuron disorders are believed to leave the peripheral nervous system (PNS) intact. In this study we examined whether there is evidence of PNS involvement in spinal cord injury (SCI). Methods: Twelve subjects with chronic low cervical or thoracic SCI were included...

  2. Injury timing alters metabolic, inflammatory and functional outcomes following repeated mild traumatic brain injury.

    Science.gov (United States)

    Weil, Zachary M; Gaier, Kristopher R; Karelina, Kate

    2014-10-01

    Repeated head injuries are a major public health concern both for athletes, and members of the police and armed forces. There is ample experimental and clinical evidence that there is a period of enhanced vulnerability to subsequent injury following head trauma. Injuries that occur close together in time produce greater cognitive, histological, and behavioral impairments than do injuries separated by a longer period. Traumatic brain injuries alter cerebral glucose metabolism and the resolution of altered glucose metabolism may signal the end of the period of greater vulnerability. Here, we injured mice either once or twice separated by three or 20days. Repeated injuries that were separated by three days were associated with greater axonal degeneration, enhanced inflammatory responses, and poorer performance in a spatial learning and memory task. A single injury induced a transient but marked increase in local cerebral glucose utilization in the injured hippocampus and sensorimotor cortex, whereas a second injury, three days after the first, failed to induce an increase in glucose utilization at the same time point. In contrast, when the second injury occurred substantially later (20days after the first injury), an increase in glucose utilization occurred that paralleled the increase observed following a single injury. The increased glucose utilization observed after a single injury appears to be an adaptive component of recovery, while mice with 2 injuries separated by three days were not able to mount this response, thus this second injury may have produced a significant energetic crisis such that energetic demands outstripped the ability of the damaged cells to utilize energy. These data strongly reinforce the idea that too rapid return to activity after a traumatic brain injury can induce permanent damage and disability, and that monitoring cerebral energy utilization may be a tool to determine when it is safe to return to the activity that caused the initial

  3. Dexmedetomidine Postconditioning Reduces Brain Injury after Brain Hypoxia-Ischemia in Neonatal Rats.

    Science.gov (United States)

    Ren, Xiaoyan; Ma, Hong; Zuo, Zhiyi

    2016-06-01

    Perinatal asphyxia can lead to death and severe disability. Brain hypoxia-ischemia (HI) injury is the major pathophysiology contributing to death and severe disability after perinatal asphyxia. Here, seven-day old Sprague-Dawley rats were subjected to left brain HI. Dexmedetomidine was given intraperitoneally after the brain HI. Yohimbine or atipamezole, two α2 adrenergic receptor antagonists, were given 10 min before the dexmedetomidine injection. Neurological outcome was evaluated 7 or 28 days after the brain HI. Frontal cerebral cortex was harvested 6 h after the brain HI. Left brain HI reduced the left cerebral hemisphere weight assessed 7 days after the brain HI. This brain tissue loss was dose-dependently attenuated by dexmedetomidine. Dexmedetomidine applied within 1 h after the brain HI produced this effect. Dexmedetomidine attenuated the brain HI-induced brain tissue and cell loss as well as neurological and cognitive dysfunction assessed from 28 days after the brain HI. Dexmedetomidine postconditioning-induced neuroprotection was abolished by yohimbine or atipamezole. Brain HI increased tumor necrosis factor α and interleukin 1β in the brain tissues. This increase was attenuated by dexmedetomidine. Atipamezole inhibited this dexmedetomidine effect. Our results suggest that dexmedetomidine postconditioning reduces HI-induced brain injury in the neonatal rats. This effect may be mediated by α2 adrenergic receptor activation that inhibits inflammation in the ischemic brain tissues. PMID:26932203

  4. Role of Melatonin in Traumatic Brain Injury and Spinal Cord Injury

    Directory of Open Access Journals (Sweden)

    Mehar Naseem

    2014-01-01

    Full Text Available Brain and spinal cord are implicated in incidences of two of the most severe injuries of central nervous system (CNS. Traumatic brain injury (TBI is a devastating neurological deficit involving primary and secondary injury cascades. The primary and secondary mechanisms include complex consequences of activation of proinflammatory cytokines, cerebral edema, upregulation of NF-κβ, disruption of blood-brain barrier (BBB, and oxidative stress. Spinal cord injury (SCI includes primary and secondary injury cascades. Primary injury leads to secondary injury in which generation of free radicals and oxidative or nitrative damage play an important pathophysiological role. The indoleamine melatonin is a hormone secreted or synthesized by pineal gland in the brain which helps to regulate sleep and wake cycle. Melatonin has been shown to be a versatile hormone having antioxidative, antiapoptotic, neuroprotective, and anti-inflammatory properties. It has a special characteristic of crossing BBB. Melatonin has neuroprotective role in the injured part of the CNS after TBI and SCI. A number of studies have successfully shown its therapeutic value as a neuroprotective agent in the treatment of neurodegenerative diseases. Here in this review we have compiled the literature supporting consequences of CNS injuries, TBI and SCI, and the protective role of melatonin in it.

  5. Lateral fluid percussion: model of traumatic brain injury in mice.

    Science.gov (United States)

    Alder, Janet; Fujioka, Wendy; Lifshitz, Jonathan; Crockett, David P; Thakker-Varia, Smita

    2011-01-01

    Traumatic brain injury (TBI) research has attained renewed momentum due to the increasing awareness of head injuries, which result in morbidity and mortality. Based on the nature of primary injury following TBI, complex and heterogeneous secondary consequences result, which are followed by regenerative processes (1,2). Primary injury can be induced by a direct contusion to the brain from skull fracture or from shearing and stretching of tissue causing displacement of brain due to movement (3,4). The resulting hematomas and lacerations cause a vascular response (3,5), and the morphological and functional damage of the white matter leads to diffuse axonal injury (6-8). Additional secondary changes commonly seen in the brain are edema and increased intracranial pressure (9). Following TBI there are microscopic alterations in biochemical and physiological pathways involving the release of excitotoxic neurotransmitters, immune mediators and oxygen radicals (10-12), which ultimately result in long-term neurological disabilities (13,14). Thus choosing appropriate animal models of TBI that present similar cellular and molecular events in human and rodent TBI is critical for studying the mechanisms underlying injury and repair. Various experimental models of TBI have been developed to reproduce aspects of TBI observed in humans, among them three specific models are widely adapted for rodents: fluid percussion, cortical impact and weight drop/impact acceleration (1). The fluid percussion device produces an injury through a craniectomy by applying a brief fluid pressure pulse on to the intact dura. The pulse is created by a pendulum striking the piston of a reservoir of fluid. The percussion produces brief displacement and deformation of neural tissue (1,15). Conversely, cortical impact injury delivers mechanical energy to the intact dura via a rigid impactor under pneumatic pressure (16,17). The weight drop/impact model is characterized by the fall of a rod with a specific

  6. The Role of Cytokines and Inflammatory Cells in Perinatal Brain Injury

    OpenAIRE

    McAdams, Ryan M.; Juul, Sandra E.

    2012-01-01

    Perinatal brain injury frequently complicates preterm birth and leads to significant long-term morbidity. Cytokines and inflammatory cells are mediators in the common pathways associated with perinatal brain injury induced by a variety of insults, such as hypoxic-ischemic injury, reperfusion injury, toxin-mediated injury, and infection. This paper examines our current knowledge regarding cytokine-related perinatal brain injury and specifically discusses strategies for attenuating cytokine-med...

  7. Correlation of brain-derived neurotrophic factor to cognitive impairment following traumatic brain injury in rats

    Institute of Scientific and Technical Information of China (English)

    Dezhi Kang; Zhang Guo

    2008-01-01

    BACKGROUND: In vitro and in vivo studies have confirmed that brain-derived neurotrophic factor (BDNF) can promote survival and differentiation of cholinergic, dopaminergic and motor neurons, and axonal regeneration. BDNF has neuroprotective effects on the nervous system. OBJECTIVE: To explore changes in BDNF expression and cognitive function in rats after brain injury DESIGN, TIME AND SETTING: The neuropathology experiment was performed at the Second Research Room, Department of Neurosurgery, Fujian Medical University (China) from July 2007 to July 2008. MATERIALS: A total of 72 healthy, male, Sprague Dawley, rats were selected for this study. METHODS: Rat models of mild and moderate traumatic brain injury were created by percussion, according to Feeney's method (n = 24, each group). A bone window was made in rats from the sham operation group (n = 24), but no attack was conducted. MAIN OUTCOME MEASURES: At days 1,2, 4 and 7 following injury, BDNF expression in the rat frontal lobe cortex, hippocampus and basal forebrain was examined by immunohistochemistry (streptavidin-biotin-peroxidase complex method). Changes in rat cognitive function were assessed by the walking test, balance-beam test and memory function detection. RESULTS: Cognitive impairment was aggravated at day 2, and recovered to normal at days 3 and 7 in rats from the mild and moderate traumatic brain injury groups. BDNF expression in the rat frontal lobe cortex, hippocampus and basal forebrain was increased at 1 day, decreased at day 2, and then gradually increased in the mild and moderate traumatic brain injury groups. BDNF expression was greater in rats from the moderate traumatic brain injury group than in the sham operation and mild traumatic brain injury groups (P < 0.05). CONCLUSION: BDNF expression in the rat frontal lobe cortex, hippocampus and basal forebrain is correlated to cognitive impairment after traumatic brain injury. BDNF has a protective effect on cognitive function in rats

  8. [Treatment of delayed brain injury after pituitary irradiation].

    Science.gov (United States)

    Fujii, T; Misumi, S; Shibasaki, T; Tamura, M; Kunimine, H; Hayakawa, K; Niibe, H; Miyazaki, M; Miyagi, O

    1988-03-01

    Treatment for delayed brain injury after pituitary irradiation is discussed. Six cases with delayed brain injury were treated with a combination of dexamethasone or betamethasone, with heparin, glycerol, dextran 40 and some vasodilators. Two cases with temporal lobe syndrome were treated in the early stages of brain injury for a period of over 12 months were almost completely cured, another two cases with chiasma syndrome were treated in the relatively late stages, showed a partial improvement. One case which was irradiated 120 GY during 13 years did not improve. The final case treated with steroids for a short period also resulted in failure and the patient underwent an operation for the removal of the necrotic mass three years after the radiotherapy. Steroid therapy started in the early stages of brain injury after irradiation for over the 12 months is thought to be effective. Heparin therapy was also effective in one out of three cases, but in one of the cases subarachnoid hemorrhage from a traumatic aneurysm occurred during the therapy. In an acute phase, showing edematous change of the injured brain, the administration of glycerol is also thought to be useful. But the effectiveness of the other medicines containing some vasodilators was obscure or doubtful. We propose the following: (1) A meticulous observation is essential for the patients who received high doses of irradiation to diagnose brain injury in the early reversible stage. (2) Steroids should be given immediately in this reversible stage of brain injury before the irreversible "necrosis" occurs. (3) Steroids should be maintained for a long period over 12 months.(ABSTRACT TRUNCATED AT 250 WORDS) PMID:2453809

  9. Hypothalamic-Pituitary Autoimmunity and Traumatic Brain Injury

    Directory of Open Access Journals (Sweden)

    Federica Guaraldi

    2015-05-01

    Full Text Available Background: Traumatic brain injury (TBI is a leading cause of secondary hypopituitarism in children and adults, and is responsible for impaired quality of life, disabilities and compromised development. Alterations of pituitary function can occur at any time after the traumatic event, presenting in various ways and evolving during time, so they require appropriate screening for early detection and treatment. Although the exact pathophysiology is unknown, several mechanisms have been hypothesized, including hypothalamic-pituitary autoimmunity (HP-A. The aim of this study was to systematically review literature on the association between HP-A and TBI-induced hypopituitarism. Major pitfalls related to the HP-A investigation were also discussed. Methods: The PubMed database was searched with a string developed for this purpose, without temporal or language limits, for original articles assessing the association of HP-A and TBI-induced hypopituitarism. Results: Three articles from the same group met the inclusion criteria. Anti-pituitary and anti-hypothalamic antibodies were detected using indirect immunofluorescence in a significant number of patients with acute and chronic TBI. Elevated antibody titer was associated with an increased risk of persistent hypopituitarism, especially somatotroph and gonadotroph deficiency, while no correlations were found with clinical parameters. Conclusion: HPA seems to contribute to TBI-induced pituitary damage, although major methodological issues need to be overcome and larger studies are warranted to confirm these preliminary data.

  10. Brain injury markers (S100B and NSE in chronic cocaine dependents Marcadores de lesão cerebral (S100B e NSE em dependentes crônicos de cocaína

    Directory of Open Access Journals (Sweden)

    Felix Henrique Paim Kessler

    2007-06-01

    Full Text Available OBJECTIVE: Studies have shown signs of brain damage caused by different mechanisms in cocaine users. The serum neuron specific enolase and S100B protein are considered specific biochemical markers of neuronal and glial cell injury. This study aimed at comparing blood levels of S100B and NSE in chronic cocaine users and in volunteers who did not use cocaine or other illicit drugs. METHOD: Twenty subjects dependent on cocaine but not on alcohol or marijuana, and 20 non-substance using controls were recruited. Subjects were selected by consecutive and non-probabilistic sampling. Neuron specific enolase and S100B levels were determined by luminescence assay. RESULTS: Cocaine users had significantly higher scores than controls in all psychiatric dimensions of the SCL-90 and had cognitive deficits in the subtest cubes of WAIS and the word span. Mean serum S100B level was 0.09 ± 0.04 µg/l among cocaine users and 0.08 ± 0.04 µg/l among controls. Mean serum neuron specific enolase level was 9.7 ± 3.5 ng/l among cocaine users and 8.3 ± 2.6 ng/l among controls. CONCLUSIONS: In this first study using these specific brain damage markers in cocaine users, serum levels of S100B and neuron specific enolase were not statistically different between cocaine dependent subjects and controls.OBJETIVO: Estudos têm demonstrado sinais de lesão cerebral causadas por diferentes mecanismos em usuários de cocaína. A enolase sérica neurônio-específica e a proteína S100B são consideradas marcadores bioquímicos específicos de lesão neuronal e glial. Este estudo objetivou comparar os níveis sangüíneos de S100B e enolase sérica neurônio-específica em usuários crônicos de cocaína e em voluntários que não usam cocaína ou outras drogas ilícitas. MÉTODO: Vinte sujeitos dependentes de cocaína, mas não dependentes de álcool, maconha ou outra droga, e 20 sujeitos controles não usuários de drogas foram recrutados. Os sujeitos foram selecionados por

  11. Mechanism of Chronic Pain in Rodent Brain Imaging

    Science.gov (United States)

    Chang, Pei-Ching

    Chronic pain is a significant health problem that greatly impacts the quality of life of individuals and imparts high costs to society. Despite intense research effort in understanding of the mechanism of pain, chronic pain remains a clinical problem that has few effective therapies. The advent of human brain imaging research in recent years has changed the way that chronic pain is viewed. To further extend the use of human brain imaging techniques for better therapies, the adoption of imaging technique onto the animal pain models is essential, in which underlying brain mechanisms can be systematically studied using various combination of imaging and invasive techniques. The general goal of this thesis is to addresses how brain develops and maintains chronic pain in an animal model using fMRI. We demonstrate that nucleus accumbens, the central component of mesolimbic circuitry, is essential in development of chronic pain. To advance our imaging technique, we develop an innovative methodology to carry out fMRI in awake, conscious rat. Using this cutting-edge technique, we show that allodynia is assoicated with shift brain response toward neural circuits associated nucleus accumbens and prefrontal cortex that regulate affective and cognitive component of pain. Taken together, this thesis provides a deeper understanding of how brain mediates pain. It builds on the existing body of knowledge through maximizing the depth of insight into brain imaging of chronic pain.

  12. Neuroinflammatory responses to traumatic brain injury: etiology, clinical consequences, and therapeutic opportunities

    Directory of Open Access Journals (Sweden)

    Lozano D

    2015-01-01

    Full Text Available Diego Lozano,* Gabriel S Gonzales-Portillo,* Sandra Acosta, Ike de la Pena, Naoki Tajiri, Yuji Kaneko, Cesar V Borlongan Department of Neurosurgery and Brain Repair, University of South Florida Morsani College of Medicine, Tampa, FL, USA *These authors contributed equally to this work Abstract: Traumatic brain injury (TBI is a serious public health problem accounting for 1.4 million emergency room visits by US citizens each year. Although TBI has been traditionally considered an acute injury, chronic symptoms reminiscent of neurodegenerative disorders have now been recognized. These progressive neurodegenerative-like symptoms manifest as impaired motor and cognitive skills, as well as stress, anxiety, and mood affective behavioral alterations. TBI, characterized by external bumps or blows to the head exceeding the brain’s protective capacity, causes physical damage to the central nervous system with accompanying neurological dysfunctions. The primary impact results in direct neural cell loss predominantly exhibiting necrotic death, which is then followed by a wave of secondary injury cascades including excitotoxicity, oxidative stress, mitochondrial dysfunction, blood–brain barrier disruption, and inflammation. All these processes exacerbate the damage, worsen the clinical outcomes, and persist as an evolving pathological hallmark of what we now describe as chronic TBI. Neuroinflammation in the acute stage of TBI mobilizes immune cells, astrocytes, cytokines, and chemokines toward the site of injury to mount an antiinflammatory response against brain damage; however, in the chronic stage, excess activation of these inflammatory elements contributes to an “inflamed” brain microenvironment that principally contributes to secondary cell death in TBI. Modulating these inflammatory cells by changing their phenotype from proinflammatory to antiinflammatory would likely promote therapeutic effects on TBI. Because neuroinflammation occurs at

  13. [Headache as the consequence of brain concussion and contusion in closed head injuries in children].

    Science.gov (United States)

    Lemka, M

    1999-01-01

    The most frequent type of head injury in children is closed head trauma with brain concussion or contusion, and headache is the dominant complaint of early and late postinjury period. Because of scant number of studies on the problem of occurrence, characteristics and persistence of posttraumatic headache this study was undertaken in a group of 100 children (29 girls and 71 boys), aged 3-14 years old, 90 after brain concussion and 10 after contusion. Children with a history of injuries, central nervous system infections, with headaches before injury and chronic diseases were excluded. In 9 cases linear skull fracture was present after injury. The material was examined within one week after trauma, and then after 3, 6, and 12 months. After 3 months EEG was performed and repeated after 6 and 12 months in children with persistent headache or those without headache but with abnormal EEG results in the first examination. According to the additional diagnostic examinations, I excluded other causes of headache, besides head injury. In my observation 83% of children had headache after brain concussion and contusion. The majority--56%--had acute posttraumatic headache, but 27% of children complained of chronic headache, mainly tension type headache. Only 3% had migraine. In 21% of all group of 100 children, I noticed the headache persisting during the whole year of my observation. The important risk factor for the occurrence of posttraumatic headache were the age of child at the moment injury and the period of unconsciousness. The electroencephalographic recording still remains the important additional examination of posttraumatic consequences. PMID:10719686

  14. Synaptic Mechanisms of Blast-Induced Brain Injury.

    Science.gov (United States)

    Przekwas, Andrzej; Somayaji, Mahadevabharath R; Gupta, Raj K

    2016-01-01

    Blast wave-induced traumatic brain injury (TBI) is one of the most common injuries to military personnel. Brain tissue compression/tension due to blast-induced cranial deformations and shear waves due to head rotation may generate diffuse micro-damage to neuro-axonal structures and trigger a cascade of neurobiological events culminating in cognitive and neurodegenerative disorders. Although diffuse axonal injury is regarded as a signature wound of mild TBI (mTBI), blast loads may also cause synaptic injury wherein neuronal synapses are stretched and sheared. This synaptic injury may result in temporary disconnect of the neural circuitry and transient loss in neuronal communication. We hypothesize that mTBI symptoms such as loss of consciousness or dizziness, which start immediately after the insult, could be attributed to synaptic injury. Although empirical evidence is beginning to emerge; the detailed mechanisms underlying synaptic injury are still elusive. Coordinated in vitro-in vivo experiments and mathematical modeling studies can shed light into the synaptic injury mechanisms and their role in the potentiation of mTBI symptoms. PMID:26834697

  15. Increased leakage of brain antigens after traumatic brain injury and effect of immune tolerance induced by cells on traumatic brain injury

    Institute of Scientific and Technical Information of China (English)

    YAN Hua; ZHANG Hong-wei; WU Qiao-li; ZHANG Guo-bin; LIU Kui; ZHI Da-shi; HU Zhen-bo; ZENG Xian-wei

    2012-01-01

    Background Although traumatic brain injury can lead to opening the blood-brain barrier and leaking of blood substances (including water) into brain tissue,few studies of brain antigens leaking into the blood and the pathways have been reported.Brain antigens result in damage to brain tissues by stimulating the immune system to produce anti-brain antibodies,but no treatment has been reported to reduce the production of anti-brain antibodies and protect the brain tissue.The aim of the study is to confirm the relationship between immune injury and arachnoid granulations following traumatic brain injury,and provide some new methods to inhibit the immune injury.Methods In part one,methylene blue was injected into the rabbits' cisterna magna after traumatic brain injury,and concentrations of methylene blue and tumor necrosis factor (TNF)-α in blood were detected to determine the permeability of arachnoid granulations.In part two,umbilical cord mesenchymal stem cells and immature dendritic cells were injected into veins,and concentrations of interleukin 1 (IL-1),IL-10,interferon (IFN)-y,transforming growth factor (TGF)-β,anti-brain antibodies (ABAb),and IL-12 were measured by ELISA on days 1,3,7,14 and 21 after injury,and the numbers of leukocytes in the blood were counted.Twenty-one days after injury,expression of glutamate in brain tissue was determined by immunohistochemical staining,and neuronal degeneration was detected by H&E staining.Results In part one,blood concentrations of methylene blue and TNF-α in the traumatic brain injury group were higher than in the control group (P <0.05).Concentrations of methylene blue and TNF-α in the trauma cerebrospinal fluid (CSF)injected group were higher than in the control cerebrospinal fluid injected group (P <0.05).In part two,concentrations of IL-1,IFN-y,ABAb,IL-12,expression of glutamate (Glu),neuronal degeneration and number of peripheral blood leukocytes were lower in the group with cell treatment compared to the

  16. Suicide after traumatic brain injury: a population study

    DEFF Research Database (Denmark)

    Teasdale, T W; Engberg, A W

    2001-01-01

    OBJECTIVES: To determine the rates of suicide among patients who have had a traumatic brain injury. METHODS: From a Danish population register of admissions to hospital covering the years 1979-93 patients were selected who had had either a concussion (n=126 114), a cranial fracture (n=7560), or a......). There was, however, no evidence of a specific risk period for suicide after injury. CONCLUSION: The increased risk of suicide among patients who had a mild traumatic brain injury may result from concomitant risk factors such as psychiatric conditions and psychosocial disadvantage. The greater risk among...... the more serious cases implicates additionally the physical, psychological, and social consequences of the injuries as directly contributing to the suicides....

  17. Detecting Behavioral Deficits Post Traumatic Brain Injury in Rats.

    Science.gov (United States)

    Awwad, Hibah O

    2016-01-01

    Traumatic brain injury (TBI), ranging from mild to severe, almost always elicits an array of behavioral deficits in injured subjects. Some of these TBI-induced behavioral deficits include cognitive and vestibulomotor deficits as well as anxiety and other consequences. Rodent models of TBI have been (and still are) fundamental in establishing many of the pathophysiological mechanisms of TBI. Animal models are also utilized in screening and testing pharmacological effects of potential therapeutic agents for brain injury treatment. This chapter details validated protocols for each of these behavioral deficits post traumatic brain injury in Sprague-Dawley male rats. The elevated plus maze (EPM) protocol is described for assessing anxiety-like behavior; the Morris water maze protocol for assessing cognitive deficits in learning memory and spatial working memory and the rotarod test for assessing vestibulomotor deficits. PMID:27604739

  18. Study Suggests Brain Is Hard-Wired for Chronic Pain

    Science.gov (United States)

    ... News Release Tuesday, September 17, 2013 NIH-funded study suggests brain is hard-wired for chronic pain ... Apkarian, Ph.D., a senior author of the study and professor of physiology at Northwestern University Feinberg ...

  19. Radiologic Determination of Corpus Callosum Injury in Patients with Mild Traumatic Brain Injury and Associated Clinical Characteristics

    OpenAIRE

    Kim, Dong Shin; Choi, Hyuk Jai; Yang, Jin Seo; Cho, Yong Jun; Kang, Suk Hyung

    2015-01-01

    Objective To investigate the incidence of corpus callosum injury (CCI) in patients with mild traumatic brain injury (TBI) using brain MRI. We also performed a review of the clinical characteristics associated with this injury. Methods A total of 356 patients in the study were diagnosed with TBI, with 94 patients classified as having mild TBI. We included patients with mild TBI for further evaluation if they had normal findings via brain computed tomography (CT) scans and also underwent brain ...

  20. Propofol Attenuates Early Brain Injury After Subarachnoid Hemorrhage in Rats.

    Science.gov (United States)

    Shi, Song-sheng; Zhang, Hua-bin; Wang, Chun-hua; Yang, Wei-zhong; Liang, Ri-sheng; Chen, Ye; Tu, Xian-kun

    2015-12-01

    Our previous studies demonstrated that propofol protects rat brain against focal cerebral ischemia. However, whether propofol attenuates early brain injury after subarachnoid hemorrhage in rats remains unknown until now. The present study was performed to evaluate the effect of propofol on early brain injury after subarachnoid hemorrhage in rats and further explore the potential mechanisms. Sprague-Dawley rats underwent subarachnoid hemorrhage (SAH) by endovascular perforation then received treatment with propofol (10 or 50 mg/kg) or vehicle after 2 and 12 h of SAH. SAH grading, neurological scores, brain water content, Evans blue extravasation, the myeloperoxidase activity, and malondialdehyde (MDA) content were measured 24 h after SAH. Expression of nuclear factor erythroid-related factor 2 (Nrf2), nuclear factor-kappa B (NF-κB) p65, and aquaporin 4 (AQP4) expression in rat brain were detected by Western blot. Expression of cyclooxygenase-2 (COX-2) and matrix metalloproteinase-9 (MMP-9) were determined by reverse transcription-polymerase chain reaction (RT-PCR). Expressions of tumor necrosis factor-α (TNF-α) and interleukin-1β (IL-1β) were assessed by ELISA. Neurological scores, brain water content, Evans blue extravasation, the myeloperoxidase activity, and MDA content were significantly reduced by propofol. Furthermore, expression of Nrf2 in rat brain was upregulated by propofol, and expression of NF-κB p65, AQP4, COX-2, MMP-9, TNF-α, and IL-1β in rat brain were attenuated by propofol. Our results demonstrated that propofol improves neurological scores, reduces brain edema, blood-brain barrier (BBB) permeability, inflammatory reaction, and lipid peroxidation in rats of SAH. Propofol exerts neuroprotection against SAH-induced early brain injury, which might be associated with the inhibition of inflammation and lipid peroxidation. PMID:26342279

  1. The profile of head injuries and traumatic brain injury deaths in Kashmir

    Directory of Open Access Journals (Sweden)

    Tabish Amin

    2008-06-01

    Full Text Available Abstract This study was conducted on patients of head injury admitted through Accident & Emergency Department of Sher-i-Kashmir Institute of Medical Sciences during the year 2004 to determine the number of head injury patients, nature of head injuries, condition at presentation, treatment given in hospital and the outcome of intervention. Traumatic brain injury (TBI deaths were also studied retrospectively for a period of eight years (1996 to 2003. The traumatic brain injury deaths showed a steady increase in number from year 1996 to 2003 except for 1999 that showed decline in TBI deaths. TBI deaths were highest in age group of 21–30 years (18.8%, followed by 11–20 years age group (17.8% and 31–40 years (14.3%. The TBI death was more common in males. Maximum number of traumatic brain injury deaths was from rural areas as compared to urban areas. To minimize the morbidity and mortality resulting from head injury there is a need for better maintenance of roads, improvement of road visibility and lighting, proper mechanical maintenance of automobile and other vehicles, rigid enforcement of traffic rules, compulsory wearing of crash helmets by motor cyclist and scooterists and shoulder belt in cars and imparting compulsory road safety education to school children from primary education level. Moreover, appropriate medical care facilities (including trauma centres need to be established at district level, sub-divisional and block levels to provide prompt and quality care to head injury patients

  2. Outcome from Complicated versus Uncomplicated Mild Traumatic Brain Injury

    OpenAIRE

    Iverson, Grant L.; Lange, Rael T.; Minna Wäljas; Suvi Liimatainen; Prasun Dastidar; Hartikainen, Kaisa M.; Seppo Soimakallio; Juha Öhman

    2012-01-01

    Objective. To compare acute outcome following complicated versus uncomplicated mild traumatic brain injury (MTBI) using neurocognitive and self-report measures. Method. Participants were 47 patients who presented to the emergency department of Tampere University Hospital, Finland. All completed MRI scanning, self-report measures, and neurocognitive testing at 3-4 weeks after injury. Participants were classified into the complicated MTBI or uncomplicated MTBI group based on the presence/absenc...

  3. Energy Drinks, Alcohol, Sports and Traumatic Brain Injuries among Adolescents

    OpenAIRE

    Ilie, Gabriela; Boak, Angela; Mann, Robert E.; Adlaf, Edward M.; Hamilton, Hayley; Asbridge, Mark; Rehm, Jürgen; Cusimano, Michael D.

    2015-01-01

    Importance The high prevalence of traumatic brain injuries (TBI) among adolescents has brought much focus to this area in recent years. Sports injuries have been identified as a main mechanism. Although energy drinks, including those mixed with alcohol, are often used by young athletes and other adolescents they have not been examined in relation to TBI. Objective We report on the prevalence of adolescent TBI and its associations with energy drinks, alcohol and energy drink mixed in with alco...

  4. Abnormal Corticospinal Excitability in Traumatic Diffuse Axonal Brain Injury

    OpenAIRE

    Bernabeu, Montse; Demirtas-Tatlidede, Asli; Opisso, Eloy; Lopez, Raquel; Tormos, Jose Mª; Pascual-Leone, Alvaro

    2009-01-01

    This study aimed to investigate the cortical motor excitability characteristics in diffuse axonal injury (DAI) due to severe traumatic brain injury (TBI). A variety of excitatory and inhibitory transcranial magnetic stimulation (TMS) paradigms were applied to primary motor cortices of 17 patients and 11 healthy controls. The parameters of testing included resting motor threshold (MT), motor evoked potential (MEP) area under the curve, input-output curves, MEP variability, and silent period (S...

  5. Trial of Oral Metoclopramide on Diurnal Bruxism of Brain Injury

    OpenAIRE

    Yi, Ho Sung; Kim, Hyoung Seop; Seo, Mi Ri

    2013-01-01

    Bruxism is a diurnal or nocturnal parafunctional activity that includes tooth clenching, bracing, gnashing, and grinding. The dopaminergic system seems to be the key pathophysiology of bruxism and diminution of dopaminergic transmission at the prefrontal cortex seems to induce it. We report two patients with diurnal bruxism in whom a bilateral frontal lobe injury resulted from hemorrhagic stroke or traumatic brain injury. These patients' bruxism was refractory to bromocriptine but responded t...

  6. New means to assess neonatal inflammatory brain injury

    OpenAIRE

    Jin, Chen; Londono, Irene; Mallard, Carina; Lodygensky, Gregory A

    2015-01-01

    Preterm infants are especially vulnerable to infection-induced white matter injury, associated with cerebral palsy, cognitive and psychomotor impairment, and other adverse neurological outcomes. The etiology of such lesions is complex and multifactorial. Furthermore, timing and length of exposure to infection also influence neurodevelopmental outcomes. Different mechanisms have been posited to mediate the observed brain injury including microglial activation followed by subsequent release of ...

  7. Dysautonomia after traumatic brain injury: a forgotten syndrome?

    OpenAIRE

    Baguley, I.; Nicholls, J; Felmingham, K.; Crooks, J; Gurka, J.; Wade, L.

    1999-01-01

    OBJECTIVES—To better establish the clinical features, natural history, clinical management, and rehabilitation implications of dysautonomia after traumatic brain injury, and to highlight difficulties with previous nomenclature.
METHODS—Retrospective file review on 35 patients with dysautonomia and 35 sex and Glasgow coma scale score matched controls. Groups were compared on injury details, CT findings, physiological indices, and evidence of infections over the first 28 da...

  8. The paradox of chronic neuroinflammation, systemic immune suppression and autoimmunity after traumatic chronic spinal cord injury

    OpenAIRE

    Schwab, Jan M.; Zhang, Yi; Kopp, Marcel A; Brommer, Benedikt; Popovich, Phillip G.

    2014-01-01

    During the transition from acute to chronic stages of recovery after spinal cord injury (SCI), there is an evolving state of immunologic dysfunction that exacerbates the problems associated with the more clinically obvious neurologic deficits. Since injury directly affects cells embedded within the “immune privileged/specialized” milieu of the spinal cord, maladaptive or inefficient responses are likely to occur. Collectively, these responses qualify as part of the continuum of “SCI disease” ...

  9. Early Bifrontal Brain Injury: Disturbances in Cognitive Function Development

    Directory of Open Access Journals (Sweden)

    Christine Bonnier

    2010-01-01

    Full Text Available We describe six psychomotor, language, and neuropsychological sequential developmental evaluations in a boy who sustained a severe bifrontal traumatic brain injury (TBI at 19 months of age. Visuospatial, drawing, and writing skills failed to develop normally. Gradually increasing difficulties were noted in language leading to reading and spontaneous speech difficulties. The last two evaluations showed executive deficits in inhibition, flexibility, and working memory. Those executive abnormalities seemed to be involved in the other impairments. In conclusion, early frontal brain injury disorganizes the development of cognitive functions, and interactions exist between executive function and other cognitive functions during development.

  10. [Scandinavian guidelines for prehospital management of severe traumatic brain injury

    DEFF Research Database (Denmark)

    Sollid, S.; Sundstrom, T.; Kock-Jensen, C.;

    2008-01-01

    Head trauma is the cause the death for many young persons. The number of fatalities can be reduced through systematic management. Prevention of secondary brain injury combined with the fastest possible transport to a neurosurgical unit, have been shown to effectively reduce mortality and morbidity....... Evidence-based guidelines already exist that focus on all steps in the process. In the present article members of the Scandinavian Neurotrauma Committee present recommendations on prehospital management of traumatic brain injury adapted to the infrastructure of the Nordic region Udgivelsesdato: 2008/6/26...

  11. Do metals that translocate to the brain exacerbate traumatic brain injury?

    Science.gov (United States)

    Kalinich, John F; Kasper, Christine E

    2014-05-01

    Metal translocation to the brain is strictly controlled and often prevented by the blood-brain barrier. For the most part, only those metals required to maintain normal function are transported into the brain where they are under tight metabolic control. From the literature, there are reports that traumatic brain injury disrupts the blood-brain barrier. This could allow the influx of metals that would normally have been excluded from the brain. We also have preliminary data showing that metal pellets, surgically-implanted into the leg muscle of a rat to simulate a shrapnel wound, solubilize and the metals comprising the pellet can enter the brain. Surprisingly, rats implanted with a military-grade tungsten alloy composed of tungsten, nickel, and cobalt also showed significantly elevated uranium levels in their brains as early as 1 month after pellet implantation. The only source of uranium was low levels that are naturally found in food and water. Conversely, rats implanted with depleted uranium pellets demonstrated elevated uranium levels in brain resulting from degradation of the implanted pellets. However, when cobalt levels were measured, there were no significant increases in the brain until the rats had reached old age. The only source of cobalt for these rats was the low levels found in their food and water. These data suggest that some metals or metal mixtures (i.e., tungsten alloy), when embedded into muscle, can enhance the translocation of other, endogenous metals (e.g., uranium) across the blood-brain barrier. For other embedded metals (i.e., depleted uranium), this effect is not observed until the animal is of advanced age. This raises the possibility that metal body-burdens can affect blood-brain barrier permeability in a metal-specific and age-dependent manner. This possibility is disconcerting when traumatic brain injury is considered. Traumatic brain injury has been called the "signature" wound of the conflicts in Iraq and Afghanistan, often, an

  12. Misconceptions on neuropsychological rehabilitation and traumatic brain injury.

    Directory of Open Access Journals (Sweden)

    Alberto García- Molina

    2013-12-01

    Full Text Available There are many misconceptions about traumatic brain injuries, their recovery and outcome; misconceptions that have their origin in a lack of information influenced by the image that the media show of the brain damage. Development. Based on clinical experience, the authors of this essay sets out his personal view on some of the most frequent misconceptions in the field of neuropsychological rehabilitation of traumatic brain injury: 1 All deficits are evident; 2 The recovery depends mainly on the involvement of the patient: more effort, more rapid recovery; 3 Two years after traumatic brain injury there is no possibility of improvement and recovery; and 4 The “miracle” of recovery will occur when is found the appropriate professional or treatment. These and other beliefs may influence directly or indirectly on the recovery process and the expectations placed on it by the families and patients. Conclusions. Provide accurate, clear and honest information, at the right time, helps patients and their families to better understand the deficits, the course of recovery and to adapt to the new reality resulting from a traumatic brain injury.

  13. Hyperbaric oxygen therapy improves cognitive functioning after brain injury

    Institute of Scientific and Technical Information of China (English)

    Su Liu; Guangyu Shen; Shukun Deng; Xiubin Wang; Qinfeng Wu; Aisong Guo

    2013-01-01

    Hyperbaric oxygen therapy has been widely applied and recognized in the treatment of brain injury;however, the correlation between the protective effect of hyperbaric oxygen therapy and changes of metabolites in the brain remains unclear. To investigate the effect and potential mechanism of hyperbaric oxygen therapy on cognitive functioning in rats, we established traumatic brain injury models using Feeney’s free fal ing method. We treated rat models with hyperbaric oxygen therapy at 0.2 MPa for 60 minutes per day. The Morris water maze test for spatial navigation showed that the average escape latency was significantly prolonged and cognitive function decreased in rats with brain injury. After treatment with hyperbaric oxygen therapy for 1 and 2 weeks, the rats’ spatial learning and memory abilities were improved. Hydrogen proton magnetic resonance spectroscopy analysis showed that the N-acetylaspartate/creatine ratio in the hippocampal CA3 region was sig-nificantly increased at 1 week, and the N-acetylaspartate/choline ratio was significantly increased at 2 weeks after hyperbaric oxygen therapy. Nissl staining and immunohistochemical staining showed that the number of nerve cells and Nissl bodies in the hippocampal CA3 region was significantly increased, and glial fibril ary acidic protein positive cells were decreased after a 2-week hyperbaric oxygen therapy treatment. Our findings indicate that hyperbaric oxygen therapy significantly im-proves cognitive functioning in rats with traumatic brain injury, and the potential mechanism is me-diated by metabolic changes and nerve cellrestoration in the hippocampal CA3 region.

  14. The Evolution of Post-Traumatic Stress Disorder following Moderate-to-Severe Traumatic Brain Injury.

    Science.gov (United States)

    Alway, Yvette; Gould, Kate Rachel; McKay, Adam; Johnston, Lisa; Ponsford, Jennie

    2016-05-01

    Increasing evidence indicates that post-traumatic stress disorder (PTSD) may develop following traumatic brain injury (TBI), despite most patients having no conscious memory of their accident. This prospective study examined the frequency, timing of onset, symptom profile, and trajectory of PTSD and its psychiatric comorbidities during the first 4 years following moderate-to-severe TBI. Participants were 85 individuals (78.8% male) with moderate or severe TBI recruited following admission to acute rehabilitation between 2005 and 2010. Using the Structured Clinical Interview for Diagnostic and Statistical Manual of Mental Disorders, Fourth Edition, Disorders (SCID-I), participants were evaluated for pre- and post-injury PTSD soon after injury and reassessed at 6 months, 12 months, 2 years, 3 years, and 4 years post-injury. Over the first 4 years post-injury, 17.6% developed injury-related PTSD, none of whom had PTSD prior to injury. PTSD onset peaked between 6 and 12 months post-injury. The majority of PTSD cases (66.7%) had a delayed-onset, which for a third was preceded by subsyndromal symptoms in the first 6 months post-injury. PTSD frequency increased over the first year post-injury, remained stable during the second year, and gradually declined thereafter. The majority of subjects with PTSD experienced a chronic symptom course and all developed one or more than one comorbid psychiatric disorder, with mood, other anxiety, and substance-use disorders being the most common. Despite event-related amnesia, post-traumatic stress symptoms, including vivid re-experiencing phenomena, may develop following moderate-to-severe TBI. Onset is typically delayed and symptoms may persist for several years post-injury. PMID:26176500

  15. Making waves in the brain: What are oscillations, and why modulating them makes sense for brain injury

    Directory of Open Access Journals (Sweden)

    Aleksandr ePevzner

    2016-04-01

    Full Text Available Traumatic brain injury (TBI can result in persistent cognitive, behavioral and emotional deficits. However, the vast majority of patients are not chronically hospitalized; rather they have to manage their disabilities once they are discharged to home. Promoting recovery to pre-injury level is important from a patient care as well as a societal perspective. Electrical neuromodulation is one approach that has shown promise in alleviating symptoms associated with neurological disorders such as in Parkinson’s disease and epilepsy. Consistent with this perspective, both animal and clinical studies have revealed that TBI alters physiological oscillatory rhythms. More recently several studies demonstrated that low frequency stimulation improves cognitive outcome in models of TBI. Specifically, stimulation of the septohippocampal circuit in the theta frequency entrained oscillations and improved spatial learning following traumatic brain injury. In order to evaluate the potential of electrical deep brain stimulation for clinical translation we review the basic neurophysiology of oscillations, their role in cognition and how they are changed post-TBI. Furthermore, we highlight several factors for future pre-clinical and clinical studies to consider, with the hope that it will promote a hypothesis driven approach to subsequent experimental designs and ultimately successful translation to improve outcome in patients with TBI.

  16. Nonlinear Dynamic Theory of Acute Cell Injuries and Brain Ischemia

    Science.gov (United States)

    Taha, Doaa; Anggraini, Fika; Degracia, Donald; Huang, Zhi-Feng

    2015-03-01

    Cerebral ischemia in the form of stroke and cardiac arrest brain damage affect over 1 million people per year in the USA alone. In spite of close to 200 clinical trials and decades of research, there are no treatments to stop post-ischemic neuron death. We have argued that a major weakness of current brain ischemia research is lack of a deductive theoretical framework of acute cell injury to guide empirical studies. A previously published autonomous model based on the concept of nonlinear dynamic network was shown to capture important facets of cell injury, linking the concept of therapeutic to bistable dynamics. Here we present an improved, non-autonomous formulation of the nonlinear dynamic model of cell injury that allows multiple acute injuries over time, thereby allowing simulations of both therapeutic treatment and preconditioning. Our results are connected to the experimental data of gene expression and proteomics of neuron cells. Importantly, this new model may be construed as a novel approach to pharmacodynamics of acute cell injury. The model makes explicit that any pro-survival therapy is always a form of sub-lethal injury. This insight is expected to widely influence treatment of acute injury conditions that have defied successful treatment to date. This work is supported by NIH NINDS (NS081347) and Wayne State University President's Research Enhancement Award.

  17. Animal models of traumatic brain injury : a critical evaluation

    OpenAIRE

    O'Connor, William; Smyth, Aoife; Gilchrist, M. D.

    2011-01-01

    Animal models are necessary to elucidate changes occurring after brain injury and to establish new therapeutic strategies towards a stage where drug efficacy in brain injured patients (against all classes of symptoms) can be predicted. In this review, six established animal models of head trauma, namely fluid percussion, rigid indentation, inertial acceleration, impact acceleration, weight-drop and dynamic cortical deformation are evaluated. While no single animal model is entirely successful...

  18. Pharmacologic resuscitation for hemorrhagic shock combined with traumatic brain injury

    DEFF Research Database (Denmark)

    Jin, Guang; Duggan, Michael; Imam, Ayesha;

    2012-01-01

    We have previously demonstrated that valproic acid (VPA), a histone deacetylase inhibitor, can improve survival after hemorrhagic shock (HS), protect neurons from hypoxia-induced apoptosis, and attenuate the inflammatory response. We have also shown that administration of 6% hetastarch (Hextend [...... [Hex]) after traumatic brain injury (TBI) decreases brain swelling, without affecting size of the lesion. This study was performed to determine whether addition of VPA to Hex would decrease the lesion size in a clinically relevant large animal model of TBI + HS....

  19. Oligodendrogenesis after Cerebral Ischaemia and Traumatic Brain Injury

    Directory of Open Access Journals (Sweden)

    Zheng Gang Zhang

    2013-08-01

    Full Text Available Stroke and traumatic brain injury (TBI damage white and grey matter. Loss of oligodendrocytes and their myelin, impairs axonal function. Remyelination involves oligodendrogenesis during which new myelinating oligodendrocytes are generated by differentiated oligodendrocyte progenitor cells (OPCs. This article briefly reviews the processes of oligodendrogenesis in adult rodent brains, and promising experimental therapies targeting the neurovascular unit that reduce oligodendrocyte damage and amplify endogenous oligodendrogenesis after stroke and TBI.

  20. Is Goshinjo therapy effective in cognitive impairment after severe traumatic brain injury?

    Institute of Scientific and Technical Information of China (English)

    Keiji Hashimoto; Kisho Kida

    2013-01-01

    We report a case of a 21-year-old man who had severe traumatic brain injury as a result of an accident at the age of 16 years. Two years and 4 months after the trauma, at the age of 19 years, he still had severe right hemiplegia and cognitive dysfunction including aphasia and attention and memory disturbance. Conventional rehabilitation programs could not resolve all of the neuropsychological problems. He started receiving Goshinjo therapy over a period of 22 months. Following the therapy, significant improvements in verbal intelligence quotient (assessed by the Wechsler Adult Intelligence Scale-Third Edition) and attention and concentration function (using the Wechsler Memory Scale-Revised), and remission of traumatic epilepsy were observed. Goshinjo therapy is suspected to be effective in the treatment of cognitive dysfunction in the chronic stage after severe traumatic brain injury.

  1. Measuring and inducing brain plasticity in chronic aphasia

    OpenAIRE

    Fridriksson, Julius

    2011-01-01

    Brain plasticity associated with anomia recovery in aphasia is poorly understood. Here, I review four recent studies from my lab that focused on brain modulation associated with long-term anomia outcome, its behavioral treatment, and the use of transcranial brain stimulation to enhance anomia treatment success in individuals with chronic aphasia caused by left hemisphere stroke. In a study that included 15 participants with aphasia who were compared to a group of 10 normal control subjects, w...

  2. Altered Neuroinflammation and Behavior after Traumatic Brain Injury in a Mouse Model of Alzheimer's Disease.

    Science.gov (United States)

    Kokiko-Cochran, Olga; Ransohoff, Lena; Veenstra, Mike; Lee, Sungho; Saber, Maha; Sikora, Matt; Teknipp, Ryan; Xu, Guixiang; Bemiller, Shane; Wilson, Gina; Crish, Samuel; Bhaskar, Kiran; Lee, Yu-Shang; Ransohoff, Richard M; Lamb, Bruce T

    2016-04-01

    Traumatic brain injury (TBI) has acute and chronic sequelae, including an increased risk for the development of Alzheimer's disease (AD). TBI-associated neuroinflammation is characterized by activation of brain-resident microglia and infiltration of monocytes; however, recent studies have implicated beta-amyloid as a major manipulator of the inflammatory response. To examine neuroinflammation after TBI and development of AD-like features, these studies examined the effects of TBI in the presence and absence of beta-amyloid. The R1.40 mouse model of cerebral amyloidosis was used, with a focus on time points well before robust AD pathologies. Unexpectedly, in R1.40 mice, the acute neuroinflammatory response to TBI was strikingly muted, with reduced numbers of CNS myeloid cells acquiring a macrophage phenotype and decreased expression of inflammatory cytokines. At chronic time points, macrophage activation substantially declined in non-Tg TBI mice; however, it was relatively unchanged in R1.40 TBI mice. The persistent inflammatory response coincided with significant tissue loss between 3 and 120 days post-injury in R1.40 TBI mice, which was not observed in non-Tg TBI mice. Surprisingly, inflammatory cytokine expression was enhanced in R1.40 mice compared with non-Tg mice, regardless of injury group. Although R1.40 TBI mice demonstrated task-specific deficits in cognition, overall functional recovery was similar to non-Tg TBI mice. These findings suggest that accumulating beta-amyloid leads to an altered post-injury macrophage response at acute and chronic time points. Together, these studies emphasize the role of post-injury neuroinflammation in regulating long-term sequelae after TBI and also support recent studies implicating beta-amyloid as an immunomodulator. PMID:26414955

  3. White matter disruption in moderate/severe pediatric traumatic brain injury: Advanced tract-based analyses

    Directory of Open Access Journals (Sweden)

    Emily L. Dennis

    2015-01-01

    Full Text Available Traumatic brain injury (TBI is the leading cause of death and disability in children and can lead to a wide range of impairments. Brain imaging methods such as DTI (diffusion tensor imaging are uniquely sensitive to the white matter (WM damage that is common in TBI. However, higher-level analyses using tractography are complicated by the damage and decreased FA (fractional anisotropy characteristic of TBI, which can result in premature tract endings. We used the newly developed autoMATE (automated multi-atlas tract extraction method to identify differences in WM integrity. 63 pediatric patients aged 8–19 years with moderate/severe TBI were examined with cross sectional scanning at one or two time points after injury: a post-acute assessment 1–5 months post-injury and a chronic assessment 13–19 months post-injury. A battery of cognitive function tests was performed in the same time periods. 56 children were examined in the first phase, 28 TBI patients and 28 healthy controls. In the second phase 34 children were studied, 17 TBI patients and 17 controls (27 participants completed both post-acute and chronic phases. We did not find any significant group differences in the post-acute phase. Chronically, we found extensive group differences, mainly for mean and radial diffusivity (MD and RD. In the chronic phase, we found higher MD and RD across a wide range of WM. Additionally, we found correlations between these WM integrity measures and cognitive deficits. This suggests a distributed pattern of WM disruption that continues over the first year following a TBI in children.

  4. Pivotal role of anterior cingulate cortex in working memory after traumatic brain injury in youth

    Directory of Open Access Journals (Sweden)

    Fabienne eCazalis

    2011-01-01

    Full Text Available In this fMRI study, the functions of the Anterior Cingulate Cortex were studied in a group of adolescents who had sustained a moderate to severe Traumatic Brain Injury. A spatial working memory task with varying working memory loads, representing experimental conditions of increasing difficulty, was administered.In a cross-sectional comparison between the patients and a matched control group, patients performed worse than Controls, showing longer reaction times and lower response accuracy on the spatial working memory task. Brain imaging findings suggest a possible double-dissociation: activity of the Anterior Cingulate Cortex in the Traumatic Brain Injury group, but not in the Control group, was associated with task difficulty; conversely, activity of the left Sensorimotor Cortex in the Control group, but not in the TBI group, was correlated with task difficulty.In addition to the main cross-sectional study, a longitudinal study of a group of adolescent patients with moderate to severe Traumatic Brain Injury was done using fMRI and the same spatial working memory task. The patient group was studied at two time points: one time point during the post-acute phase and one time point 12 months later, during the chronic phase. Results indicated that patients' behavioral performance improved over time, suggesting cognitive recovery. Brain imaging findings suggest that, over this 12 month period, patients recruited less of the Anterior Cingulate Cortex and more of the left Sensorimotor Cortex in response to increasing task difficulty.The role of Anterior Cingulate Cortex in executive functions following a moderate to severe brain injury in adolescence is discussed within the context of conflicting models of the Anterior Cingulate Cortex functions in the existing literature.

  5. Brain stimulation: Neuromodulation as a potential treatment for motor recovery following traumatic brain injury.

    Science.gov (United States)

    Clayton, E; Kinley-Cooper, S K; Weber, R A; Adkins, D L

    2016-06-01

    There is growing evidence that electrical and magnetic brain stimulation can improve motor function and motor learning following brain damage. Rodent and primate studies have strongly demonstrated that combining cortical stimulation (CS) with skilled motor rehabilitative training enhances functional motor recovery following stroke. Brain stimulation following traumatic brain injury (TBI) is less well studied, but early pre-clinical and human pilot studies suggest that it is a promising treatment for TBI-induced motor impairments as well. This review will first discuss the evidence supporting brain stimulation efficacy derived from the stroke research field as proof of principle and then will review the few studies exploring neuromodulation in experimental TBI studies. This article is part of a Special Issue entitled SI:Brain injury and recovery. PMID:26855256

  6. Pilot study: bone marrow stem cells as a treatment for dogs with chronic spinal cord injury

    OpenAIRE

    Sarmento, Carlos Alberto Palmeira; Rodrigues, Marcio Nogueira; Bocabello, Renato Zonzini; Mess, Andrea Maria; Miglino, Maria Angelica

    2014-01-01

    Background Chronic Spinal Cord injury is a common, severe, and medically untreatable disease. Since the functional outcomes of acute and experimental chronic spinal cord injury have been shown to improve with stem cell therapy, a case study was conducted to test if the application of stem cell also regenerates chronic SCI dysfunction. Transplantation of foetal bone marrow stem cells was applied in seven dogs with chronic spinal cord injury. Magnetic resonance images and assessments of symptom...

  7. Behavioural alteration in chronic pain: are brain glia involved?

    Science.gov (United States)

    Panigada, T; Gosselin, R-D

    2011-10-01

    Behavioural symptoms such as abnormal emotionality (including anxious and depressive episodes) and cognition (for instance weakened decision-making) are highly frequent in both chronic pain patients and their animal models. The theory developed in the present article posits that alterations in glial cells (astrocytes and microglia) in cortical and limbic brain regions might be the origin of such emotional and cognitive chronic pain-associated impairments. Indeed, in mood disorders (unipolar depression, anxiety disorders, autism or schizophrenia) glial changes in brain regions involved in mood control (prefrontal and cingulate cortices, amygdala and the hippocampus) have been recurrently described. Besides, glial cells have been undoubtedly identified as key actors in the sensory component of chronic pain, owing to the profound phenotypical changes they undergo throughout the sensory pathway. Hence, the possibility arises that brain astrocytes and microglia react in upper brain structures as well, mediating the related mood and cognitive dysfunctions in chronic pain. So far, only very few studies have provided results in this prospect, mainly indirectly in pain-independent researches. Nevertheless, the first scant available data seem to merge in a unified description of a brain glial reaction occurring after chronic peripheral lesion. The present article uses this scarce literature to formulate the provocative theory of a glia-driven mood and cognitive dysfunction in chronic pain, expounding upon its validity and putative therapeutical impact as well as its current limitations and expected future developments. PMID:21741179

  8. Human plasma DNP level after severe brain injury

    Institute of Scientific and Technical Information of China (English)

    GAO Yi-lu; XIN Hui-ning; FENG Yi; FAN Ji-wei

    2006-01-01

    Objective: To determine the relationship between DNP level after human severe brain injury and hyponatremia as well as isorrhea.Methods: The peripheral venous plasma as control was collected from 8 volunteers. The peripheral venous plasma from 14 severe brain injury patients were collected in the 1, 3, 7 days after injury. Radioimmunoassay was used to detect the DNP concentration. Meanwhile, daily plasma and urine electrolytes, osmotic pressure as well as 24 h liquid intake and output volume were detected.Results: The normal adult human plasma DNP level was 62. 46 pg/ml ± 27. 56 pg/ml. In the experimental group, the plasma DNP levels were higher from day 1 today 3 in 8 of the 14 patients than those in the control group (P1 =0.05, P3 =0.03). Negative fluid balance occurred in 8 patients and hyponatremia in 7 patients. The increase of plasma DNP level was significantly correlated with the development of a negative fluid balance (r=-0.69,P<0.01) and hyponatremia (x2 =4.38, P<0.05).Conclusions: The increase of plasma DNP level is accompanied by the enhancement of natriuretic and diuretic responses in severe brain-injured patients, which is associated with the development of a negative fluid balance and hyponatremia after brain injury.

  9. Integration of Neuropsychology in Educational Planning Following Traumatic Brain Injury

    Science.gov (United States)

    Stavinoha, Peter L.

    2005-01-01

    Traumatic brain injuries (TBIs) have the potential to significantly disrupt a student's cognitive, academic, social, emotional, behavioral, and physical functioning. It is important for educators to appreciate the array of difficulties students with TBI may experience in order to appropriately assess needs and create an educational plan that…

  10. Cognitive Rehabilitation for Children with Acquired Brain Injury

    Science.gov (United States)

    Slomine, Beth; Locascio, Gianna

    2009-01-01

    Cognitive deficits are frequent consequences of acquired brain injury (ABI) and often require intervention. We review the theoretical and empirical literature on cognitive rehabilitation in a variety of treatment domains including attention, memory, unilateral neglect, speech and language, executive functioning, and family involvement/education.…

  11. Practitioner Review: Cognitive Rehabilitation for Children with Acquired Brain Injury

    Science.gov (United States)

    Limond, Jenny; Leeke, Rachel

    2005-01-01

    Background: The need to address acquired cognitive impairments is increasing in child populations seen across a range of settings. However, current clinical practice following brain injury in children does not necessarily incorporate the use of cognitive rehabilitation models or techniques. The aim of this paper is to review the literature in this…

  12. Low level laser therapy for traumatic brain injury

    Science.gov (United States)

    Wu, Qiuhe; Huang, Ying-Ying; Dhital, Saphala; Sharma, Sulbha K.; Chen, Aaron C.-H.; Whalen, Michael J.; Hamblin, Michael R.

    2010-02-01

    Low level laser (or light) therapy (LLLT) has been clinically applied for many indications in medicine that require the following processes: protection from cell and tissue death, stimulation of healing and repair of injuries, and reduction of pain, swelling and inflammation. One area that is attracting growing interest is the use of transcranial LLLT to treat stroke and traumatic brain injury (TBI). The fact that near-infrared light can penetrate into the brain would allow non-invasive treatment to be carried out with a low likelihood of treatment-related adverse events. LLLT may have beneficial effects in the acute treatment of brain damage injury by increasing respiration in the mitochondria, causing activation of transcription factors, reducing key inflammatory mediators, and inhibiting apoptosis. We tested LLLT in a mouse model of TBI produced by a controlled weight drop onto the skull. Mice received a single treatment with 660-nm, 810-nm or 980-nm laser (36 J/cm2) four hours post-injury and were followed up by neurological performance testing for 4 weeks. Mice with moderate to severe TBI treated with 660- nm and 810-nm laser had a significant improvement in neurological score over the course of the follow-up and histological examination of the brains at sacrifice revealed less lesion area compared to untreated controls. Further studies are underway.

  13. Swallowing Disorders in Severe Brain Injury in the Arousal Phase.

    Science.gov (United States)

    Bremare, A; Rapin, A; Veber, B; Beuret-Blanquart, F; Verin, E

    2016-08-01

    The objective of this study was to determine the clinical characteristics of swallowing disorders in severe brain injury in the arousal phase after coma. Between December 1, 2013 and June 30, 2014, eleven patients with severe acquired brain injury who were admitted to rehabilitation center (Male 81.8 %; 40.7 ± 14.6 years) were included in the study. Evaluation of swallowing included a functional examination, clinical functional swallowing test, and naso-endoscopic swallowing test. All patients had swallowing disorders at admission. The first functional swallowing test showed oral (77.8 %) and pharyngeal (66.7 %) food bolus transport disorders; and alterations in airway protection mechanisms (80 %). Swallowing test under endoscopic control showed a disorder in swallowing coordination in 55.6 % of patients tested. Seven (63.6 %) patients resumed oral feeding within an average of 6 weeks after admission to rehabilitation center and 14 weeks after acquired brain injury. Six (85.7 %) of these seven patients continued to require modified solid and liquid textures. Swallowing disorders are a major concern in severe brain injury in the arousal phase. Early bedside assessment of swallowing is essential for detection of swallowing disorders to propose appropriate medical rehabilitation care to these patients in a state of altered consciousness. PMID:27090424

  14. Brain injury and severe eating difficulties at admission

    DEFF Research Database (Denmark)

    Kjærsgaard, Annette; Kaae Kristensen, Hanne

    acquired brain injury were interviewed via qualitative semi-structured interviews. An explorative study was conducted to study eating difficulties. Qualitative content analysis was used. Results: Four main themes emerged from the analysis: personal values related to eating, swallowing difficulties, eating...

  15. Death Associated Protein Kinases: Molecular Structure and Brain Injury

    Directory of Open Access Journals (Sweden)

    Claire Thornton

    2013-07-01

    Full Text Available Perinatal brain damage underlies an important share of motor and neurodevelopmental disabilities, such as cerebral palsy, cognitive impairment, visual dysfunction and epilepsy. Clinical, epidemiological, and experimental studies have revealed that factors such as inflammation, excitotoxicity and oxidative stress contribute considerably to both white and grey matter injury in the immature brain. A member of the death associated protein kinase (DAPk family, DAPk1, has been implicated in cerebral ischemic damage, whereby DAPk1 potentiates NMDA receptor-mediated excitotoxicity through interaction with the NR2BR subunit. DAPk1 also mediate a range of activities from autophagy, membrane blebbing and DNA fragmentation ultimately leading to cell death. DAPk mRNA levels are particularly highly expressed in the developing brain and thus, we hypothesize that DAPk1 may play a role in perinatal brain injury. In addition to reviewing current knowledge, we present new aspects of the molecular structure of DAPk domains, and relate these findings to interacting partners of DAPk1, DAPk-regulation in NMDA-induced cerebral injury and novel approaches to blocking the injurious effects of DAPk1.

  16. Risks of Brain Injury after Blunt Head Trauma

    Directory of Open Access Journals (Sweden)

    J Gordon Millichap

    2004-06-01

    Full Text Available The association of loss of consciousness (LOC and/or amnesia with traumatic brain injury (TBI identified on CT and TBI requiring acute intervention was evaluated in 2043 children <18 years old enrolled prospectively in a level 1 trauma center ED at University of California, Davis School of Medicine, CA.

  17. Sex, Gender, and Traumatic Brain Injury: A Commentary.

    Science.gov (United States)

    Colantonio, Angela

    2016-02-01

    The goal of this supplemental issue is to address major knowledge, research, and clinical practice gaps regarding the limited focus on brain injury in girls and women as well as limited analysis of the effect of sex and gender in research on acquired brain injury. Integrating sex and gender in research is recognized as leading to better science and, ultimately, to better clinical practice. A sex and gender analytical approach to rehabilitation research is crucial to understanding traumatic brain injury and improving quality of life outcomes for survivors. Put another way, the lack of focus on sex and gender reduces the rigor of research design, the generalizability of study findings, and the effectiveness of clinical implementation and knowledge dissemination practices. The articles in this supplement examine sex and gender using a variety of methodological approaches and research contexts. Recommendations for future research on acquired brain injury that consciously incorporates sex and gender are made throughout this issue. This supplement is a product of the Girls and Women with ABI Task Force of the American Congress of Rehabilitation Medicine. PMID:26804988

  18. Endogenous lipoid pneumonia in a cachectic patient after brain injury.

    Science.gov (United States)

    Zhang, Ji; Mu, Jiao; Lin, Wei; Dong, Hongmei

    2015-01-01

    Endogenous lipoid pneumonia (EnLP) is an uncommon non-life-threatening inflammatory lung disease that usually occurs in patients with conditions such as lung cancers, primary sclerosing cholangitis, and undifferentiated connective tissue disease. Here we report a case of EnLP in a paralytic and cachectic patient with bronchopneumonia after brain injury. A 40-year-old man experienced a severe brain injury in an automobile accident. He was treated for 1 month and his status plateaued. However, he became paralyzed and developed cachexia and ultimately died 145 days after the accident. Macroscopically, multifocal yellowish firm nodules were visible on scattered gross lesions throughout the lungs. Histologically, many foam cells had accumulated within the alveoli and alveolar walls accompanied by a surrounding interstitial infiltration of lymphocytes. The findings were in accordance with a diagnosis of EnLP. Bronchopneumonia was also noted. To our knowledge, there have been few reports of EnLP associated with bronchopneumonia and cachexia after brain injury. This uncommon pathogenesis should be well recognized by clinicians and forensic pathologists. The case reported here should prompt medical staff to increase the nutritional status and fight pulmonary infections in patients with brain injury to prevent the development of EnLP. PMID:26097618

  19. School-Based Traumatic Brain Injury and Concussion Management Program

    Science.gov (United States)

    Davies, Susan C.

    2016-01-01

    Traumatic brain injuries (TBIs), including concussions, can result in a constellation of physical, cognitive, emotional, and behavioral symptoms that affect students' well-being and performance at school. Despite these effects, school personnel remain underprepared identify, educate, and assist this population of students. This article describes a…

  20. Blissfully unaware: Anosognosia and anosodiaphoria after acquired brain injury.

    Science.gov (United States)

    Gasquoine, Philip Gerard

    2016-01-01

    Historically, anosognosia referred to under-report of striking symptoms of acquired brain injury (e.g., hemiplegia) with debilitating functional consequences and was linked with anosodiaphoria, an emotional reaction of indifference. It was later extended to include under-report of all manner of symptoms of acquired brain injury by the patient compared to clinicians, family members, or functional performance. Anosognosia is related to time since onset of brain injury but not consistently to demographic variables, lesion location (except that it is more common after unilateral right than left hemispheric injury), or specific neuropsychological test scores. This review considers all manifestations of anosognosia as a unitary phenomenon with differing clinical characteristics dictated by variability in linked cognitive impairments. It is concluded that anosognosia has three chief contributing factors: (1) procedural: measurement differences across studies in terms of symptom selection and the designation of a "gold standard" of patient symptomatology; (2) psychological: a tendency towards positive self-evaluation and the avoidance of adverse information, that also occurs in neurologically intact individuals; and (3) neuropathological: an increased likelihood of error recognition failure from disconnections that disrupt feedback between injured brain regions governing specific behaviours (symptoms) and anterior cingulate/insular cortex. Anosodiaphoria is considered as an associated symptom, resulting from the same psychological and neuropathological factors. PMID:25686381

  1. Neuroprotective Therapies after Perinatal Hypoxic-Ischemic Brain Injury

    Directory of Open Access Journals (Sweden)

    Enrique Hilario

    2013-03-01

    Full Text Available Hypoxic-ischemic (HI brain injury is one of the main causes of disabilities in term-born infants. It is the result of a deprivation of oxygen and glucose in the neural tissue. As one of the most important causes of brain damage in the newborn period, the neonatal HI event is a devastating condition that can lead to long-term neurological deficits or even death. The pattern of this injury occurs in two phases, the first one is a primary energy failure related to the HI event and the second phase is an energy failure that takes place some hours later. Injuries that occur in response to these events are often manifested as severe cognitive and motor disturbances over time. Due to difficulties regarding the early diagnosis and treatment of HI injury, there is an increasing need to find effective therapies as new opportunities for the reduction of brain damage and its long term effects. Some of these therapies are focused on prevention of the production of reactive oxygen species, anti-inflammatory effects, anti-apoptotic interventions and in a later stage, the stimulation of neurotrophic properties in the neonatal brain which could be targeted to promote neuronal and oligodendrocyte regeneration.

  2. Traumatic Brain Injury and Its Effect on Students

    Science.gov (United States)

    Rosenthal, Stacy B.

    2012-01-01

    Over one million people suffer a traumatic brain injury every year, many of whom are students between the ages of 5 and 18. Using a qualitative case study approach, I wanted to discover the specific factors that both impede and help the school re-entry process for students in grades kindergarten through twelve so that these students can return to…

  3. Evaluation of a Health Education Programme about Traumatic Brain Injury

    Science.gov (United States)

    Garcia, Jane Mertz; Sellers, Debra M.; Hilgendorf, Amy E.; Burnett, Debra L.

    2014-01-01

    Objective: Our aim was to evaluate a health education programme (TBIoptions: Promoting Knowledge) designed to increase public awareness and understanding about traumatic brain injury (TBI) through in-person (classroom) and computer-based (electronic) learning environments. Design: We used a pre-post survey design with randomization of participants…

  4. Spoken Persuasive Discourse Abilities of Adolescents with Acquired Brain Injury

    Science.gov (United States)

    Moran, Catherine; Kirk, Cecilia; Powell, Emma

    2012-01-01

    Purpose: The aim of this study was to examine the performance of adolescents with acquired brain injury (ABI) during a spoken persuasive discourse task. Persuasive discourse is frequently used in social and academic settings and is of importance in the study of adolescent language. Method: Participants included 8 adolescents with ABI and 8 peers…

  5. Neurogenesis and gliogenesis in brain injury and learning

    Czech Academy of Sciences Publication Activity Database

    Šimonová, Zuzana; Náměstková, Kateřina; Jendelová, Pavla; Syková, Eva

    Fyziologický ústav AV ČR, v. v. i.. s. 37 ISSN 0862-8408. [Fyziologické dny /80./. 03.02.2004-05.02.2004, Praha] R&D Projects: GA MŠk LN00A065; GA ČR GA304/03/1189 Keywords : neurogenesis * gliogenesis * brain injury Subject RIV: FH - Neurology

  6. Hypofibrinogenemia in isolated traumatic brain injury in Indian patients

    Directory of Open Access Journals (Sweden)

    Chhabra Gaurav

    2010-12-01

    Full Text Available Coagulation abnormalities are common in patients with head injuries. However, the effect of brain injury on fibrinogen levels has not been well studied prospectively to assess coagulation abnormalities in patients with moderate and severe head injuries and correlate these abnormalities with the neurologic outcome. Consecutive patients with moderate (Glasgow Comma Scale (GCS,9-12 and severe (GCS≤8 head injuries were the subjects of this pilot study, All patients had coagulation parameters, including plasma fibrinogen levels measured. Clinical and computed tomography (CT scan findings and immediate clinical outcome were analyzed. Of the 100 patients enrolled, only seven (7% patients had hypofibrinogenemia (fibrinogen ≤200 mg/dL. The head injury was moderate in two patients and severe in five patients. Fibrinogen levels showed a progressively increasing trend in four patients (three with severe head injuries and one with moderate head injury. CT scan revealed subdural hematoma in five patients; extradural hematoma in one; and subarachnoid hemorrhage in another patient. Of the seven patients, two patients died during hospital. Large-scale prospective studies are needed to assess the fibrinogen level in patients with head injury and its impact on outcome.

  7. Metabolic changes in concussed American football players during the acute and chronic post-injury phases

    Directory of Open Access Journals (Sweden)

    Ellemberg Dave

    2011-08-01

    Full Text Available Abstract Background Despite negative neuroimaging findings many athletes display neurophysiological alterations and post-concussion symptoms that may be attributable to neurometabolic alterations. Methods The present study investigated the effects of sports concussion on brain metabolism using 1H-MR Spectroscopy by comparing a group of 10 non-concussed athletes with a group of 10 concussed athletes of the same age (mean: 22.5 years and education (mean: 16 years within both the acute and chronic post-injury phases. All athletes were scanned 1-6 days post-concussion and again 6-months later in a 3T Siemens MRI. Results Concussed athletes demonstrated neurometabolic impairment in prefrontal and motor (M1 cortices in the acute phase where NAA:Cr levels remained depressed relative to controls. There was some recovery observed in the chronic phase where Glu:Cr levels returned to those of control athletes; however, there was a pathological increase of m-I:Cr levels in M1 that was only present in the chronic phase. Conclusions These results confirm cortical neurometabolic changes in the acute post-concussion phase as well as recovery and continued metabolic abnormalities in the chronic phase. The results indicate that complex pathophysiological processes differ depending on the post-injury phase and the neurometabolite in question.

  8. Signs and Strategies for Educating Students with Brain Injuries: A Practical Guide for Teachers and Schools.

    Science.gov (United States)

    Wolcott, Gary; And Others

    This resource guide offers strategies for working with children having mild to severe brain injuries. Chapter 1 corrects common misunderstandings about brain injuries and gives suggestions and illustrative case examples. Chapter 2 discusses 12 common changes in students with brain injuries such as tiredness, irritability, passivity, depression,…

  9. Study of pathogenesis and the change of immune system of radiation brain injury

    International Nuclear Information System (INIS)

    Radiation brain injury is a severe complication of the pate tumour after radiotherapy. Review the pathogenesis of radiation brain injury and ion irradiation and the change of immune system then conclude the change of immune system that radiation brain injury can cause. (authors)

  10. 77 FR 73366 - Secondary Service Connection for Diagnosable Illnesses Associated With Traumatic Brain Injury

    Science.gov (United States)

    2012-12-10

    ... Traumatic Brain Injury AGENCY: Department of Veterans Affairs. ACTION: Proposed rule. SUMMARY: The... Medicine (IOM), Gulf War and Health, Volume 7: Long-Term Consequences of Traumatic Brain Injury, regarding the association between traumatic brain injury (TBI) and five diagnosable illnesses. The...

  11. Triple Peripheral Nerve Injury Accompanying to Traumatic Brain Injury: A Case Report

    Directory of Open Access Journals (Sweden)

    Ižlknur Can

    2014-02-01

    Full Text Available Secondary injuries especially extremity fractures may be seen concurrently with traumatic brain injury (TBI. Peripheral nerve damages may accompany to these fractures and may be missed out, especially in acute stage. In this case report; damage of radial, ulnar and median nerves which was developed secondarily to distal humerus fracture that could not be detected in acute stage, in a patient who had motor vehicle accident (MVA. 29-year-old male patient was admitted with weakness in the right upper extremity. 9 months ago, he had traumatic brain injury because of MVA, and fracture of distal humerus was detected in follow-ups. Upon the suspect of the peripheral nerve injury, the diagnosis was confirmed with ENMG. The patient responded well to the rehabilitation program treatment. In a TBI patient, it must be kept in mind that there might be a secondary trauma and therefore peripheral nerve lesions may accompany to TBI.

  12. Penetrating Brain Injury after Suicide Attempt with Speargun

    Directory of Open Access Journals (Sweden)

    John Ross Williams

    2014-07-01

    Full Text Available Penetrating cranial injury by mechanisms other than are exceedingly rare, and so strategies and guidelines for the management of PBI are largely informed by data from higher-velocity penetrating injuries. Here we present a case of penetrating brain injury by the low velocity mechanism of a harpoon from an underwater fishing speargun in an attempted suicide by a 56-year-old Caucasian male. The case raised a number of interesting points in management of lower-velocity penetrating brain injury (LVPBI, including benefit in delaying foreign body removal to allow for tamponade; the importance of history taking in establishing the social/legal significance of the events surrounding the injury; the use of cerebral angiogram in all cases of PBI; advantages of using DECT to reduce artifact when available; and antibiotic prophylaxis in the context of idiosyncratic histories of usage of penetrating objects before coming in contact with the intracranial environment. We present here the management of the case in full along with an extended discussion and review of existing literature regarding key points in management of LVPBI vs. higher velocity forms of intracranial injury.

  13. Early CT signs of progressive hemorrhagic injury following acute traumatic brain injury

    Energy Technology Data Exchange (ETDEWEB)

    Tong, Wu-song; Zheng, Ping; Xu, Jun-fa; Guo, Yi-jun; Zeng, Jing-song; Yang, Wen-jin; Li, Gao-yi; He, Bin; Yu, Hui [Pudong New Area People' s Hospital, Department of Neurosurgery, Shanghai (China)

    2011-05-15

    Since progressive hemorrhagic injury (PHI) was introduced in neurosurgical literatures, several studies have been performed, the results of which have influenced doctors but do not define guidelines for the best treatment of PHI. PHI may be confirmed by a serial computerized tomography (CT) scan, and it has been shown to be associated with a fivefold increase in the risk of clinical worsening and is a significant cause of morbidity and mortality as well. So, early detection of PHI is practically important in a clinical situation. To analyze the early CT signs of progressive hemorrhagic injury following acute traumatic brain injury (TBI) and explore their clinical significances, PHI was confirmed by comparing the first and repeated CT scans. Data were analyzed and compared including times from injury to the first CT and signs of the early CT scan. Logistic regression analysis was used to show the risk factors related to PHI. A cohort of 630 TBI patients was evaluated, and there were 189 (30%) patients who suffered from PHI. For patients with their first CT scan obtained as early as 2 h post-injury, there were 116 (77.25%) cases who suffered from PHI. The differences between PHIs and non-PHIs were significant in the initial CT scans showing fracture, subarachnoid hemorrhage (SAH), brain contusion, epidural hematoma (EDH), subdural hematoma (SDH), and multiple hematoma as well as the times from injury to the first CT scan (P < 0.01). Logistic regression analysis showed that early CT scans (EDH, SDH, SAH, fracture, and brain contusion) were predictors of PHI (P < 0.01). For patients with the first CT scan obtained as early as 2 h post-injury, a follow-up CT scan should be performed promptly. If the initial CT scan shows SAH, brain contusion, and primary hematoma with brain swelling, an earlier and dynamic CT scan should be performed for detection of PHI as early as possible and the medical intervention would be enforced in time. (orig.)

  14. Early CT signs of progressive hemorrhagic injury following acute traumatic brain injury

    International Nuclear Information System (INIS)

    Since progressive hemorrhagic injury (PHI) was introduced in neurosurgical literatures, several studies have been performed, the results of which have influenced doctors but do not define guidelines for the best treatment of PHI. PHI may be confirmed by a serial computerized tomography (CT) scan, and it has been shown to be associated with a fivefold increase in the risk of clinical worsening and is a significant cause of morbidity and mortality as well. So, early detection of PHI is practically important in a clinical situation. To analyze the early CT signs of progressive hemorrhagic injury following acute traumatic brain injury (TBI) and explore their clinical significances, PHI was confirmed by comparing the first and repeated CT scans. Data were analyzed and compared including times from injury to the first CT and signs of the early CT scan. Logistic regression analysis was used to show the risk factors related to PHI. A cohort of 630 TBI patients was evaluated, and there were 189 (30%) patients who suffered from PHI. For patients with their first CT scan obtained as early as 2 h post-injury, there were 116 (77.25%) cases who suffered from PHI. The differences between PHIs and non-PHIs were significant in the initial CT scans showing fracture, subarachnoid hemorrhage (SAH), brain contusion, epidural hematoma (EDH), subdural hematoma (SDH), and multiple hematoma as well as the times from injury to the first CT scan (P < 0.01). Logistic regression analysis showed that early CT scans (EDH, SDH, SAH, fracture, and brain contusion) were predictors of PHI (P < 0.01). For patients with the first CT scan obtained as early as 2 h post-injury, a follow-up CT scan should be performed promptly. If the initial CT scan shows SAH, brain contusion, and primary hematoma with brain swelling, an earlier and dynamic CT scan should be performed for detection of PHI as early as possible and the medical intervention would be enforced in time. (orig.)

  15. Ceftriaxone attenuates hypoxic-ischemic brain injury in neonatal rats

    Directory of Open Access Journals (Sweden)

    Huang Yen

    2011-09-01

    Full Text Available Abstract Background Perinatal brain injury is the leading cause of subsequent neurological disability in both term and preterm baby. Glutamate excitotoxicity is one of the major factors involved in perinatal hypoxic-ischemic encephalopathy (HIE. Glutamate transporter GLT1, expressed mainly in mature astrocytes, is the major glutamate transporter in the brain. HIE induced excessive glutamate release which is not reuptaked by immature astrocytes may induce neuronal damage. Compounds, such as ceftriaxone, that enhance the expression of GLT1 may exert neuroprotective effect in HIE. Methods We used a neonatal rat model of HIE by unilateral ligation of carotid artery and subsequent exposure to 8% oxygen for 2 hrs on postnatal day 7 (P7 rats. Neonatal rats were administered three dosages of an antibiotic, ceftriaxone, 48 hrs prior to experimental HIE. Neurobehavioral tests of treated rats were assessed. Brain sections from P14 rats were examined with Nissl and immunohistochemical stain, and TUNEL assay. GLT1 protein expression was evaluated by Western blot and immunohistochemistry. Results Pre-treatment with 200 mg/kg ceftriaxone significantly reduced the brain injury scores and apoptotic cells in the hippocampus, restored myelination in the external capsule of P14 rats, and improved the hypoxia-ischemia induced learning and memory deficit of P23-24 rats. GLT1 expression was observed in the cortical neurons of ceftriaxone treated rats. Conclusion These results suggest that pre-treatment of infants at risk for HIE with ceftriaxone may reduce subsequent brain injury.

  16. Brain plasticity and recovery from early cortical injury.

    Science.gov (United States)

    Kolb, Bryan; Mychasiuk, Richelle; Williams, Preston; Gibb, Robbin

    2011-09-01

    Neocortical development represents more than a simple unfolding of a genetic blueprint: rather, it represents a complex dance of genetic and environmental events that interact to adapt the brain to fit a particular environmental context. Most cortical regions are sensitive to a wide range of experiential factors during development and later in life, but the injured cortex appears to be unusually sensitive to perinatal experiences. This paper reviews the factors that influence how normal and injured brains (both focal and ischemic injuries) develop and adapt into adulthood. Such factors include prenatal experiences in utero as well as postnatal experiences throughout life. Examples include the effects of sensory and motor stimulation, psychoactive drugs (including illicit and prescription drugs), maternal and postnatal stress, neurotrophic factors, and pre- and postnatal diet. All these factors influence cerebral development and influence recovery from brain injury during development. PMID:21950386

  17. MRI and clinical symptoms in chronic cervical cord injury

    Energy Technology Data Exchange (ETDEWEB)

    Soeda, Shuichi; Maruiwa, Hirofumi; Yokoi, Masahiro; Saitoh, Seiya (Tsukigase Rehabilitation Center, Shizuoka (Japan)); Yamauchi, Kenji

    1992-08-01

    To assess the ability of magnetic resonance (MR) imaging to determine the prognosis of spinal cord injury in the chronic stage and to detect the injured myelomere, 39 patients were examined with MR images obtained by T1-weighted spin echo method 5 months to 4 years and 8 months (mean, one year and 5 months) after they had sustained spinal cord injury. According to hypointensity area of the ventrodorsad diameter of the spinal cord, MR images were classified as non-hypointensity (I), discrete (II), central (III), large cavity (IV), and transverse (V). The most common type was III (25%), followed by IV (26%), II (18%), V (15%), and I (13%). In 21 patients with bone injury, 14 (67%) had type IV or V, in contrast to 2 (11%) of 18 patients without bone injury. Increased hypointensity on MR images was associated with severer injury of the spinal cord. When hypointensity accounted for less than 1/2 of the ventrodorsad diameter of the spinal cord, walking ability was recovered in more than 80% of the patients. When less than 1/3 of the ventrodorsad diameter of the spinal cord was seen as hypointensity, arm function was well preserved, and the anterior horn of gray matter was found less injured. In 60% of the patients, there was difference in the injured level of myelomere between MR images and the neurological examination; the injured level of myelomere tended to be more cephalad level in the neurological examination than MR appearance.(N.K.).

  18. MRI and clinical symptoms in chronic cervical cord injury

    International Nuclear Information System (INIS)

    To assess the ability of magnetic resonance (MR) imaging to determine the prognosis of spinal cord injury in the chronic stage and to detect the injured myelomere, 39 patients were examined with MR images obtained by T1-weighted spin echo method 5 months to 4 years and 8 months (mean, one year and 5 months) after they had sustained spinal cord injury. According to hypointensity area of the ventrodorsad diameter of the spinal cord, MR images were classified as non-hypointensity (I), discrete (II), central (III), large cavity (IV), and transverse (V). The most common type was III (25%), followed by IV (26%), II (18%), V (15%), and I (13%). In 21 patients with bone injury, 14 (67%) had type IV or V, in contrast to 2 (11%) of 18 patients without bone injury. Increased hypointensity on MR images was associated with severer injury of the spinal cord. When hypointensity accounted for less than 1/2 of the ventrodorsad diameter of the spinal cord, walking ability was recovered in more than 80% of the patients. When less than 1/3 of the ventrodorsad diameter of the spinal cord was seen as hypointensity, arm function was well preserved, and the anterior horn of gray matter was found less injured. In 60% of the patients, there was difference in the injured level of myelomere between MR images and the neurological examination; the injured level of myelomere tended to be more cephalad level in the neurological examination than MR appearance.(N.K.)

  19. Does Caspase-6 Have a Role in Perinatal Brain Injury?

    Science.gov (United States)

    Baburamani, Ana A.; Miyakuni, Yasuka; Vontell, Regina; Supramaniam, Veena G.; Svedin, Pernilla; Rutherford, Mary; Gressens, Pierre; Mallard, Carina; Takeda, Satoru; Thornton, Claire; Hagberg, Henrik

    2015-01-01

    Apoptotic mechanisms are centre stage for the development of injury in the immature brain, and caspases have been shown to play a pivotal role during brain development and in response to injury. The inhibition of caspases using broad-spectrum agents such as Q-VD-OPh is neuroprotective in the immature brain. Caspase-6, an effector caspase, has been widely researched in neurodevelopmental disorders and found to be important following adult stroke, but its function in the neonatal brain has yet to be detailed. Furthermore, caspases may be important in microglial activation; microglia are required for optimal brain development and following injury, and their close involvement during neuronal cell death suggests that apoptotic cues such as caspase activation may be important in microglial activation. Therefore, in this study we aimed to investigate the possible apoptotic and non-apoptotic functions caspase-6 may have in the immature brain in response to hypoxia-ischaemia. We examined whether caspases are involved in microglial activation. We assessed cleaved caspase-6 expression following hypoxia-ischaemia and conducted primary microglial cultures to assess whether the broad-spectrum inhibitor Q-VD-OPh or caspase-6 gene deletion affected lipopolysaccharide (LPS)-mediated microglial activation and phenotype. We observed cleaved caspase-6 expression to be low but present in the cell body and cell processes in both a human case of white matter injury and 72 h following hypoxia-ischaemia in the rat. Gene deletion of caspase-6 did not affect the outcome of brain injury following mild (50 min) or severe (60 min) hypoxia-ischaemia. Interestingly, we did note that cleaved caspase-6 was co-localised with microglia that were not of apoptotic morphology. We observed that mRNA of a number of caspases was modulated by low-dose LPS stimulation of primary microglia. Q-VD-OPh treatment and caspase-6 gene deletion did not affect microglial activation but modified slightly the M2b

  20. Neural Bases of Recovery after Brain Injury

    Science.gov (United States)

    Nudo, Randolph J.

    2011-01-01

    Substantial data have accumulated over the past decade indicating that the adult brain is capable of substantial structural and functional reorganization after stroke. While some limited recovery is known to occur spontaneously, especially within the first month post-stroke, there is currently significant optimism that new interventions based on…

  1. Fetal Brain Injury in Survivors of Twin Pregnancies Complicated by Demise of One Twin: A Review.

    Science.gov (United States)

    Mackie, Fiona L; Morris, R Katie; Kilby, Mark D

    2016-06-01

    Perinatal mortality is increased considerably in multiple pregnancies compared to singleton pregnancies, with single intrauterine fetal demise (sIUFD) presenting a rare but unique perinatal problem. Monochorionic pregnancies are at particular risk of sIUFD due to bidirectional inter-twin placental vascular anastomoses. The resulting inter-twin blood flow can become unbalanced, causing acute and chronic inter-twin transfusion and profound anemia secondary to fetal exsanguination into the low-pressure circulation of the dead fetus. If the sIUFD occurs after 14 weeks' gestation it is believed to have the most significant effect on the continuing pregnancy as the co-twin is at increased risk of preterm delivery, long-term neurological complications, and death. This article will focus on fetal brain injury in the surviving co-twin in the case of sIUFD, as it is the most common kind of injury in sIUFD, and one which concerns parents and may be the basis for terminating the pregnancy. We will outline how these brain injuries are thought to occur and describe potential pathophysiological mechanisms. We will discuss risk factors for brain injury in cases of sIUFD, including: chorionicity, cause of the sIUFD (spontaneous or secondary to an underlying pathological process such as twin-to-twin transfusion syndrome), gestation of delivery and how to prevent brain injury in the co-twin. We also review modes of imaging, discuss the difficulties in predicting the long-term outcome for co-twin survivors, and highlight the dearth of research in this area. PMID:27203608

  2. Neuroprotective effect of estrogen after chronic spinal cord injury in ovariectomized rats

    Institute of Scientific and Technical Information of China (English)

    2007-01-01

    BACKGROUND: At present, there is still lack of effective drugs for chronic spinal cord injury, whereas it is found recently that estrogen has a neuroprotective effect on brain and spinal cord injuries.OBJECTIVE: To observe the effect of estrogen on the apoptosis of nerve cells after gradual chronic spinal cord injury in ovariectomized rats.DESIGN: A randomized controlled animal trial.SETTING: Institute of Orthopaedics, the Second Hospital of Lanzhou University.MATERIALS: Sixty-five female Wistar rats of common degree, weighing 220 - 250 g, were provided by the experimental animal center of Lanzhou University. The rats were randomly divided into sham-operated group (n =5), estrogen-treated group (n =30) and saline control group (n =30), and the latter two groups were observed at 1, 3, 7, 14, 28 and 60 days respectively, and 5 rats for each time point.METHODS: All the rats were treated with bilateral oophorectomy 2 weeks before the experiment. T10 vertebral lamina was revolved into using plastic screw. The spinal canal impingement was not induced initially. After that, the original incision was opened to expose the screw every 7 - 10 days.MAIN OUTCOME MEASURES: The apoptosis and Caspase-3 positive cells in the damaged spinal cord were detected using terminal deoxynucleotidal transferase-mediated dUTP-biotin nick end labeling (TUNEL) method and Caspase-3 immunohistochemical staining at 1, 3, 7, 14, 28 and 60 days after chronic spinal cord injury respectively.RESULTS: Totally 65 rats were used, and the deleted ones during the experiment were supplemented by others. Changes of Caspase-3 expression after spinal cord injury: In the sham-operated group, only a small amount of Caspase-3 proteins were observed in the rat spinal cord, mainly located in motor neurons of spinal cord anterior horn. In the estrogen-treated group and saline control group, positive cells expressed occasionally at 1 day postoperatively, began to increase obviously at 7 days after injury, strongly

  3. Pituitary dysfunction following traumatic brain injury or subarachnoid haemorrhage - in "Endocrine Management in the Intensive Care Unit".

    LENUS (Irish Health Repository)

    Hannon, M J

    2012-02-01

    Traumatic brain injury and subarachnoid haemorrhage are important causes of morbidity and mortality in the developed world. There is a large body of evidence that demonstrates that both conditions may adversely affect pituitary function in both the acute and chronic phases of recovery. Diagnosis of hypopituitarism and accurate treatment of pituitary disorders offers the opportunity to improve mortality and outcome in both traumatic brain injury and subarachnoid haemorrhage. In this article, we will review the history and pathophysiology of pituitary function in the acute phase following traumatic brain injury and subarachnoid haemorrhage, and we will discuss in detail three key aspects of pituitary dysfunction which occur in the early course of TBI; acute cortisol deficiency, diabetes insipidus and SIAD.

  4. Efficacy of N-acetyl cysteine in traumatic brain injury.

    Science.gov (United States)

    Eakin, Katharine; Baratz-Goldstein, Renana; Pick, Chiam G; Zindel, Ofra; Balaban, Carey D; Hoffer, Michael E; Lockwood, Megan; Miller, Jonathan; Hoffer, Barry J

    2014-01-01

    In this study, using two different injury models in two different species, we found that early post-injury treatment with N-Acetyl Cysteine (NAC) reversed the behavioral deficits associated with the TBI. These data suggest generalization of a protocol similar to our recent clinical trial with NAC in blast-induced mTBI in a battlefield setting, to mild concussion from blunt trauma. This study used both weight drop in mice and fluid percussion injury in rats. These were chosen to simulate either mild or moderate traumatic brain injury (TBI). For mice, we used novel object recognition and the Y maze. For rats, we used the Morris water maze. NAC was administered beginning 30-60 minutes after injury. Behavioral deficits due to injury in both species were significantly reversed by NAC treatment. We thus conclude NAC produces significant behavioral recovery after injury. Future preclinical studies are needed to define the mechanism of action, perhaps leading to more effective therapies in man. PMID:24740427

  5. Efficacy of N-Acetyl Cysteine in Traumatic Brain Injury

    Science.gov (United States)

    Eakin, Katharine; Baratz-Goldstein, Renana; Pick, Chiam G.; Zindel, Ofra; Balaban, Carey D.; Hoffer, Michael E.; Lockwood, Megan; Miller, Jonathan; Hoffer, Barry J.

    2014-01-01

    In this study, using two different injury models in two different species, we found that early post-injury treatment with N-Acetyl Cysteine (NAC) reversed the behavioral deficits associated with the TBI. These data suggest generalization of a protocol similar to our recent clinical trial with NAC in blast-induced mTBI in a battlefield setting [1], to mild concussion from blunt trauma. This study used both weight drop in mice and fluid percussion injury in rats. These were chosen to simulate either mild or moderate traumatic brain injury (TBI). For mice, we used novel object recognition and the Y maze. For rats, we used the Morris water maze. NAC was administered beginning 30–60 minutes after injury. Behavioral deficits due to injury in both species were significantly reversed by NAC treatment. We thus conclude NAC produces significant behavioral recovery after injury. Future preclinical studies are needed to define the mechanism of action, perhaps leading to more effective therapies in man. PMID:24740427

  6. Efficacy of N-acetyl cysteine in traumatic brain injury.

    Directory of Open Access Journals (Sweden)

    Katharine Eakin

    Full Text Available In this study, using two different injury models in two different species, we found that early post-injury treatment with N-Acetyl Cysteine (NAC reversed the behavioral deficits associated with the TBI. These data suggest generalization of a protocol similar to our recent clinical trial with NAC in blast-induced mTBI in a battlefield setting, to mild concussion from blunt trauma. This study used both weight drop in mice and fluid percussion injury in rats. These were chosen to simulate either mild or moderate traumatic brain injury (TBI. For mice, we used novel object recognition and the Y maze. For rats, we used the Morris water maze. NAC was administered beginning 30-60 minutes after injury. Behavioral deficits due to injury in both species were significantly reversed by NAC treatment. We thus conclude NAC produces significant behavioral recovery after injury. Future preclinical studies are needed to define the mechanism of action, perhaps leading to more effective therapies in man.

  7. Reorganization of Functional Connectivity as a Correlate of Cognitive Recovery in Acquired Brain Injury

    Science.gov (United States)

    Castellanos, Nazareth P.; Paul, Nuria; Ordonez, Victoria E.; Demuynck, Olivier; Bajo, Ricardo; Campo, Pablo; Bilbao, Alvaro; Ortiz, Tomas; del-Pozo, Francisco; Maestu, Fernando

    2010-01-01

    Cognitive processes require a functional interaction between specialized multiple, local and remote brain regions. Although these interactions can be strongly altered by an acquired brain injury, brain plasticity allows network reorganization to be principally responsible for recovery. The present work evaluates the impact of brain injury on…

  8. Characterization of pressure distribution in penetrating traumatic brain injuries.

    Science.gov (United States)

    Davidsson, Johan; Risling, Mårten

    2015-01-01

    Severe impacts to the head commonly lead to localized brain damage. Such impacts may also give rise to temporary pressure changes that produce secondary injuries in brain volumes distal to the impact site. Monitoring pressure changes in a clinical setting is difficult; detailed studies into the effect of pressure changes in the brain call for the development and use of animal models. The aim of this study is to characterize the pressure distribution in an animal model of penetrating traumatic brain injuries (pTBI). This data may be used to validate mathematical models of the animal model and to facilitate correlation studies between pressure changes and pathology. Pressure changes were measured in rat brains while subjected to pTBI for a variety of different probe velocities and shapes; pointy, blunt, and flat. Experiments on ballistic gel samples were carried out to study the formation of any temporary cavities. In addition, pressure recordings from the gel experiments were compared to values recorded in the animal experiments. The pTBI generated short lasting pressure changes in the brain tissue; the pressure in the contralateral ventricle (CLV) increased to 8 bar followed by a drop to 0.4 bar when applying flat probes. The pressure changes in the periphery of the probe, in the Cisterna Magna, and the spinal canal, were significantly less than those recorded in the CLV or the vicinity of the skull base. High-speed videos of the gel samples revealed the formation of spherically shaped cavities when flat and spherical probes were applied. Pressure changes in the gel were similar to those recorded in the animals, although amplitudes were lower in the gel samples. We concluded cavity expansion rate rather than cavity size correlated with pressure changes in the gel or brain secondary to probe impact. The new data can serve as validation data for finite element models of the trauma model and the animal and to correlate physical measurements with secondary injuries

  9. Pain and sleep in post-concussion/mild traumatic brain injury.

    Science.gov (United States)

    Lavigne, Gilles; Khoury, Samar; Chauny, Jean-Marc; Desautels, Alex

    2015-04-01

    Concussion after a force to the head is called mild traumatic brain injury (mTBI). Approximately 1 in 5 patients with mTBI will develop chronic pain (headache and widespread pain, possibly of central origin) and/or sleep problems (insomnia, disordered breathing, periodic limb movements). However, the predisposing mechanisms for chronic pain in patients with mTBI are unknown. Mild traumatic brain injury is a rare model to prospectively assess the risk factors and mechanisms for pain chronification from the injury onset in the absence of pretrauma comorbidity or medication. In the acute phase, headaches and sleep disturbances seem to predict the poorest long-term cognitive and mood outcomes. Although recent studies suggest that certain brain biomarkers and mood alterations (eg, anxiety, depression) contribute, the causality of chronic pain remains unclear. In mTBI patients with pain, poor sleep quality was correlated with fast beta and gamma electroencephalographic activity in frontal, central, and occipital electroencephalographic (EEG) derivations in all sleep stages. Sleep recuperative function seems to be disturbed by persistent wake EEG activity, corroborating patient complaints such as feeling awake when asleep. Pain and sleep management in mTBI is not yet evidence-based. Treatments include cognitive behavioral and light therapies, medications, and continuous positive airway pressure (CPAP) or oral appliances for disordered sleep breathing. Customized approaches are indicated for mTBI, pain, and sleep complaints. Further studies in pediatric, sport, and transportation populations are needed to prevent TBI chronification. Improvements are emerging in biomarker sensitivity and specificity and management strategies for TBI, pain, and sleep comorbidities. PMID:25789439

  10. Establishing a cat model of chronic optic nerve compression injury

    Institute of Scientific and Technical Information of China (English)

    Feng Yu; Shaoji Yuan; Rongwei Zhang; Yicheng Lu; Meiqing Lou

    2009-01-01

    BACKGROUND:An animal model of chronic optic nerve injury is necessary to further understand the pathological mechanisms involved.OBJECTIVE:To establish a stabilized,chronic,optic nerve crush model,which is similar to the clinical situation to explore histopathological and optic electrophysiological changes involved in this injury.DESIGN,TIME AND SETTING:A randomized and controlled animal trial was performed at Shanghai Institute of Neurosurgery from May to October 2004.MATERIALS:A BAL3XRAY undetachable balloon and Magic-BD catheter were provided by BLAT,France;JX-2000 biological signal processing system by Second Military Medical University of Chinese PLA,China;inverted phase contrast microscopy by Olympus,Japan.METHODS:A total of twenty normal adult cats were randomly assigned to control (n = 5) and model (n = 15) groups,according to different doses of contrast agent injected through balloons as follows:0.2 mL injection,0.25 mL injection,and 0.35 mL injection,with each group containing 5 animals.Imitating the clinical pterion approach,the optic nerves were exposed using micro-surgical methods.An engorged undetachable balloon was implanted beneath the nerve and connected to a catheter.Balloon size was controlled with a contrast agent injection (0.1 mL/10 min) to form an occupying lesion model similar to sellar tumors.MAIN OUTCOME MEASURES:The visually evoked potential examination was used to study optical electrophysiology changes in pre-post chronic optical nerve injury.Ultrastructural pathological changes to the optic nerve were analyzed by electron microscopy.RESULTS:During the early period (day 11 after modeling),visually evoked potential demonstrated no significant changes.In the late period (day 51 after modeling),recorded VEP demonstrated that P1 wave latency was prolonged and P1 wave amplitude was obviously reduced.Following injury,the endoneurium,myelin sheath,lamella,axolemma,and axon appeared disordered.CONCLUSION:Results demonstrated that the chronic

  11. MICROGLIA ACTIVATION AS A BIOMARKER FOR TRAUMATIC BRAIN INJURY

    Directory of Open Access Journals (Sweden)

    CesarVBorlongan

    2013-03-01

    Full Text Available Traumatic brain injury (TBI has become the signature wound of wars in Afghanistan and Iraq. Injury may result from a mechanical force, a rapid acceleration-deceleration movement, or a blast wave. A cascade of secondary cell death events ensues after the initial injury. In particular, multiple inflammatory responses accompany TBI. A series of inflammatory cytokines and chemokines spreads to normal brain areas juxtaposed to the core impacted tissue. Among the repertoire of immune cells involved, microglia is a key player in propagating inflammation to tissues neighboring the core site of injury. Neuroprotective drug trials in TBI have failed, likely due to their sole focus on abrogating neuronal cell death and ignoring the microglia response despite these inflammatory cells’ detrimental effects on the brain. Another relevant point to consider is the veracity of results of animal experiments due to deficiencies in experimental design, such as incomplete or inadequate method description, data misinterpretation and reporting may introduce bias and give false-positive results. Thus, scientific publications should follow strict guidelines that include randomization, blinding, sample-size estimation and accurate handling of all data (Landis et al., 2012. A prolonged state of inflammation after brain injury may linger for years and predispose patients to develop other neurological disorders, such as Alzheimer’s disease. TBI patients display progressive and long-lasting impairments in their physical, cognitive, behavioral, and social performance. Here, we discuss inflammatory mechanisms that accompany TBI in an effort to increase our understanding of the dynamic pathological condition as the disease evolves over time and begin to translate these findings for defining new and existing inflammation-based biomarkers and treatments for TBI.

  12. Perinatal Hypoxic-Ischemic brain injury; MR findings

    International Nuclear Information System (INIS)

    To characterize the MR findings of hypoxic-ischemic brain injury and to assess the value of the MR imaging. SE T1-, T2-weighted, and IR brain MR images of 44 infants and children with the past history of perinatal hypoxic insults were reviewed. Abnormal brain MR findings of 8 patients with birth history of prematurity and 36 patients with birth history of full-term/posterm including 7 with severe anoxic insult history, were compared in regard to the location and the character of the lesions. MRI demonstrated the followings; (1)abnormal signal intensity lesions of subcortical and/or deep cerebral white matter, cortex, and deep gray matter, (2)atrophy of the cerebral white matter, cortex and corpus callosum, with/without ventriculomegaly, and (3)delay in myelination. Periventricular and deep white matter lesions were demonstrated in the prematurity, the deep white matter lesions and/ or subcortical white matter lesions in the term/post-term, and deep gray matter lesions in the 7 patients with severe anoxic insults history. MR imaging was useful in the diagnosis of the hypoxic-ischemic brain injury, and the white and gray matter lesions were correlated with the time of the injury and the severity of hypoxic insult

  13. Systemic progesterone for modulating electrocautery-induced secondary brain injury.

    Science.gov (United States)

    Un, Ka Chun; Wang, Yue Chun; Wu, Wutian; Leung, Gilberto Ka Kit

    2013-09-01

    Bipolar electrocautery is an effective and commonly used haemostatic technique but it may also cause iatrogenic brain trauma due to thermal injury and secondary inflammatory reactions. Progesterone has anti-inflammatory and neuroprotective actions in traumatic brain injury. However, its potential use in preventing iatrogenic brain trauma has not been explored. We conducted a pilot animal study to investigate the effect of systemic progesterone on brain cellular responses to electrocautery-induced injury. Adult male Sprague-Dawley rats received standardized bipolar electrocautery (40 W for 2 seconds) over the right cerebral cortex. The treatment group received progesterone intraperitoneally 2 hours prior to surgery; the control group received the drug vehicle only. Immunohistochemical studies showed that progesterone could significantly reduce astrocytic hypertrophy on postoperative day 1, 3 and 7, as well as macrophage infiltration on day 3. The number of astrocytes, however, was unaffected. Our findings suggest that progesterone should be further explored as a neuroprotective agent against electrocautery-induced or other forms of iatrogenic trauma during routine neurosurgical procedures. Future studies may focus on different dosing regimens, neuronal survival, functional outcome, and to compare progesterone with other agents such as dexamethasone. PMID:23830688

  14. Sleep deprivation does not affect neuronal susceptibility to mild traumatic brain injury in the rat.

    Science.gov (United States)

    Caron, Aimee M; Stephenson, Richard

    2015-01-01

    Mild and moderate traumatic brain injuries (TBIs) (and concussion) occur frequently as a result of falls, automobile accidents, and sporting activities, and are a major cause of acute and chronic disability. Fatigue and excessive sleepiness are associated with increased risk of accidents, but it is unknown whether prior sleep debt also affects the pathophysiological outcome of concussive injury. Using the "dark neuron" (DN) as a marker of reversible neuronal damage, we tested the hypothesis that acute (48 hours) total sleep deprivation (TSD) and chronic sleep restriction (CSR; 10 days, 6-hour sleep/day) affect DN formation following mild TBI in the rat. TSD and CSR were administered using a walking wheel apparatus. Mild TBI was administered under anesthesia using a weight-drop impact model, and the acute neuronal response was observed without recovery. DNs were detected using standard bright-field microscopy with toluidine blue stain following appropriate tissue fixation. DN density was low under home cage and sleep deprivation control conditions (respective median DN densities, 0.14% and 0.22% of neurons), and this was unaffected by TSD alone (0.1%). Mild TBI caused significantly higher DN densities (0.76%), and this was unchanged by preexisting acute or chronic sleep debt (TSD, 0.23%; CSR, 0.7%). Thus, although sleep debt may be predicted to increase the incidence of concussive injury, the present data suggest that sleep debt does not exacerbate the resulting neuronal damage. PMID:26124685

  15. Neurobehavioral Effects of Levetiracetam in Patients with Traumatic Brain Injury

    Directory of Open Access Journals (Sweden)

    Jared F Benge

    2013-12-01

    Full Text Available Moderate to severe traumatic brain injury (TBI is one of the leading causes of acquired epilepsy. Prophylaxis for seizures is the standard of care for individuals with moderate to severe injuries at risk for developing seizures, though relatively limited comparative data is available to guide clinicians in their choice of agents. There have however been experimental studies which demonstrate potential neuroprotective qualities of levetiracetam after TBI, and in turn there is hope that eventually such agents may improve neurobehavioral outcomes post-TBI. This mini-review summarizes the available studies and suggests areas for future studies.

  16. Association football injuries to the brain. A preliminary report.

    OpenAIRE

    Tysvaer, A.; Storli, O.

    1981-01-01

    In 1975 the authors sent a questionnaire to all players in the Norwegian First Division League Clubs to record the incidence of head injuries due to heading. The conclusion of the questionnaire is that there seems to be a low percentage of serious head injuries. None of the players had been operated on for epi- or subdural hematoma or other brain damage and only a few have had concussion due to heading. In sixty per cent of the players a full neurological examination and EEG recording was und...

  17. Neuropsychological, Metabolic, and GABAA Receptor Studies in Subjects with Repetitive Traumatic Brain Injury.

    Science.gov (United States)

    Bang, Seong Ae; Song, Yoo Sung; Moon, Byung Seok; Lee, Byung Chul; Lee, Ho-Young; Kim, Jong-Min; Kim, Sang Eun

    2016-06-01

    Repetitive traumatic brain injury (rTBI) occurs as a result of mild and accumulative brain damage. A prototype of rTBI is chronic traumatic encephalopathy (CTE), which is a degenerative disease that occurs in patients with histories of multiple concussions or head injuries. Boxers have been the most commonly studied patient group because they may experience thousands of subconcussive hits over the course of a career. This study examined the consequences of rTBI with structural brain imaging and biomolecular imaging and investigated whether the neuropsychological features of rTBI were related to the findings of the imaging studies. Five retired professional boxers (mean age, 46.8 ± 3.19 years) and four age-matched controls (mean age, 48.5 ± 3.32 years) were studied. Cognitive-motor related functional impairment was assessed, and all subjects underwent neuropsychological evaluation and behavioral tasks, as well as structural brain imaging and functional-molecular imaging. In neuropsychological tests, boxers showed deficits in delayed retrieval of visuospatial memory and motor coordination, which had a meaningful relationship with biomolecular imaging results indicative of neuronal injury. Morphometric abnormalities were not found in professional boxers by structural magnetic resonance imaging (MRI). Glucose metabolism was impaired in frontal areas associated with cognitive dysfunction, similar to findings in Alzheimer's disease. Low binding potential (BP) of (18)F-flumazenil (FMZ) was found in the angular gyrus and temporal cortical regions, revealing neuronal deficits. These results suggested that cognitive impairment and motor dysfunction reflect chronic damage to neurons in professional boxers with rTBI. PMID:26414498

  18. Remyelination after chronic spinal cord injury is associated with proliferation of endogenous adult progenitor cells after systemic administration of guanosine

    OpenAIRE

    Jiang, Shucui; Ballerini, Patrizia; Buccella, Silvana; Giuliani, Patricia; Jiang, Cai; Huang, Xinjie; Rathbone, Michel P.

    2008-01-01

    Axonal demyelination is a consistent pathological sequel to chronic brain and spinal cord injuries and disorders that slows or disrupts impulse conduction, causing further functional loss. Since oligodendroglial progenitors are present in the demyelinated areas, failure of remyelination may be due to lack of sufficient proliferation and differentiation of oligodendroglial progenitors. Guanosine stimulates proliferation and differentiation of many types of cells in vitro and exerts neuroprotec...

  19. Dissociated Horizontal Deviation after Traumatic Brain Injury

    OpenAIRE

    Lee, Tae-Eun; Cha, Deok-Sun; Koh, Seong-Beom; Kim, Seung-Hyun

    2010-01-01

    A 4-year-old boy visited the hospital with exotropia after brain hemorrhage caused by trauma. He had undergone decompressive craniectomy and cranioplasty 18 months prior to presentation at our hospital. An alternate prism cover test showed more than 50 prism diopters (PD) of left exotropia when he was fixing with the right eye and 30 PD of right exotropia when he was fixing with the left eye at near and far distance. On the Hirschberg test, 60 PD of left exotropia was noted in the primary pos...

  20. Chronic pain: The role of learning and brain plasticity

    OpenAIRE

    Mansour, A.R.; Farmer, M.A.; Baliki, M. N.; Apkarian, A. Vania

    2014-01-01

    Based on theoretical considerations and recent observations, we argue that continued suffering of chronic pain is critically dependent on the state of motivational and emotional mesolimbic-prefrontal circuitry of the brain. The plastic changes that occur within this circuitry in relation to nociceptive inputs dictate the transition to chronic pain, rendering the pain less somatic and more affective in nature. This theoretical construct is a strong departure from the traditional scientific vie...

  1. MR imaging of late radiation brain injury

    International Nuclear Information System (INIS)

    One hundred and four patients treated with radiotherapy for intracranial tumors and their related conditions were reviewed to evaluate the usefulness of magnetic resonance (MR) imaging in demonstrating increased signal intensity areas on T2-weighted images that were considered to be late adverse effects of irradiation of the brain. High signal intensity areas of the white matter were divided into five patterns according to their size and extension. Severity was found to increase with age and irradiation doses of more than 50 Gy. In patients with irradiation doses of more than 60 Gy, the severity of increased with shorter interval after radiotherapy than in those given low irradiation doses. Clinical findings such as mental deterioration, motor abnormality, and visual defect were observed in 12 patients. These findings were closely correlated with the severity of the MR pattern. In most patients, high signal intensity areas were stable or progressive during the course of follow-up. However, these areas were regressive in three patients. Imaging with Gd-DTPA was performed in 36 patients, six of whom showed enhancement. Pathological findings on enhancement included astrocyte proliferation and coalescing vacuoles in neural tissue. MR imaging is an excellent method with which to monitor the adverse effects of radiotherapy of the brain. (author)

  2. Facilitated assessment of tissue loss following traumatic brain injury

    Directory of Open Access Journals (Sweden)

    Anders eHånell

    2012-03-01

    Full Text Available All experimental models of traumatic brain injury (TBI result in a progressive loss of brain tissue. The extent of tissue loss reflects the injury severity and can be measured to evaluate the potential neuroprotective effect of experimental treatments. Quantitation of tissue volumes is commonly performed using evenly spaced brain sections stained using routine histochemical methods and digitally captured. The brain tissue areas are then measured and the corresponding volumes are calculated using the distance between the sections. Measurements of areas are usually performed using a general purpose image analysis software and the results are then transferred to another program for volume calculations. To facilitate the measurement of brain tissue loss we developed novel algorithms which automatically separate the areas of brain tissue from the surrounding image background and identify the ventricles. We implemented these new algorithms by creating a new computer program (SectionToVolume which also has functions for image organization, image adjustments and volume calculations. We analyzed brain sections from mice subjected to severe focal TBI using both SectionToVolume and ImageJ, a commonly used image analysis program. The volume measurements made by the two programs were highly correlated and analysis using SectionToVolume required considerably less time. The inter-rater reliability was high. Given the extensive use of brain tissue loss measurements in TBI research, SectionToVolume will likely be a useful tool for TBI research. We therefore provide both the source code and the program as attachments to this article.

  3. Lipotoxic brain microvascular injury is mediated by activating transcription factor 3-dependent inflammatory and oxidative stress pathways.

    Science.gov (United States)

    Aung, Hnin Hnin; Altman, Robin; Nyunt, Tun; Kim, Jeffrey; Nuthikattu, Saivageethi; Budamagunta, Madhu; Voss, John C; Wilson, Dennis; Rutledge, John C; Villablanca, Amparo C

    2016-06-01

    Dysfunction of the cerebrovasculature plays an important role in vascular cognitive impairment (VCI). Lipotoxic injury of the systemic endothelium in response to hydrolyzed triglyceride-rich lipoproteins (TGRLs; TGRL lipolysis products) or a high-fat Western diet (WD) suggests similar mechanisms may be present in brain microvascular endothelium. We investigated the hypothesis that TGRL lipolysis products cause lipotoxic injury to brain microvascular endothelium by generating increased mitochondrial superoxide radical generation, upregulation of activating transcription factor 3 (ATF3)-dependent inflammatory pathways, and activation of cellular oxidative stress and apoptotic pathways. Human brain microvascular endothelial cells were treated with human TGRL lipolysis products that induced intracellular lipid droplet formation, mitochondrial superoxide generation, ATF3-dependent transcription of proinflammatory, stress response, and oxidative stress genes, as well as activation of proapoptotic cascades. Male apoE knockout mice were fed a high-fat/high-cholesterol WD for 2 months, and brain microvessels were isolated by laser capture microdissection. ATF3 gene transcription was elevated 8-fold in the hippocampus and cerebellar brain region of the WD-fed animals compared with chow-fed control animals. The microvascular injury phenotypes observed in vitro and in vivo were similar. ATF3 plays an important role in mediating brain microvascular responses to acute and chronic lipotoxic injury and may be an important preventative and therapeutic target for endothelial dysfunction in VCI. PMID:27087439

  4. Assessment of traumatic brain injury degree in animal model

    Institute of Scientific and Technical Information of China (English)

    Jian-Qiang Chen; Cheng-Cheng Zhang; Hong Lu; Wei Wang

    2014-01-01

    Objective:To establish stable and controllable brain injury with accurate degree and good repeatability in rat model.Methods:Controlled cortical impact(CCI) device was used to prepare for the rat brain injury model by the impact head of different model(GroupANo.4,GroupBNo.5, GroupCNo.6) and the impact depth(GroupA:1.5-2.0 mm,GroupB:2.5-3.0 mm,GroupC:3.5-4.0 mm) with impact time of0.1 s and impact velocity of2.5 m/s.Twelve rats with three months of age were used in each group(the impact depth of every two rats was added1 mm respectively).After modeling for1 h, magnetic resonance imaging(MRI) was received and brain histopathology was observed to assess degree of injury by model parameters of three groups.Results:After modeling ofGroupA,MRI showed that the cortex structure was damaged with a small amount of bleeding in center and mild edema around, and the total volume of injury was(28.69±4.94) mm3.Pathology revealed the injury was confined to the superficial cortical with mild edema of nerve cell, which was assessed as mild cerebral contusion.While after modeling,MRI ofGroupB showed that the structure of cortex and medulla were damaged simultaneously and extended to cerebral nuclei zone, with4 cases of hematoma in the center and larger edema range around, and the total volume of injury was(78.38±9.28) mm3.Pathology revealed the injury range was reached nuclei zone, with swell of nerve cell and mitochondria, which was assessed to moderate cerebral contusion. After modeling ofGroupC,MRI showed that extensive tissue injury was appeared in cortex and medulla and deep nuclei, with9 cases of hematoma and large edema signal of surrounding tissue T2WI, while in5 cases, lateral nucleus of injury signal was increased, and the total volume of injury was(135.89±24.80) mm3.Pathology revealed the deep cerebral nuclei was damaged, with the disappearance of neuronal structure and vacuolization of mitochondria, which was assessed as severe cerebral contusion.MRI changes were

  5. Coated-Platelet Levels Increase with Number of Injuries in Patients with Mild Traumatic Brain Injury.

    Science.gov (United States)

    Prodan, Calin I; Vincent, Andrea S; Dale, George L

    2016-05-01

    Coated-platelets are procoagulant platelets that are elevated in stroke and are associated with stroke recurrence. In a previous study, prompted by data showing an increased risk for stroke following traumatic brain injury (TBI), we found that coated-platelet levels are elevated in patients with combat-related mild TBI (mTBI) several years after the injury, compared with controls. We now investigate in an expanded patient population whether parameters commonly recorded in mTBI are related to increased coated-platelet potential. Coated-platelet levels were assayed in 120 mTBI patients at intervals ranging from 6 months to 10 years from the last injury. Correlations were calculated between coated-platelet levels and age, gender, race/ethnicity, loss of consciousness, alteration in consciousness, post-traumatic amnesia, number of injuries, mechanism of injury, time since first and last injury, smoking, medications that may influence coated-platelet levels, and pertinent comorbid conditions. Significant correlations were detected between coated-platelet levels and number of injuries (p = 0.026), gender (p = 0.01), and time since last injury (p = 0.04). A multi-variable linear model analysis, including these three parameters and an additional three parameters (race/ethnicity, smoking, and mechanism of injury) that reached a p value of <0.2, showed that the number of injuries were predictive of coated-platelet levels (p = 0.004). These results support a mechanistic link between increased coated-platelet levels and repeated injuries in mTBI. Long-term studies will be required to determine the impact of increased prothrombotic potential in mTBI patients. PMID:26414016

  6. Traumatic brain injury in children: acute care management.

    Science.gov (United States)

    Geyer, Kristen; Meller, Karen; Kulpan, Carol; Mowery, Bernice D

    2013-01-01

    The care of the pediatric patient with a severe traumatic brain injury (TBI) is an all-encompassing nursing challenge. Nursing vigilance is required to maintain a physiological balance that protects the injured brain. From the time a child and family first enter the hospital, they are met with the risk of potential death and an uncertain future. The family is subjected to an influx of complex medical and nursing terminology and interventions. Nurses need to understand the complexities of TBI and the modalities of treatment, as well as provide patients and families with support throughout all phases of care. PMID:24640314

  7. Relationship between changes of N-methyl-D-aspartate receptor activity and brain edema after brain injury in rats

    Institute of Scientific and Technical Information of China (English)

    2001-01-01

    Objective: To investigate the relationship between the changes of N-methyl-D-aspartate (NMDA) receptor activity and brain edema after injury in rats.   Methods: The brain injury models were made by using a free-falling body. The treatment model was induced by means of injecting AP5 into lateral ventricle before brain injury; water contents in brain cortex were measured with dry-wet method; and NMDA receptor activity was detected with a radio ligand binding assay.   Results: The water contents began to increase at 30 minutes and reached the peak at 6 hours after brain injury. The maximal binding (Bmax) of NMDA receptor increased significantly at 15 minutes and reached the peak at 30 minutes, then decreased gradually and had the lowest value 6 hours after brain injury. Followed the treatment with AP5, NMDA receptor activity in the injured brain showed a normal value; and the water contents were lower than that of AP5-free injury group 24 hours after brain injury.   Conclusions: It suggests that excessive activation of NMDA receptor may be one of the most important factors to induce the secondary cerebral impairments, and AP5 may protect the brain from edema after brain injury.

  8. Sigma-1 Receptor Modulates Neuroinflammation After Traumatic Brain Injury.

    Science.gov (United States)

    Dong, Hui; Ma, Yunfu; Ren, Zengxi; Xu, Bin; Zhang, Yunhe; Chen, Jing; Yang, Bo

    2016-07-01

    Traumatic brain injury (TBI) remains a significant clinical problem and contributes to one-third of all injury-related deaths. Activated microglia-mediated inflammatory response is a distinct characteristic underlying pathophysiology of TBI. Here, we evaluated the effect and possible mechanisms of the selective Sigma-1 receptor agonist 2-(4-morpholinethyl)-1-phenylcyclohexanecarboxylate (PRE-084) in mice TBI model. A single intraperitoneal injection 10 μg/g PRE-084, given 15 min after TBI significantly reduced lesion volume, lessened brain edema, attenuated modified neurological severity score, increased the latency time in wire hang test, and accelerated body weight recovery. Moreover, immunohistochemical analysis with Iba1 staining showed that PRE-084 lessened microglia activation. Meanwhile, PRE-084 reduced nitrosative and oxidative stress to proteins. Thus, Sigma-1 receptors play a major role in inflammatory response after TBI and may serve as useful target for TBI treatment in the future. PMID:26228028

  9. Minding and Caring about Ethics in Brain Injury.

    Science.gov (United States)

    Gillett, Grant

    2016-05-01

    Joseph Fins's book Rights Come to Mind: Brain Injury, Ethics, and the Struggle for Consciousness (Cambridge UP, 2015) is a considerable addition to the literature on disorders of consciousness and the murky area of minimally conscious states. Fins brings to this fraught area of clinical practice and neuroethical analysis a series of stories and reflections resulting in a pressing and sustained ethical challenge both to clinicians and to health care systems. The challenge is multifaceted, with diagnostic and therapeutic demands to be met by clinicians and a mix of moral, scientific-economic, and political resonances for health care analysts. Everything in the book resonates with my own clinical experience and the often messy and emotionally wrenching business of providing ongoing care for patients with severe brain injuries and disorders, people who frequently resist the categorizations that well-organized health care systems prefer and that can dictate terms of patient management. PMID:27150418

  10. Acute respiratory distress syndrome assessment after traumatic brain injury

    Directory of Open Access Journals (Sweden)

    Shahrooz Kazemi

    2016-01-01

    Full Text Available Background: Acute respiratory distress syndrome (ARDS is one of the most important complications associated with traumatic brain injury (TBI. ARDS is caused by inflammation of the lungs and hypoxic damage with lung physiology abnormalities associated with acute respiratory distress syndrome. Aim of this study is to determine the epidemiology of ARDS and the prevalence of risk factors. Methods: This prospective study performed on patients with acute traumatic head injury hospitalization in the intensive care unit of the Shohaday-e Haftom-e-Tir Hospital (September 2012 to September 2013 done. About 12 months, the data were evaluated. Information including age, sex, education, employment, drug and alcohol addiction, were collected and analyzed. The inclusion criteria were head traumatic patients and exclusion was the patients with chest trauma. Questionnaire was designed with doctors supervision of neurosurgery. Then the collected data were analysis. Results: In this study, the incidence of ARDS was 23.8% and prevalence of metabolic acidosis was 31.4%. Most injury with metabolic acidosis was Subarachnoid hemorrhage (SAH 48 (60% and Subdural hemorrhage (SDH was Next Level with 39 (48% Correlation between Glasgow Coma Scale (GCS and Respiratory Distress Syndrome (ARDS were significantly decreased (P< 0.0001. The level of consciousness in patients with skull fractures significantly lower than those without fractures (P= 0.009 [(2.3±4.6 vs (4.02±7.07]. Prevalence of metabolic acidosis during hospitalization was 80 patients (31.4%. Conclusion: Acute respiratory distress syndrome is a common complication of traumatic brain injury. Management and treatment is essential to reduce the mortality. In this study it was found the age of patients with ARDS was higher than patients without complications. ARDS risk factor for high blood pressure was higher in men. Most victims were pedestrians. The most common injury associated with ARDS was SDH. Our analysis

  11. Quantitative Brain Electrical Activity in the Initial Screening of Mild Traumatic Brain Injuries

    OpenAIRE

    O'Neil, Brian; Prichep, Leslie S.; Naunheim, Roseanne; Chabot, Robert

    2012-01-01

    Introduction: The incidence of emergency department (ED) visits for Traumatic Brain Injury (TBI) in the United States exceeds 1,000,000 cases/year with the vast majority classified as mild (mTBI). Using existing computed tomography (CT) decision rules for selecting patients to be referred for CT, such as the New Orleans Criteria (NOC), approximately 70% of those scanned are found to have a negative CT. This study investigates the use of quantified brain electrical activity to assess its possi...

  12. Feasibility of computerized brain plasticity-based cognitive training after traumatic brain injury

    OpenAIRE

    Matthew S. Lebowitz, AB; Kristen Dams-O’Connor, PhD; Joshua B. Cantor, PhD

    2013-01-01

    The present study investigates the feasibility and utility of using a computerized brain plasticity-based cognitive training (BPCT) program as an intervention for community-dwelling individuals with traumatic brain injury (TBI). In a pre-post pilot study, 10 individuals with mild to severe TBI who were 6 mo to 22 yr postinjury were asked to use a computerized BPCT intervention—designed to improve cognitive functioning through a graduated series of structured exercises—at their homes in an urb...

  13. Hypothalamic-Pituitary Autoimmunity and Traumatic Brain Injury

    OpenAIRE

    Federica Guaraldi; Silvia Grottoli; Emanuela Arvat; Ezio Ghigo

    2015-01-01

    Background: Traumatic brain injury (TBI) is a leading cause of secondary hypopituitarism in children and adults, and is responsible for impaired quality of life, disabilities and compromised development. Alterations of pituitary function can occur at any time after the traumatic event, presenting in various ways and evolving during time, so they require appropriate screening for early detection and treatment. Although the exact pathophysiology is unknown, several mechanisms have been hypoth...

  14. Understanding paroxysmal sympathetic hyperactivity after traumatic brain injury

    OpenAIRE

    Meyer, Kimberly S.

    2014-01-01

    Background: Paroxysmal sympathetic hyperactivity (PSH) is a condition occurring in a small percentage of patients with severe traumatic brain injury (TBI). It is characterized by a constellation of symptoms associated with excessive adrenergic output, including tachycardia, hypertension, tachypnea, and diaphoresis. Diagnosis is one of exclusion and, therefore, is often delayed. Treatment is aimed at minimizing triggers and pharmacologic management of symptoms. Methods: A literature review...

  15. Cognitive rehabilitation in children with acquired brain injuries

    OpenAIRE

    Hagberg-van't Hooft, Ingrid

    2005-01-01

    Deficits in attention, memory and executive functions are the most common cognitive dysfunctions after acquired brain injuries (ABI) and may have a major negative influence on academic and social adjustment. Neuropsychological measures can assess these dysfunctions and shortcomings in academic and social life, but there is a great need for new efficacious cognitive treatment programmes. The main aims of this thesis were to evaluate the direct and maintained effects of a ...

  16. Rehabilitation Outcome of Unconscious Traumatic Brain Injury Patients

    OpenAIRE

    Klein, Anke-Maria; Howell, Kaitlen; Vogler, Jana; Grill, Eva; Straube, Andreas; Bender, Andreas

    2013-01-01

    Outcome prediction of traumatic brain injury (TBI) patients with severe disorders of consciousness (DOC) at the end of their time in an intensive care setting is important for clinical decision making and counseling of relatives, and constitutes a major challenge. Even the question of what constitutes an improved outcome is controversially discussed. We have conducted a retrospective cohort study for the rehabilitation dynamics and outcome of TBI patients with DOC. Out of 188 patients, 37.2% ...

  17. Cost-effectiveness of early rehabilitation after Traumatic brain injury

    OpenAIRE

    2013-01-01

    Traumatic brain injury (TBI) is a craniocerebral trauma which causes long-term physical, cognitive and emotional impairment and adds substantially to the healthcare burden. The cost of TBIs is believed to be huge in Norway. Moderate and severe TBIs require rehabilitation, which helps reduce disability and improves the quality of life of patients. It is important to determine the efficacy of early rehabilitation as a form of treatment after severe TBI both in terms of its costs and effectivene...

  18. Adolescents’ experience of a parental traumatic brain injury

    Directory of Open Access Journals (Sweden)

    D Harris

    2006-04-01

    Full Text Available This study explores the experiences of four adolescents, each living with a parent who has sustained a traumatic brain injury, against the theoretical backdrop of existential-phenomenological psychology. Opsomming Hierdie navorsing verken die belewenisse van vier adolessente wat saam met ‘n ouer wat ‘n traumatiese breinbesering opgedoen het, leef. *Please note: This is a reduced version of the abstract. Please refer to PDF for full text.

  19. Inhibitory Control after Traumatic Brain Injury in Children

    OpenAIRE

    Sinopoli, Katia J.; Dennis, Maureen

    2011-01-01

    Inhibitory control describes a number of distinct processes. Effortless inhibition refers to acts of control that are automatic and reflexive. Effortful inhibition refers to voluntary, goal-directed acts of control such as response flexibility, interference control, cancellation inhibition, and restraint inhibition. Disruptions to a number of inhibitory control processes occur as a consequence of childhood traumatic brain injury (TBI). This paper reviews the current knowledge of inhibition de...

  20. Deficits in analogical reasoning in adolescents with traumatic brain injury

    OpenAIRE

    Krawczyk, Daniel C.; Gerri Hanten; Elisabeth A. Wilde; Levin, Harvey S.

    2010-01-01

    Individuals with traumatic brain injury (TBI) exhibit deficits in executive control, which may impact their reasoning abilities. Analogical reasoning requires working memory and inhibitory abilities. In this study, we tested adolescents with moderate to severe TBI and typically-developing (TD) controls on a set of picture analogy problems. Three factors were varied: complexity (number of relations in the problems), distraction (distractor item present or absent), and animacy (living or non-li...

  1. Deficits in Analogical Reasoning in Adolescents with Traumatic Brain Injury

    OpenAIRE

    Krawczyk, Daniel C.; Hanten, Gerri; Elisabeth A. Wilde; Li, Xiaoqi; Schnelle, Kathleen P.; Merkley, Tricia L.; Vasquez, Ana C.; Cook, Lori G.; McClelland, Michelle; Chapman, Sandra B.; Levin, Harvey S.

    2010-01-01

    Individuals with traumatic brain injury (TBI) exhibit deficits in executive control, which may impact their reasoning abilities. Analogical reasoning requires working memory and inhibitory abilities. In this study, we tested adolescents with moderate to severe TBI and typically developing (TD) controls on a set of picture analogy problems. Three factors were varied: complexity (number of relations in the problems), distraction (distractor item present or absent), and animacy (living or non-li...

  2. Could Cord Blood Cell Therapy Reduce Preterm Brain Injury?

    OpenAIRE

    Li, Jingang; McDonald, Courtney A.; Fahey, Michael C.; Jenkin, Graham; Miller, Suzanne L.

    2014-01-01

    Major advances in neonatal care have led to significant improvements in survival rates for preterm infants, but this occurs at a cost, with a strong causal link between preterm birth and neurological deficits, including cerebral palsy (CP). Indeed, in high-income countries, up to 50% of children with CP were born preterm. The pathways that link preterm birth and brain injury are complex and multifactorial, but it is clear that preterm birth is strongly associated with damage to the white matt...

  3. Persistent giant U wave inversion with anoxic brain injury

    OpenAIRE

    Peters, Matthew N.; Katz, Morgan J.; Howell, Lucius A.; Moscona, John C.; Turnage, Thomas A.; Delafontaine, Patrice

    2013-01-01

    Various electrocardiographic changes have been reported in the setting of acute neurological events, among them large, upright U waves. In contrast, the occurrence of inverted U waves is strongly suggestive of cardiovascular disease, most commonly hypertension, coronary artery disease, or valvular abnormalities. Presented herein is the case of a 29-year-old man with previous anoxic brain injury (but without apparent cardiovascular disease) whose electrocardiogram demonstrated persistent giant...

  4. The Relationship between Mid-face Fractures and Brain Injuries

    OpenAIRE

    Khalighi Sigaroudi A.; Vadiati Saberi B.; Yousefzadeh Chabok Sh.

    2012-01-01

    Statement of Problem: Although advances in technology have led to improvements in man’s life in different aspects, statistics show that the incidence of fractures is increasing in different regions of the body. Recent studies show that midface fractures are strongly associated with patient's death. The exact relationship between different types of facial fractures and brain injuries is still controversial. Purpose: To evaluate individuals with midface fractures from different causes and deter...

  5. Common astrocytic programs during brain development, injury and cancer

    OpenAIRE

    Silver, Daniel J.; Steindler, Dennis A.

    2009-01-01

    In addition to radial glial cells of neurohistogenesis, immature astrocytes with stem-cell-like properties cordon off emerging functional patterns in the developing brain. Astrocytes also can be stem cells during adult neurogenesis, and a proposed potency of injury-associated reactive astrocytes has recently been substantiated. Astrocytic cells might additionally be involved in cancer stem cell-associated gliomagenesis. Thus, there are distinguishing roles for stem-cell-like astrocytes during...

  6. Mechanisms of gender-linked ischemic brain injury

    OpenAIRE

    Liu, Mingyue; Dziennis, Suzan; Hurn, Patricia D.; Alkayed, Nabil J.

    2009-01-01

    Biological sex is an important determinant of stroke risk and outcome. Women are protected from cerebrovascular disease relative to men, an observation commonly attributed to the protective effect of female sex hormones, estrogen and progesterone. However, sex differences in brain injury persist well beyond the menopause and can be found in the pediatric population, suggesting that the effects of reproductive steroids may not completely explain sexual dimorphism in stroke. We review recent ad...

  7. Clinical Traumatic Brain Injury in the Preclinical Setting.

    Science.gov (United States)

    Berkner, Justin; Mannix, Rebekah; Qiu, Jianhua

    2016-01-01

    Traumatic brain injury (TBI) is the leading cause of death and disability for people under 45 years of age. Clinical TBI is often the result of disparate forces resulting in heterogeneous injuries. Preclinical modeling of TBI is a vital tool for studying the complex cascade of metabolic, cellular, and molecular post-TBI events collectively termed secondary injury. Preclinical models also provide an important platform for studying therapeutic interventions. However, modeling TBI in the preclinical setting is challenging, and most models replicate only certain aspects of clinical TBI. This chapter details the most widely used models of preclinical TBI, including the controlled cortical impact, fluid percussion, blast, and closed head models. Each of these models replicates particular critical aspects of clinical TBI. Prior to selecting a preclinical TBI model, it is important to address what aspect of human TBI is being sought to evaluate. PMID:27604710

  8. Predictors of Personality Change Due to Traumatic Brain Injury in Children and Adolescents in the First Six Months after Injury.

    Science.gov (United States)

    Max, Jeffrey E.; Levin, Harvey S.; Landis, Julie; Schachar, Russell; Saunders, Ann; Ewing-Cobbs, Linda; Chapman, Sandra B.; Dennis, Maureen

    2005-01-01

    Objective: To assess the phenomenology and predictive factors of personality change due to traumatic brain injury. Method: Children (N = 177), aged 5 to 14 years with traumatic brain injury from consecutive admissions to five trauma centers, were followed prospectively at baseline and 6 months with semistructured psychiatric interviews. Injury…

  9. Magnetic micelles for DNA delivery to rat brains after mild traumatic brain injury.

    Science.gov (United States)

    Das, Mahasweta; Wang, Chunyan; Bedi, Raminder; Mohapatra, Shyam S; Mohapatra, Subhra

    2014-10-01

    Traumatic brain injury (TBI) causes significant mortality, long term disability and psychological symptoms. Gene therapy is a promising approach for treatment of different pathological conditions. Here we tested chitosan and polyethyleneimine (PEI)-coated magnetic micelles (CP-mag micelles or CPMMs), a potential MRI contrast agent, to deliver a reporter DNA to the brain after mild TBI (mTBI). CPMM-tomato plasmid (ptd) conjugate expressing a red-fluorescent protein (RFP) was administered intranasally immediately after mTBI or sham surgery in male SD rats. Evans blue extravasation following mTBI suggested CPMM-ptd entry into the brain via the compromised blood-brain barrier. Magnetofection increased the concentration of CPMMs in the brain. RFP expression was observed in the brain (cortex and hippocampus), lung and liver 48 h after mTBI. CPMM did not evoke any inflammatory response by themselves and were excreted from the body. These results indicate the possibility of using intranasally administered CPMM as a theranostic vehicle for mTBI. From the clinical editor: In this study, chitosan and PEI-coated magnetic micelles (CPMM) were demonstrated as potentially useful vehicles in traumatic brain injury in a rodent model. Magnetofection increased the concentration of CPMMs in the brain and, after intranasal delivery, CPMM did not evoke any inflammatory response and were excreted from the body. PMID:24486465

  10. Effects of magnesium sulfate on brain mitochondrial respiratory function in rats after experimental traumatic brain injury

    Institute of Scientific and Technical Information of China (English)

    许民辉; 代文光; 邓洵鼎

    2002-01-01

    Objective: To study the effects of magnesium sulfate on brain mitochondrial respiratory function in rats after experimental traumatic brain injury and the possible mechanism.Methods: The middle degree brain injury in rats was made by BIM-III multi-function impacting machine. The brain mitochondrial respiratory function was measured with oxygen electrode and the ultra-structural changes were observed with transmission electron microscope (TEM).Results: 1. The brain mitochondrial respiratory stage III and respiration control rate reduced significantly in the untreated groups within 24 and 72 hours. But treated Group A showed certain degree of recovery of respiratory function; treated Group B showed further improvement. 2. Untreated Group, treated Groups A and B had different degrees of mitochondrial ultra-structural damage respectively, which could be attenuated after the treatment with magnesium sulfate.Conclusions: The mitochondrial respiratory function decreases significantly after traumatic brain injury. But it can be apparently improved after magnesium sulfate management along with the attenuated damage of mitochondria discovered by TEM. The longer course of treatment can obtain a better improvement of mitochondrial respiratory function.

  11. Cognitive and psychopathological sequelae of pediatric traumatic brain injury.

    Science.gov (United States)

    Beauchamp, M H; Anderson, V

    2013-01-01

    Childhood traumatic brain injury (TBI) is a frequent cause of acquired disability in childhood and can have a serious impact on development across the lifespan. The consequences of early TBI vary according to injury severity, with severe injuries usually resulting in more serious physical, cognitive and behavioral sequelae. Both clinical and research reports document residual deficits in a range of skills, including intellectual function, attention, memory, learning, and executive function. In addition, recent investigations suggest that early brain injury also affects psychological and social development and that problems in these domains may increase in the long term postinjury. Together, these deficits affect children's ability to function effectively at school, in the home, and in their social environment, resulting in impaired acquisition of knowledge, psychological and social problems, and overall reduced quality of life. Ultimately, recovery from childhood TBI depends on a range of complex biological, developmental, and psychosocial factors making prognosis difficult to predict. This chapter will detail the cognitive (intellectual, attentional, mnesic, executive, educational, and vocational) and psychopathological (behavioral, adaptive, psychological, social) sequelae of childhood TBI with a particular focus on postinjury recovery patterns in the acute, short-, and long-term phases, as well as into adulthood. PMID:23622301

  12. Brain injury impairs working memory and prefrontal circuit function

    Directory of Open Access Journals (Sweden)

    Colin James Smith

    2015-11-01

    Full Text Available More than 2.5 million Americans suffer a traumatic brain injury (TBI each year. Even mild to moderate traumatic brain injury causes long-lasting neurological effects. Despite its prevalence, no therapy currently exists to treat the underlying cause of cognitive impairment suffered by TBI patients. Following lateral fluid percussion injury (LFPI, the most widely used experimental model of TBI, we investigated alterations in working memory and excitatory/inhibitory synaptic balance in the prefrontal cortex. LFPI impaired working memory as assessed with a T-maze behavioral task. Field excitatory postsynaptic potentials recorded in the prefrontal cortex were reduced in slices derived from brain-injured mice. Spontaneous and miniature excitatory postsynaptic currents onto layer 2/3 neurons were more frequent in slices derived from LFPI mice while inhibitory currents onto layer 2/3 neurons were smaller after LFPI. Additionally, an increase in action potential threshold and concomitant decrease in firing rate was observed in layer 2/3 neurons in slices from injured animals. Conversely, no differences in excitatory or inhibitory synaptic transmission onto layer 5 neurons were observed; however, layer 5 neurons demonstrated a decrease in input resistance and action potential duration after LFPI. These results demonstrate synaptic and intrinsic alterations in prefrontal circuitry that may underlie working memory impairment caused by TBI.

  13. Speed of perceptual grouping in acquired brain injury.

    Science.gov (United States)

    Kurylo, Daniel D; Larkin, Gabriella Brick; Waxman, Richard; Bukhari, Farhan

    2014-09-01

    Evidence exists that damage to white matter connections may contribute to reduced speed of information processing in traumatic brain injury and stroke. Damage to such axonal projections suggests a particular vulnerability to functions requiring integration across cortical sites. To test this prediction, measurements were made of perceptual grouping, which requires integration of stimulus components. A group of traumatic brain injury and cerebral vascular accident patients and a group of age-matched healthy control subjects viewed arrays of dots and indicated the pattern into which stimuli were perceptually grouped. Psychophysical measurements were made of perceptual grouping as well as processing speed. The patient group showed elevated grouping thresholds as well as extended processing time. In addition, most patients showed progressive slowing of processing speed across levels of difficulty, suggesting reduced resources to accommodate increased demands on grouping. These results support the prediction that brain injury results in a particular vulnerability to functions requiring integration of information across the cortex, which may result from dysfunction of long-range axonal connection. PMID:24820289

  14. Percutaneous dilatational tracheostomy for ICU patients with severe brain injury

    Directory of Open Access Journals (Sweden)

    Guo Dongyuan

    2014-12-01

    Full Text Available 【Abstract】Objective: To sum up our experience in percutaneous dilatational tracheostomy (PDT in ICU patient with severe brain injury. Methods: Between November 2011 and April 2014, PDTs were performed on 32 severe brain injury patients in ICU by a team of physicians and intensivists. The success rate, effi cacy, safety, and complications including stomal infection and bleeding, paratracheal insertion, pneumothorax, pneumomediastinum, tracheal laceration, as well as clinically significant tracheal stenosis were carefully monitored and recorded respectively. Results: The operations took 4-15 minutes (mean 9.1 minutes±4.2 minutes. Totally 4 cases suffered from complications in the operations: 3 cases of stomal bleeding, and 1 case of intratracheal bloody secretion, but none required intervention. Paratracheal insertion, pneumothorax, pneumomediastinum, tracheal laceration, or clinically signifi cant tracheal stenosis were not found in PDT patients. There was no procedure-related death occurring during or after PDT. Conclusion: Our study demonstrats that PDT is a safe, highly effective, and minimally invasive procedure. The appropriate sedation and airway management perioperatively help to reduce complication rates. PDT should be performed or supervised by a team of physicians with extensive experience in this procedure, and also an intensivist with experience in diffi cult airway management. Key words: Brain injuries; Percutaneous dilatational tracheostomy; ICU

  15. Male pituitary-gonadal dysfunction following severe traumatic brain injury.

    Science.gov (United States)

    Lee, S C; Zasler, N D; Kreutzer, J S

    1994-01-01

    A prospective study was conducted to evaluate pituitary-gonadal function and correlated parameters in 21 adult males with severe traumatic brain injury during acute inpatient rehabilitation. Serum concentrations of testosterone, follicle-stimulating hormone (FSH) and luteinizing hormone (LH) were measured within 1 week after the patient was transferred to the rehabilitation unit. Fourteen of 21 patients (67%) had abnormally low testosterone levels. One of 21 patients had a subnormal FSH level and one had a supranormal level. Three of 21 patients had subnormal LH levels and two had supranormal levels. There was no correlation between the severity of brain injury and the levels of testosterone, FSH or LH. The presence of increased intracranial pressure, hypoxia, skull fracture or abnormal CT findings had no significant influence on the levels of testosterone, FSH or LH. The high incidence of hypotestosteronaemia in survivors of severe traumatic brain injury is seemingly more related to accompanying physiological stressors rather than structural or neurochemical disruption of the hypothalamic-pituitary-gonadal axis. Early identification is important relative to the potential neuromedical and rehabilitative consequences of prolonged hypotestosteronaemia in this patient population. PMID:7987293

  16. The paradox of chronic neuroinflammation, systemic immune suppression, autoimmunity after traumatic chronic spinal cord injury.

    Science.gov (United States)

    Schwab, Jan M; Zhang, Yi; Kopp, Marcel A; Brommer, Benedikt; Popovich, Phillip G

    2014-08-01

    During the transition from acute to chronic stages of recovery after spinal cord injury (SCI), there is an evolving state of immunologic dysfunction that exacerbates the problems associated with the more clinically obvious neurologic deficits. Since injury directly affects cells embedded within the "immune privileged/specialized" milieu of the spinal cord, maladaptive or inefficient responses are likely to occur. Collectively, these responses qualify as part of the continuum of "SCI disease" and are important therapeutic targets to improve neural repair and neurological outcome. Generic immune suppressive therapies have been largely unsuccessful, mostly because inflammation and immunity exert both beneficial (plasticity enhancing) and detrimental (e.g. glia- and neurodegenerative; secondary damage) effects and these functions change over time. Moreover, "compartimentalized" investigations, limited to only intraspinal inflammation and associated cellular or molecular changes in the spinal cord, neglect the reality that the structure and function of the CNS are influenced by systemic immune challenges and that the immune system is 'hardwired' into the nervous system. Here, we consider this interplay during the progression from acute to chronic SCI. Specifically, we survey impaired/non-resolving intraspinal inflammation and the paradox of systemic inflammatory responses in the context of ongoing chronic immune suppression and autoimmunity. The concepts of systemic inflammatory response syndrome (SIRS), compensatory anti-inflammatory response syndrome (CARS) and "neurogenic" spinal cord injury-induced immune depression syndrome (SCI-IDS) are discussed as determinants of impaired "host-defense" and trauma-induced autoimmunity. PMID:25017893

  17. Risk factors for cervical spine injury among patients with traumatic brain injury

    Directory of Open Access Journals (Sweden)

    Tomoko Fujii

    2013-01-01

    Full Text Available Background: Diagnosis of cervical spine injury (CSI is difficult in patients with an altered level of consciousness as a result of a traumatic brain injury (TBI. Patients with TBI and older adults are at increased risk for CSI. This study examined the various risk factors for CSI among trauma patients with TBI and whether adults who were older (≥55 years were at higher risk for CSI when they sustained a fall-related TBI. Materials and Methods: Data used was the 2007 National Trauma Data Bank (NTDB, National Sample Project (NSP for adults who sustained a TBI. This dataset contains 2007 admission records from 82 level I and II trauma centers. Logistic regression was used to identify potential risk factors for CSI and to test for interaction between age and injury mechanism. Additional model variables included gender, race, Glasgow Coma Score, multiple severe injuries, hypotension and respiratory distress. Results: An analysis of the NTDB NSP identified 187,709 adults with TBI, of which 16,078 were diagnosed with a concomitant CSI. In motor vehicle traffic injuries, the older age group had significantly higher odds of CSI (odds ratio [OR] = 1.26 [1.15-1.39]. In fall-related injuries the older age group did not have a higher odds of CSI compared to the younger age group. Skull/face fracture, other spine fracture/dislocation, upper limb injury, thorax injury, and hypotension were significantly associated with CSI. Pelvic injuries had an inverse association with CSI (OR = 0.60 [0.54-0.67]. Black had significantly higher odds of CSI compared to Whites (OR = 1.25 [1.07-1.46]. Conclusion: The identification of associated injuries and factors may assist physicians in evaluating CSI in patients with TBI.

  18. Bcl-2 gene therapy for apoptosis following traumatic brain injury

    Institute of Scientific and Technical Information of China (English)

    YANG Xiao-feng; ZHENG Xue-sheng; LIU Wei-guo; FENG Jun-feng

    2006-01-01

    Objective: To investigate the therapeutic effect of Bcl- 2 fusion protein on apoptosis in brain following traumatic brain injury.Methods: Bcl-2 gene was cloned by RT-PCR. Bcl-2 and EGFP genes were linked together and inserted into pAdeno-X vector. This recombinant vector was packaged into infectious adenovirus in HEK293 cells. Ninety Wistar rats were assigned randomly into experimental group(n=45) and control group (n=45). All rats were subjected to traumatic brain injury. Then recombinant adenovirus (for experimental group) or saline (for control group) was injected into the traumatic brain. The expression of Bcl-2 fusion protein was investigated by Western blotting, immunohistochemistry and fluorescence microscopy. Apoptosis in the injured brain was studied by TUNEL. Animals' behavior capacity was evaluated by tiltboard test.Results: In the experimental group, many fluorescent cells were found around the traumatic locus,which were also proven to be Bcl-2-positive by immunohistochemistry. On the contrary, few Bcl-2-positive cells and no fluorescent cell were detected in the control group. Bcl-2 expression of experimental group was much higher than that of control group, which was illustrated by Western blotting. The apoptosis index of experimental group was 0.027 ± 0.005, and that of control group was 0.141±0.025 (P<0.01). Two weeks after injury, animals of the experimental group behaved better than those of the control group.Conclusions: A recombinant adenovirus vector expressing Bcl-2 fusion protein has been constructed. Bcl-2 fusion protein can suppress apoptosis and promote cell survival. Moreover, the behavior recovery of the injured animal is promoted. Bcl-2 fusion protein provides a way to track the target cells in vivo.

  19. Atypical moral judgment following traumatic brain injury

    Directory of Open Access Journals (Sweden)

    Angelica Muresan

    2012-07-01

    Full Text Available Previous research has shown an association between emotions, particularly social emotions, and moral judgments. Some studies suggested an association between blunted emotion and the utilitarian moral judgments observed in patients with prefrontal lesions. In order to investigate how prefrontal brain damage affects moral judgment, we asked a sample of 29 TBI patients (12 females and 17 males and 41 healthy participants (16 females and 25 males to judge 22 hypothetical dilemmas split into three different categories (non-moral, impersonal and personal moral. The TBI group presented a higher proportion of affirmative (utilitarian responses for personal moral dilemmas when compared to controls, suggesting an atypical pattern of utilitarian judgements. We also found a negative association between the performance on recognition of social emotions and the proportion of affirmative responses on personal moral dilemmas. These results suggested that the preference for utilitarian responses in this type of dilemmas is accompanied by difficulties in social emotion recognition. Overall, our findings suggest that deontological moral judgments are associated with normal social emotion processing and that frontal lobe plays an important role in both emotion and moral judgment.

  20. Positive emotions and brain reward circuits in chronic pain.

    Science.gov (United States)

    Navratilova, Edita; Morimura, Kozo; Xie, Jennifer Y; Atcherley, Christopher W; Ossipov, Michael H; Porreca, Frank

    2016-06-01

    Chronic pain is an important public health problem that negatively impacts the quality of life of affected individuals and exacts enormous socioeconomic costs. Chronic pain is often accompanied by comorbid emotional disorders including anxiety, depression, and possibly anhedonia. The neural circuits underlying the intersection of pain and pleasure are not well understood. We summarize recent human and animal investigations and demonstrate that aversive aspects of pain are encoded in brain regions overlapping with areas processing reward and motivation. We highlight findings revealing anatomical and functional alterations of reward/motivation circuits in chronic pain. Finally, we review supporting evidence for the concept that pain relief is rewarding and activates brain reward/motivation circuits. Adaptations in brain reward circuits may be fundamental to the pathology of chronic pain. Knowledge of brain reward processing in the context of pain could lead to the development of new therapeutics for the treatment of emotional aspects of pain and comorbid conditions. J. Comp. Neurol. 524:1646-1652, 2016. © 2016 Wiley Periodicals, Inc. PMID:26788716

  1. A peptide for targeted, systemic delivery of imaging and therapeutic compounds into acute brain injuries

    Science.gov (United States)

    Mann, Aman P.; Scodeller, Pablo; Hussain, Sazid; Joo, Jinmyoung; Kwon, Ester; Braun, Gary B.; Mölder, Tarmo; She, Zhi-Gang; Kotamraju, Venkata Ramana; Ranscht, Barbara; Krajewski, Stan; Teesalu, Tambet; Bhatia, Sangeeta; Sailor, Michael J.; Ruoslahti, Erkki

    2016-06-01

    Traumatic brain injury (TBI) is a major health and socio-economic problem, but no pharmacological agent is currently approved for the treatment of acute TBI. Thus, there is a great need for advances in this field. Here, we describe a short peptide (sequence CAQK) identified by in vivo phage display screening in mice with acute brain injury. The CAQK peptide selectively binds to injured mouse and human brain, and systemically injected CAQK specifically homes to sites of brain injury in mouse models. The CAQK target is a proteoglycan complex upregulated in brain injuries. Coupling to CAQK increased injury site accumulation of systemically administered molecules ranging from a drug-sized molecule to nanoparticles. CAQK-coated nanoparticles containing silencing oligonucleotides provided the first evidence of gene silencing in injured brain parenchyma by systemically administered siRNA. These findings present an effective targeting strategy for the delivery of therapeutics in clinical management of acute brain injuries.

  2. Repeated Closed Head Injury in Mice Results in Sustained Motor and Memory Deficits and Chronic Cellular Changes

    Science.gov (United States)

    Bolton Hall, Amanda N.; Joseph, Binoy; Brelsfoard, Jennifer M.; Saatman, Kathryn E.

    2016-01-01

    Millions of mild traumatic brain injuries (TBIs) occur every year in the United States, with many people subject to multiple head injuries that can lead to chronic behavioral dysfunction. We previously reported that mild TBI induced using closed head injuries (CHI) repeated at 24h intervals produced more acute neuron death and glial reactivity than a single CHI, and increasing the length of time between injuries to 48h reduced the cumulative acute effects of repeated CHI. To determine whether repeated CHI is associated with behavioral dysfunction or persistent cellular damage, mice receiving either five CHI at 24h intervals, five CHI at 48h intervals, or five sham injuries at 24h intervals were evaluated across a 10 week period after injury. Animals with repeated CHI exhibited motor coordination and memory deficits, but not gait abnormalities when compared to sham animals. At 10wks post-injury, no notable neuron loss or glial reactivity was observed in the cortex, hippocampus, or corpus callosum. Argyrophilic axons were found in the pyramidal tract of some injured animals, but neither silver stain accumulation nor inflammatory responses in the injury groups were statistically different from the sham group in this region. However, argyrophilic axons, microgliosis and astrogliosis were significantly increased within the optic tract of injured animals. Repeated mild CHI also resulted in microgliosis and a loss of neurofilament protein 200 in the optic nerve. Lengthening the inter-injury interval from 24h to 48h did not effectively reduce these behavioral or cellular responses. These results suggest that repeated mild CHI results in persistent behavioral dysfunction and chronic pathological changes within the visual system, neither of which was significantly attenuated by lengthening the inter-injury interval from 24h to 48h. PMID:27427961

  3. Low level primary blast injury in rodent brain

    Directory of Open Access Journals (Sweden)

    Enci MaryKan

    2011-04-01

    Full Text Available The incidence of blast attacks and resulting traumatic brain injuries has been on the rise in recent years. Primary blast is one of the mechanisms in which the blast wave can cause injury to the brain. The aim of this study was to investigate the effects of a single sub-lethal blast over pressure exposure of either 48.9 kPa (7.1 psi or 77.3 kPa (11.3 psi to rodents in an open-field setting. Brain tissue from these rats was harvested for microarray and histopathological analyses. Gross histopathology of the brains showed that cortical neurons were ‘darkened’ and shrunken with narrowed vasculature in the cerebral cortex day 1 after blast with signs of recovery at day 4 and day 7 after blast. TUNEL-positive cells were predominant in the white matter of the brain at day 1 after blast and double-labeling of brain tissue showed that these DNA-damaged cells were both oligodendrocytes and astrocytes but were mainly not apoptotic due to the low caspase-3 immunopositivity. There was also an increase in amyloid precursor protein immunoreactive cells in the white matter which suggests acute axonal damage. In contrast, Iba-1 staining for macrophages or microglia was not different from control post-blast. Blast exposure altered the expression of over 5786 genes in the brain which occurred mostly at day 1 and day 4 post-blast. These genes were narrowed down to 10 overlapping genes after time-course evaluation and functional analyses. These genes pointed towards signs of repair at day 4 and 7 post-blast. Our findings suggest that the blast over pressure levels in the study resulted in mild cellular injury to the brain as evidenced by acute neuronal, cerebrovascular and white matter perturbations that showed signs of resolution. It is unclear whether these perturbations exist at a milder level or normalize completely and will need more investigation. Specific changes in gene expression may be further evaluated to understand the mechanism of blast

  4. Application of Ultrasonic Techniques for Brain Injury Diagnosis

    International Nuclear Information System (INIS)

    In this work, we evaluate methods for detecting brain injury using ultrasound. We have used simulations of ultrasonic fields in the head to model the phase distortion of the skull. In addition we present experimental data from the crania of large animals. The experimental data help us understand and evaluate the performance of different transducers in acquiring the backscatter data from the brain through the skull. Both the simulations and acquired data illustrate the superiority of lower-frequency (<= 1 MHz) ultrasonic fields for transcranial acquisition of signals from inside the brain. Additionally, the experimental work shows that the higher-frequency (5 MHz) ultrasound can also be useful in acquiring clean nearfield data to help detect the position of the inner boundary of the skull

  5. Application of Ultrasonic Techniques for Brain Injury Diagnosis

    Energy Technology Data Exchange (ETDEWEB)

    Kasili, P.M.; Mobley, J.; Norton, S.J.; Vo-Dinh, T.

    1999-09-19

    In this work, we evaluate methods for detecting brain injury using ultrasound. We have used simulations of ultrasonic fields in the head to model the phase distortion of the skull. In addition we present experimental data from the crania of large animals. The experimental data help us understand and evaluate the performance of different transducers in acquiring the backscatter data from the brain through the skull. Both the simulations and acquired data illustrate the superiority of lower-frequency (<= 1 MHz) ultrasonic fields for transcranial acquisition of signals from inside the brain. Additionally, the experimental work shows that the higher-frequency (5 MHz) ultrasound can also be useful in acquiring clean nearfield data to help detect the position of the inner boundary of the skull.

  6. Resuscitation speed affects brain injury in a large animal model of traumatic brain injury and shock

    DEFF Research Database (Denmark)

    Sillesen, Martin; Jin, Guang; Johansson, Pär I;

    2014-01-01

    infusion speed increment NS (n¿=¿7). Hemodynamic variables over a 6-hour observation phase were recorded. Following euthanasia, brains were harvested and lesion size as well as brain swelling was measured.ResultsBolus FFP resuscitation resulted in greater brain swelling (22.36¿±¿1.03% vs. 15.58¿±¿2.52%, p...

  7. Investigation of elemental changes in brain tissues following excitotoxic injury

    International Nuclear Information System (INIS)

    Recently the ANSTO heavy ion microprobe has been used for elemental mapping of thin brain tissue sections. The fact that a very small portion of the proton energy is used for X-ray excitation combined with small variations of the major element concentrations makes μ-PIXE imaging and GeoPIXE analysis a challenging task. Excitotoxic brain injury underlies the pathology of stroke and various neurodegenerative disorders. Large fluxes in Ca+2 cytosolic concentrations are a key feature of the initiation of this pathophysiological process. In order to understand if these modifications are associated with changes in the elemental composition, several brain sections have been mapped with μ-PIXE. Increases in Ca+2 cytosolic concentrations were indicative of the pathophysiological process continuing 1 week after an initiating neural insult. We were able to measure significant variations in K and Ca concentration distribution across investigated brain tissue. These variations correlate very well with physiological changes visible in the brain tissue. Moreover, the obtained μ-PIXE results clearly demonstrate that the elemental composition changes significantly correlate with brain drauma

  8. Investigation of elemental changes in brain tissues following excitotoxic injury

    Energy Technology Data Exchange (ETDEWEB)

    Siegele, Rainer, E-mail: rns@ansto.gov.au [Institute for Environmental Research, ANSTO, Locked Bag 2001, Kirrawee DC, NSW 2232 (Australia); Howell, Nicholas R.; Callaghan, Paul D. [Life Sciences, ANSTO, Locked Bag 2001, Kirrawee DC, NSW 2232 (Australia); Pastuovic, Zeljko [Institute for Environmental Research, ANSTO, Locked Bag 2001, Kirrawee DC, NSW 2232 (Australia)

    2013-07-01

    Recently the ANSTO heavy ion microprobe has been used for elemental mapping of thin brain tissue sections. The fact that a very small portion of the proton energy is used for X-ray excitation combined with small variations of the major element concentrations makes μ-PIXE imaging and GeoPIXE analysis a challenging task. Excitotoxic brain injury underlies the pathology of stroke and various neurodegenerative disorders. Large fluxes in Ca{sup +2} cytosolic concentrations are a key feature of the initiation of this pathophysiological process. In order to understand if these modifications are associated with changes in the elemental composition, several brain sections have been mapped with μ-PIXE. Increases in Ca{sup +2} cytosolic concentrations were indicative of the pathophysiological process continuing 1 week after an initiating neural insult. We were able to measure significant variations in K and Ca concentration distribution across investigated brain tissue. These variations correlate very well with physiological changes visible in the brain tissue. Moreover, the obtained μ-PIXE results clearly demonstrate that the elemental composition changes significantly correlate with brain drauma.

  9. Plasticity in the Neonatal Brain following Hypoxic-Ischaemic Injury

    Directory of Open Access Journals (Sweden)

    Eridan Rocha-Ferreira

    2016-01-01

    Full Text Available Hypoxic-ischaemic damage to the developing brain is a leading cause of child death, with high mortality and morbidity, including cerebral palsy, epilepsy, and cognitive disabilities. The developmental stage of the brain and the severity of the insult influence the selective regional vulnerability and the subsequent clinical manifestations. The increased susceptibility to hypoxia-ischaemia (HI of periventricular white matter in preterm infants predisposes the immature brain to motor, cognitive, and sensory deficits, with cognitive impairment associated with earlier gestational age. In term infants HI causes selective damage to sensorimotor cortex, basal ganglia, thalamus, and brain stem. Even though the immature brain is more malleable to external stimuli compared to the adult one, a hypoxic-ischaemic event to the neonate interrupts the shaping of central motor pathways and can affect normal developmental plasticity through altering neurotransmission, changes in cellular signalling, neural connectivity and function, wrong targeted innervation, and interruption of developmental apoptosis. Models of neonatal HI demonstrate three morphologically different types of cell death, that is, apoptosis, necrosis, and autophagy, which crosstalk and can exist as a continuum in the same cell. In the present review we discuss the mechanisms of HI injury to the immature brain and the way they affect plasticity.

  10. Plasticity in the Neonatal Brain following Hypoxic-Ischaemic Injury.

    Science.gov (United States)

    Rocha-Ferreira, Eridan; Hristova, Mariya

    2016-01-01

    Hypoxic-ischaemic damage to the developing brain is a leading cause of child death, with high mortality and morbidity, including cerebral palsy, epilepsy, and cognitive disabilities. The developmental stage of the brain and the severity of the insult influence the selective regional vulnerability and the subsequent clinical manifestations. The increased susceptibility to hypoxia-ischaemia (HI) of periventricular white matter in preterm infants predisposes the immature brain to motor, cognitive, and sensory deficits, with cognitive impairment associated with earlier gestational age. In term infants HI causes selective damage to sensorimotor cortex, basal ganglia, thalamus, and brain stem. Even though the immature brain is more malleable to external stimuli compared to the adult one, a hypoxic-ischaemic event to the neonate interrupts the shaping of central motor pathways and can affect normal developmental plasticity through altering neurotransmission, changes in cellular signalling, neural connectivity and function, wrong targeted innervation, and interruption of developmental apoptosis. Models of neonatal HI demonstrate three morphologically different types of cell death, that is, apoptosis, necrosis, and autophagy, which crosstalk and can exist as a continuum in the same cell. In the present review we discuss the mechanisms of HI injury to the immature brain and the way they affect plasticity. PMID:27047695

  11. Demonstration of blood brain barrier injury by computed tomography

    International Nuclear Information System (INIS)

    Blood brain barrier (BBB) injury was evoked by the injection of hypertonic solution, 50% glucose or 80% sodium iothalamate, through the catheter placed in the common carotid artery of the adult mongrel dogs. Plain CT and then contrast CT were performed at 30 minutes intervals until 3 hours to determine the relationship between the degrees of contrast enhancement (CE) and the amount of injected hypertonic solution, and to examine the diminishing rates of CE according to time elapsed after the intravenous contrast injection. Another four groups of dogs received contrast CT immediately, at 1, 2 and 3 hours after the injection of hypertonic solution to examine the degree of repair of BBB injury. Contrast media, which was leaked through BBB injured by the injection of hypertonic solution, was recognized by CT, and the area of CE coincided exactly with the dyed area by Evans blue, injected intravenously after induction of BBB injury. Degrees of CE were found to correlate linearly to the amount of hypertonic solution within a certain range. These results indicate that CT can demonstrate BBB injury qualitatively and quantitatively. In sequential CT after the artificial injury of BBB, degree of CE diminished linearly with a half life of about 3 hours. Hydrocortisone accelerated this washout of leaked contrast media. Repair of BBB itself, determined by contrast CT which were performed at 1, 2 and 3 hours after the induction of BBB injury, has been accomplished until 3 hours, and not affected by the administration of hydrocortisone. These experimental results suggest that CT is the most promising method to detect quantitatively and non-invasively the degree and the extent of BBB injury in clinical cases. (J.P.N.)

  12. Brain viscoelasticity alteration in chronic-progressive multiple sclerosis.

    Directory of Open Access Journals (Sweden)

    Kaspar-Josche Streitberger

    Full Text Available INTRODUCTION: Viscoelastic properties indicate structural alterations in biological tissues at multiple scales with high sensitivity. Magnetic Resonance Elastography (MRE is a novel technique that directly visualizes and quantitatively measures biomechanical tissue properties in vivo. MRE recently revealed that early relapsing-remitting multiple sclerosis (MS is associated with a global decrease of the cerebral mechanical integrity. This study addresses MRE and MR volumetry in chronic-progressive disease courses of MS. METHODS: We determined viscoelastic parameters of the brain parenchyma in 23 MS patients with primary or secondary chronic progressive disease course in comparison to 38 age- and gender-matched healthy individuals by multifrequency MRE, and correlated the results with clinical data, T2 lesion load and brain volume. Two viscoelastic parameters, the shear elasticity μ and the powerlaw exponent α, were deduced according to the springpot model and compared to literature values of relapsing-remitting MS. RESULTS: In chronic-progressive MS patients, μ and α were reduced by 20.5% and 6.1%, respectively, compared to healthy controls. MR volumetry yielded a weaker correlation: Total brain volume loss in MS patients was in the range of 7.5% and 1.7% considering the brain parenchymal fraction. All findings were significant (P<0.001. CONCLUSIONS: Chronic-progressive MS disease courses show a pronounced reduction of the cerebral shear elasticity compared to early relapsing-remitting disease. The powerlaw exponent α decreased only in the chronic-progressive stage of MS, suggesting an alteration in the geometry of the cerebral mechanical network due to chronic neuroinflammation.

  13. Epileptogenesis after traumatic brain injury in Plaur-deficient mice.

    Science.gov (United States)

    Bolkvadze, Tamuna; Puhakka, Noora; Pitkänen, Asla

    2016-07-01

    Binding of the extracellular matrix proteinase urokinase-type plasminogen activator (uPA) to its receptor, uPAR, regulates tissue remodeling during development and after injury in different organs, including the brain. Accordingly, mutations in the Plaur gene, which encodes uPAR, have been linked to language deficits, autism, and epilepsy, both in mouse and human. Whether uPAR deficiency modulates epileptogenesis and comorbidogenesis after brain injury, however, is unknown. To address this question, we induced traumatic brain injury (TBI) by controlled cortical impact (CCI) in 10 wild-type (Wt-CCI) and 16 Plaur-deficient (uPAR-CCI) mice. Sham-operated mice served as controls (10 Wt-sham, 10 uPAR-sham). During the 4-month follow-up, the mice were neurophenotyped by assessing the somatomotor performance with the composite neuroscore test, emotional learning and memory with fear conditioning to tone and context, and epileptogenesis with videoelectroencephalography monitoring and the pentylenetetrazol (PTZ) seizure susceptibility test. At the end of the testing, the mice were perfused for histology to analyze cortical and hippocampal neurodegeneration and mossy fiber sprouting. Fourteen percent (1/7) of the mice in the Wt-CCI and 0% in the uPAR-CCI groups developed spontaneous seizures (p>0.05; chi-square). Both the Wt-CCI and uPAR-CCI groups showed increased seizure susceptibility in the PTZ test (plearning showed a genotype effect, being more impaired in uPAR-CCI than in Wt-CCI mice (p<0.05). The findings of the present study indicate that uPAR deficiency does not increase susceptibility to epileptogenesis after CCI injury but has an unfavorable comorbidity-modifying effect after TBI. PMID:27208924

  14. Art Therapy for Individuals with Traumatic Brain Injury: A Comprehensive Neurorehabilitation-Informed Approach to Treatment

    Science.gov (United States)

    Kline, Tori

    2016-01-01

    I describe an approach to art therapy treatment for survivors of traumatic brain injury developed at a rehabilitation facility for adults that serves inpatient, outpatient, and long-term residential clients. This approach is based on a review of the literature on traumatic brain injury, comprehensive neurorehabilitation, brain plasticity, and art…

  15. Effects of NOS inhibitor on dentate gyrus neurogenesis after diffuse brain injury in the adult rats

    Institute of Scientific and Technical Information of China (English)

    SunLi-Sha; XuJiang-ping

    2004-01-01

    Objective To investigate the effects of selective nitric oxide synthase (NOS) inhibitors on dentate gyrus neurogenesis after diffuse brain injury (DBI) in the adult rat brain. Methods Adult male SD rats were subjected to diffuse brain injury (DBI) model. By using systemic bromodeoxyuridine (BrdU) to label dividing cells, we compared the proliferation rate of

  16. Making Waves in the Brain: What Are Oscillations, and Why Modulating Them Makes Sense for Brain Injury.

    Science.gov (United States)

    Pevzner, Aleksandr; Izadi, Ali; Lee, Darrin J; Shahlaie, Kiarash; Gurkoff, Gene G

    2016-01-01

    Traumatic brain injury (TBI) can result in persistent cognitive, behavioral and emotional deficits. However, the vast majority of patients are not chronically hospitalized; rather they have to manage their disabilities once they are discharged to home. Promoting recovery to pre-injury level is important from a patient care as well as a societal perspective. Electrical neuromodulation is one approach that has shown promise in alleviating symptoms associated with neurological disorders such as in Parkinson's disease (PD) and epilepsy. Consistent with this perspective, both animal and clinical studies have revealed that TBI alters physiological oscillatory rhythms. More recently several studies demonstrated that low frequency stimulation improves cognitive outcome in models of TBI. Specifically, stimulation of the septohippocampal circuit in the theta frequency entrained oscillations and improved spatial learning following TBI. In order to evaluate the potential of electrical deep brain stimulation for clinical translation we review the basic neurophysiology of oscillations, their role in cognition and how they are changed post-TBI. Furthermore, we highlight several factors for future pre-clinical and clinical studies to consider, with the hope that it will promote a hypothesis driven approach to subsequent experimental designs and ultimately successful translation to improve outcome in patients with TBI. PMID:27092062

  17. Optimizing sedation in patients with acute brain injury.

    Science.gov (United States)

    Oddo, Mauro; Crippa, Ilaria Alice; Mehta, Sangeeta; Menon, David; Payen, Jean-Francois; Taccone, Fabio Silvio; Citerio, Giuseppe

    2016-01-01

    Daily interruption of sedative therapy and limitation of deep sedation have been shown in several randomized trials to reduce the duration of mechanical ventilation and hospital length of stay, and to improve the outcome of critically ill patients. However, patients with severe acute brain injury (ABI; including subjects with coma after traumatic brain injury, ischaemic/haemorrhagic stroke, cardiac arrest, status epilepticus) were excluded from these studies. Therefore, whether the new paradigm of minimal sedation can be translated to the neuro-ICU (NICU) is unclear. In patients with ABI, sedation has 'general' indications (control of anxiety, pain, discomfort, agitation, facilitation of mechanical ventilation) and 'neuro-specific' indications (reduction of cerebral metabolic demand, improved brain tolerance to ischaemia). Sedation also is an essential therapeutic component of intracranial pressure therapy, targeted temperature management and seizure control. Given the lack of large trials which have evaluated clinically relevant endpoints, sedative selection depends on the effect of each agent on cerebral and systemic haemodynamics. Titration and withdrawal of sedation in the NICU setting has to be balanced between the risk that interrupting sedation might exacerbate brain injury (e.g. intracranial pressure elevation) and the potential benefits of enhanced neurological function and reduced complications. In this review, we provide a concise summary of cerebral physiologic effects of sedatives and analgesics, the advantages/disadvantages of each agent, the comparative effects of standard sedatives (propofol and midazolam) and the emerging role of alternative drugs (ketamine). We suggest a pragmatic approach for the use of sedation-analgesia in the NICU, focusing on some practical aspects, including optimal titration and management of sedation withdrawal according to ABI severity. PMID:27145814

  18. Are boys and girls that different? An analysis of traumatic brain injury in children.

    LENUS (Irish Health Repository)

    Collins, Niamh C

    2013-08-01

    The Phillips Report on traumatic brain injury (TBI) in Ireland found that injury was more frequent in men and that gender differences were present in childhood. This study determined when gender differences emerge and examined the effect of gender on the mechanism of injury, injury type and severity and outcome.

  19. Deep brain stimulation for chronic pain.

    Science.gov (United States)

    Boccard, Sandra G J; Pereira, Erlick A C; Aziz, Tipu Z

    2015-10-01

    Deep brain stimulation (DBS) is a neurosurgical intervention popularised in movement disorders such as Parkinson's disease, and also reported to improve symptoms of epilepsy, Tourette's syndrome, obsessive compulsive disorders and cluster headache. Since the 1950s, DBS has been used as a treatment to relieve intractable pain of several aetiologies including post stroke pain, phantom limb pain, facial pain and brachial plexus avulsion. Several patient series have shown benefits in stimulating various brain areas, including the sensory thalamus (ventral posterior lateral and medial), the periaqueductal and periventricular grey, or, more recently, the anterior cingulate cortex. However, this technique remains "off label" in the USA as it does not have Federal Drug Administration approval. Consequently, only a small number of surgeons report DBS for pain using current technology and techniques and few regions approve it. Randomised, blinded and controlled clinical trials that may use novel trial methodologies are desirable to evaluate the efficacy of DBS in patients who are refractory to other therapies. New imaging techniques, including tractography, may help optimise electrode placement and clinical outcome. PMID:26122383

  20. Neuroendocrine abnormalities in patients with traumatic brain injury

    Science.gov (United States)

    Yuan, X. Q.; Wade, C. E.

    1991-01-01

    This article provides an overview of hypothalamic and pituitary alterations in brain trauma, including the incidence of hypothalamic-pituitary damage, injury mechanisms, features of the hypothalamic-pituitary defects, and major hypothalamic-pituitary disturbances in brain trauma. While hypothalamic-pituitary lesions have been commonly described at postmortem examination, only a limited number of clinical cases of traumatic hypothalamic-pituitary dysfunction have been reported, probably because head injury of sufficient severity to cause hypothalamic and pituitary damage usually leads to early death. With the improvement in rescue measures, an increasing number of severely head-injured patients with hypothalamic-pituitary dysfunction will survive to be seen by clinicians. Patterns of endocrine abnormalities following brain trauma vary depending on whether the injury site is in the hypothalamus, the anterior or posterior pituitary, or the upper or lower portion of the pituitary stalk. Injury predominantly to the hypothalamus can produce dissociated ACTH-cortisol levels with no response to insulin-induced hypoglycemia and a limited or failed metopirone test, hypothyroxinemia with a preserved thyroid-stimulating hormone response to thyrotropin-releasing hormone, low gonadotropin levels with a normal response to gonadotropin-releasing hormone, a variable growth hormone (GH) level with a paradoxical rise in GH after glucose loading, hyperprolactinemia, the syndrome of inappropriate ADH secretion (SIADH), temporary or permanent diabetes insipidus (DI), disturbed glucose metabolism, and loss of body temperature control. Severe damage to the lower pituitary stalk or anterior lobe can cause low basal levels of all anterior pituitary hormones and eliminate responses to their releasing factors. Only a few cases showed typical features of hypothalamic or pituitary dysfunction. Most severe injuries are sufficient to damage both structures and produce a mixed endocrine picture

  1. Neuroimaging in adult penetrating brain injury: a guide for radiographers

    Energy Technology Data Exchange (ETDEWEB)

    Temple, Nikki; Donald, Cortny; Skora, Amanda [Discipline of Medical Radiation Sciences, The University of Sydney, Lidcombe, New South Wales (Australia); Reed, Warren, E-mail: warren.reed@sydney.edu.au [Medical Image Optimisation and Perception Group, Discipline of Medical Radiation Sciences, The University of Sydney, Lidcombe, New South Wales (Australia)

    2015-06-15

    Penetrating brain injuries (PBI) are a medical emergency, often resulting in complex damage and high mortality rates. Neuroimaging is essential to evaluate the location and extent of injuries, and to manage them accordingly. Currently, a myriad of imaging modalities are included in the diagnostic workup for adult PBI, including skull radiography, computed tomography (CT), magnetic resonance imaging (MRI) and angiography, with each modality providing their own particular benefits. This literature review explores the current modalities available for investigating PBI and aims to assist in decision making for the appropriate use of diagnostic imaging when presented with an adult PBI. Based on the current literature, the authors have developed an imaging pathway for adult penetrating brain injury that functions as both a learning tool and reference guide for radiographers and other health professionals. Currently, CT is recommended as the imaging modality of choice for the initial assessment of PBI patients, while MRI is important in the sub-acute setting where it aids prognosis prediction and rehabilitation planning, Additional follow-up imaging, such as angiography, should be dependent upon clinical findings.

  2. Neuroimaging in adult penetrating brain injury: a guide for radiographers

    International Nuclear Information System (INIS)

    Penetrating brain injuries (PBI) are a medical emergency, often resulting in complex damage and high mortality rates. Neuroimaging is essential to evaluate the location and extent of injuries, and to manage them accordingly. Currently, a myriad of imaging modalities are included in the diagnostic workup for adult PBI, including skull radiography, computed tomography (CT), magnetic resonance imaging (MRI) and angiography, with each modality providing their own particular benefits. This literature review explores the current modalities available for investigating PBI and aims to assist in decision making for the appropriate use of diagnostic imaging when presented with an adult PBI. Based on the current literature, the authors have developed an imaging pathway for adult penetrating brain injury that functions as both a learning tool and reference guide for radiographers and other health professionals. Currently, CT is recommended as the imaging modality of choice for the initial assessment of PBI patients, while MRI is important in the sub-acute setting where it aids prognosis prediction and rehabilitation planning, Additional follow-up imaging, such as angiography, should be dependent upon clinical findings

  3. Effect of zinc supplementation on neuronal precursor proliferation in the rat hippocampus after traumatic brain injury.

    Science.gov (United States)

    Cope, Elise C; Morris, Deborah R; Gower-Winter, Shannon D; Brownstein, Naomi C; Levenson, Cathy W

    2016-05-01

    There is great deal of debate about the possible role of adult-born hippocampal cells in the prevention of depression and related mood disorders. We first showed that zinc supplementation prevents the development of the depression-like behavior anhedonia associated with an animal model of traumatic brain injury (TBI). This work then examined the effect of zinc supplementation on the proliferation of new cells in the hippocampus that have the potential to participate in neurogenesis. Rats were fed a zinc adequate (ZA, 30ppm) or zinc supplemented (ZS, 180ppm) diet for 4wk followed by TBI using controlled cortical impact. Stereological counts of EdU-positive cells showed that TBI doubled the density of proliferating cells 24h post-injury (p<0.05), and supplemental zinc significantly increased this by an additional 2-fold (p<0.0001). While the survival of these proliferating cells decreased at the same rate in ZA and in ZS rats after injury, the total density of newly born cells was approximately 60% higher in supplemented rats 1wk after TBI. Furthermore, chronic zinc supplementation resulted in significant increases in the density of new doublecortin-positive neurons one week post-TBI that were maintained for 4wk after injury (p<0.01). While the effect of zinc supplementation on neuronal precursor cells in the hippocampus was robust, use of targeted irradiation to eliminate these cells after zinc supplementation and TBI revealed that these cells are not the sole mechanism through which zinc acts to prevent depression associated with brain injury, and suggest that other zinc dependent mechanisms are needed for the anti-depressant effect of zinc in this model of TBI. PMID:26902472

  4. Cognitive, emotional and behavioral impairments following traumatic brain injury and the neuro-radiological diagnosis

    International Nuclear Information System (INIS)

    Definition and diagnostic criteria in Japan of a high order brain functional impairment are explained and recent findings of the useful imaging for the criteria are discussed. The criteria of cognitive, emotional and behavioral impairments following brain injury (BI) defined by Ministry of Health, Labour and Welfare (MHLW) and National Rehabilitation Center for Persons with Disabilities contain 4 items of major symptoms, test findings, exclusion criteria and diagnosis. The criteria contain parts of diseases F04, F06 and F7 in ICD (International Classification of Diseases) 10, and conceivably correspond to such Western terms as the neuropsychological impairment, neurobehavioral impairment, cognitive disability and post-concussion syndrome. Head trauma is the major cause of BI and in the second item (test findings) of the diagnostic criteria above, imaging confirmation of the organic BI (mainly diffuse) is essential. For imaging technology of chronic diffuse injury, discussed are on findings of the structural MRI, diffusion tensor imaging (DTI), functional MRI; 18F-fluorodeoxyglucose-positron emission tomography (FDG-PET); and single photon emission computed tomography (SPECT) with 99mTc-ethyl-cysteinate dimmer and 123I-iomazenil. Based on those findings, it is thought that the impairment of the high order brain functions by diffuse injury is caused by the dysfunction of the primarily injured region and by its consequent disorder of cingulated gyrus and frontal anterior medial region through disturbance of cerebral nerve transmission and control. It is also suggested that a part of the blast related mild traumatic BI in US ex-servicemen is caused by the light diffuse BI, which can only be identified by the fractional anisotropy-statistical parametric mapping image in DTI. Number of patients with the high order brain functional impairment is estimated to be about 300,000 in Japan, but only 1/3 of those are actually diagnosed to be of the disease. (T.T.)

  5. Treatment of mild traumatic brain injury by epidural saline and oxygen injection: report of two cases.

    Science.gov (United States)

    Takagi, Kiyoshi; Kato, Kazuyoshi; Kato, Yoko

    2013-01-01

    Mild traumatic brain injury (mTBI) is a common complication of minor head injury and a serious problem in the Iraq war returnees. Effective treatment is not yet available. We have treated 23 patients with chronic post-traumatic headache by epidural saline and oxygen injection (ESOI) with efficacy of 96 %. Among them, ten cases were cured. Two out of these cured cases fulfilled the criteria of mTBI and their improvement were objectively demonstrated by a TriIRIS C9000 (Hamamatsu Photonics K.K.) that can monitor the accommodation and convergence function simultaneously. We show the treatment protocol of ESOI and the clinical courses of the two cases in this paper. Both had symptoms somewhat similar to those of spontaneous intracranial hypotension. However, their intracranial pressure was not low and their symptoms were relieved immediately after removal of cerebrospinal fluid (CSF). Although symptoms of mTBI are believed to be attributed to brain damage, some symptoms may not be derived from brain damage itself, but from CSF circulation abnormalities. This is the first report of successfully treated mTBI by ESOI. The effectiveness of the treatment can be verified objectively by monitoring eye function. The outcome suggests that war returnees with mTBI can be treated -successfully by ESOI. PMID:23564152

  6. A Prospective Pilot Investigation of Brain Volume, White Matter Hyperintensities, and Hemorrhagic Lesions after Mild Traumatic Brain Injury

    OpenAIRE

    Jarrett, Michael; Tam, Roger; Hernández-Torres, Enedino; Martin, Nancy; Perera, Warren; Zhao, Yinshan; Shahinfard, Elham; Dadachanji, Shiroy; Taunton, Jack; Li, David K.B.; Rauscher, Alexander

    2016-01-01

    Traumatic brain injury (TBI) is among the most common neurological disorders. Hemorrhagic lesions and white matter hyperintensities (WMH) are radiological features associated with moderate and severe TBI. Brain volume reductions have also been observed during the months following injury. In concussion, no signs of injury are observed on conventional magnetic resonance imaging (MRI), which may be a true feature of concussion or merely due to the limited sensitivity of imaging techniques used s...

  7. Glucose administration after traumatic brain injury improves cerebral metabolism and reduces secondary neuronal injury

    OpenAIRE

    Moro, Nobuhiro; Ghavim, Sima; Harris, Neil G.; Hovda, David A.; Sutton, Richard L.

    2013-01-01

    Clinical studies have indicated an association between acute hyperglycemia and poor outcomes in patients with traumatic brain injury (TBI), although optimal blood glucose levels needed to maximize outcomes for these patients’ remains under investigation. Previous results from experimental animal models suggest that post-TBI hyperglycemia may be harmful, neutral, or beneficial. The current studies determined the effects of single or multiple episodes of acute hyperglycemia on cerebral glucose ...

  8. Lateral (Parasagittal) Fluid Percussion Model of Traumatic Brain Injury.

    Science.gov (United States)

    Van, Ken C; Lyeth, Bruce G

    2016-01-01

    Fluid percussion was first conceptualized in the 1940s and has evolved into one of the leading laboratory methods for studying experimental traumatic brain injury (TBI). Over the decades, fluid percussion has been used in numerous species and today is predominantly applied to the rat. The fluid percussion technique rapidly injects a small volume of fluid, such as isotonic saline, through a circular craniotomy onto the intact dura overlying the brain cortex. In brief, the methods involve surgical production of a circular craniotomy, attachment of a fluid-filled conduit between the dura overlying the cortex and the outlet port of the fluid percussion device. A fluid pulse is then generated by the free-fall of a pendulum striking a piston on the fluid-filled cylinder of the device. The fluid enters the cranium, producing a compression and displacement of the brain parenchyma resulting in a sharp, high magnitude elevation of intracranial pressure that is propagated diffusely through the brain. This results in an immediate and transient period of traumatic unconsciousness as well as a combination of focal and diffuse damage to the brain, which is evident upon histological and behavioral analysis. Numerous studies have demonstrated that the rat fluid percussion model reproduces a wide range of pathological features associated with human TBI. PMID:27604722

  9. Factors affecting radiation injury after interstitial brachytherapy for brain tumors

    International Nuclear Information System (INIS)

    The effects of brachytherapy on normal brain tissue are not easily delineated in the clinical setting because of the presence of concurrent radiation-induced changes in the coexistent brain tumor. Sequential morphologic studies performed after the implantation of radioactive sources into the brains of experimental animals have provided a better understanding of the character and magnitude of the structural changes produced by interstitial irradiation on normal brain tissue. Furthermore, the clinical experience accumulated thus far provides not only relevant information, but also some guidelines for future treatment policies. In this paper, the authors summarize the experimental findings and review the pathologic and clinical features of brain injury caused by interstitial brachytherapy. A number of studies in the older literature examined the effects of radioisotopes such as radium-226 (38--43), radon-22 (44--46), gold-198 (29,47--50), tantalum-182 (29,51,52) yttrium-9- (50,53,54), and cobalt-60 (29,50,55). This review is restricted to low- and high-activity encapsulated iodine-125 (125I) and iridium-192 (192Ir), the isotopes that are most commonly used in current clinical practice

  10. Regional brain morphometry predicts memory rehabilitation outcome after traumatic brain injury

    Directory of Open Access Journals (Sweden)

    Gary E Strangman

    2010-10-01

    Full Text Available Cognitive deficits following traumatic brain injury (TBI commonly include difficulties with memory, attention, and executive dysfunction. These deficits are amenable to cognitive rehabilitation, but optimally selecting rehabilitation programs for individual patients remains a challenge. Recent methods for quantifying regional brain morphometry allow for automated quantification of tissue volumes in numerous distinct brain structures. We hypothesized that such quantitative structural information could help identify individuals more or less likely to benefit from memory rehabilitation. Fifty individuals with TBI of all severities who reported having memory difficulties first underwent structural MRI scanning. They then participated in a 12 session memory rehabilitation program emphasizing internal memory strategies (I-MEMS. Primary outcome measures (HVLT, RBMT were collected at the time of the MRI scan, immediately following therapy, and again at one month post-therapy. Regional brain volumes were used to predict outcome, adjusting for standard predictors (e.g., injury severity, age, education, pretest scores. We identified several brain regions that provided significant predictions of rehabilitation outcome, including the volume of the hippocampus, the lateral prefrontal cortex, the thalamus, and several subregions of the cingulate cortex. The prediction range of regional brain volumes were in some cases nearly equal in magnitude to prediction ranges provided by pretest scores on the outcome variable. We conclude that specific cerebral networks including these regions may contribute to learning during I-MEMS rehabilitation, and suggest that morphometric measures may provide substantial predictive value for rehabilitation outcome in other cognitive interventions as well.

  11. Differential role of tumor necrosis factor receptors in mouse brain inflammatory responses in cryolesion brain injury

    DEFF Research Database (Denmark)

    Quintana, Albert; Giralt, Mercedes; Rojas, Santiago;

    2005-01-01

    Tumor necrosis factor-alpha (TNF-alpha) is one of the mediators dramatically increased after traumatic brain injury that leads to the activation, proliferation, and hypertrophy of mononuclear, phagocytic cells and gliosis. Eventually, TNF-alpha can induce both apoptosis and necrosis via intracell......Tumor necrosis factor-alpha (TNF-alpha) is one of the mediators dramatically increased after traumatic brain injury that leads to the activation, proliferation, and hypertrophy of mononuclear, phagocytic cells and gliosis. Eventually, TNF-alpha can induce both apoptosis and necrosis via...... intracellular signaling. This cytokine exerts its functions via interaction with two receptors: type-1 receptor (TNFR1) and type-2 receptor (TNFR2). In this work, the inflammatory response after a freeze injury (cryolesion) in the cortex was studied in wild-type (WT) animals and in mice lacking TNFR1 (TNFR1 KO...... affected by TNFR1 deficiency. Overall, these results suggest that TNFR1 is involved in the early establishment of the inflammatory response and that its deficiency causes a decreased inflammatory response and tissue damage following brain injury....

  12. Berberine Protects against Neuronal Damage via Suppression of Glia-Mediated Inflammation in Traumatic Brain Injury

    OpenAIRE

    Chien-Cheng Chen; Tai-Ho Hung; Chao Yu Lee; Liang-Fei Wang; Chun-Hu Wu; Chia-Hua Ke; Szu-Fu Chen

    2014-01-01

    Traumatic brain injury (TBI) triggers a series of neuroinflammatory processes that contribute to evolution of neuronal injury. The present study investigated the neuroprotective effects and anti-inflammatory actions of berberine, an isoquinoline alkaloid, in both in vitro and in vivo TBI models. Mice subjected to controlled cortical impact injury were injected with berberine (10 mg·kg(-1)) or vehicle 10 min after injury. In addition to behavioral studies and histology analysis, blood-brain ba...

  13. Astrocytic Ephrin-B1 Regulates Synapse Remodeling Following Traumatic Brain Injury

    OpenAIRE

    Nikolakopoulou, Angeliki M.; Koeppen, Jordan; Garcia, Michael; Leish, Joshua; Obenaus, Andre; Iryna M Ethell

    2016-01-01

    Traumatic brain injury (TBI) can result in tissue alterations distant from the site of the initial injury, which can trigger pathological changes within hippocampal circuits and are thought to contribute to long-term cognitive and neuropsychological impairments. However, our understanding of secondary injury mechanisms is limited. Astrocytes play an important role in brain repair after injury and astrocyte-mediated mechanisms that are implicated in synapse development are likely important in ...

  14. Personality Change due to Traumatic Brain Injury in Children and Adolescents: Neurocognitive Correlates

    OpenAIRE

    Wilde, Elisabeth A.; Bigler, Erin D; Hanten, Gerri; Dennis, Maureen; Schachar, Russell J.; Saunders, Ann E.; Ewing-Cobbs, Linda; Chapman, Sandra B.; Wesley K. Thompson; Yang, Tony T.; Levin, Harvey S.

    2015-01-01

    Personality Change due to traumatic brain injury (PC) in children is an important psychiatric complication of injury and is a form of severe affective dysregulation. The aim of the study was to examine neurocognitive correlates of PC. The sample included children (n=177) aged 5-14 years with traumatic brain injury from consecutive admissions to 5 trauma centers were followed prospectively at baseline and 6 months with semi-structured psychiatric interviews. Injury severity, socioeconomic stat...

  15. Impaired Cerebral Autoregulation during Head Up Tilt in Patients with Severe Brain Injury

    OpenAIRE

    Riberholt, Christian Gunge; Olesen, Niels Damkjær; Thing, Mira; Juhl, Carsten Bogh; Mehlsen, Jesper; Petersen, Tue Hvass

    2016-01-01

    Early mobilization is of importance for improving long-term outcome for patients after severe acquired brain injury. A limiting factor for early mobilization by head-up tilt is orthostatic intolerance. The purpose of the present study was to examine cerebral autoregulation in patients with severe acquired brain injury and a low level of consciousness. Fourteen patients with severe acquired brain injury and orthostatic intolerance and fifteen healthy volunteers were enrolled. Blood pressure wa...

  16. Intelligence after traumatic brain injury: meta-analysis of outcomes and prognosis.

    Science.gov (United States)

    Königs, M; Engenhorst, P J; Oosterlaan, J

    2016-01-01

    Worldwide, 54-60 million individuals sustain traumatic brain injury (TBI) each year. This meta-analysis aimed to quantify intelligence impairments after TBI and to determine the value of age and injury severity in the prognosis of TBI. An electronic database search identified 81 relevant peer-reviewed articles encompassing 3890 patients. Full-scale IQ (FSIQ), performance IQ (PIQ) and verbal IQ (VIQ) impairments were quantified (Cohen's d) for patients with mild, moderate and severe TBI in the subacute phase of recovery and the chronic phase. Meta-regressions explored prognostic values of age and injury severity measures for intelligence impairments. The results showed that, in the subacute phase, FSIQ impairments were absent for patients with mild TBI, medium-sized for patients with moderate TBI (d = -0.61, P intelligence impairments, where children may have better recovery from mild TBI and poorer recovery from severe TBI than adults. Injury severity measures predict intelligence impairments and do not outperform one another. PMID:25919757

  17. Outcome from Complicated versus Uncomplicated Mild Traumatic Brain Injury.

    Science.gov (United States)

    Iverson, Grant L; Lange, Rael T; Wäljas, Minna; Liimatainen, Suvi; Dastidar, Prasun; Hartikainen, Kaisa M; Soimakallio, Seppo; Ohman, Juha

    2012-01-01

    Objective. To compare acute outcome following complicated versus uncomplicated mild traumatic brain injury (MTBI) using neurocognitive and self-report measures. Method. Participants were 47 patients who presented to the emergency department of Tampere University Hospital, Finland. All completed MRI scanning, self-report measures, and neurocognitive testing at 3-4 weeks after injury. Participants were classified into the complicated MTBI or uncomplicated MTBI group based on the presence/absence of intracranial abnormality on day-of-injury CT scan or 3-4 week MRI scan. Results. There was a large statistically significant difference in time to return to work between groups. The patients with uncomplicated MTBIs had a median of 6.0 days (IQR = 0.75-14.75, range = 0-77) off work compared to a median of 36 days (IQR = 13.5-53, range = 3-315) for the complicated group. There were no significant differences between groups for any of the neurocognitive or self-report measures. There were no differences in the proportion of patients who (a) met criteria for ICD-10 postconcussional disorder or (b) had multiple low scores on the neurocognitive measures. Conclusion. Patients with complicated MTBIs took considerably longer to return to work. They did not perform more poorly on neurocognitive measures or report more symptoms, at 3-4 weeks after injury compared to patients with uncomplicated MTBIs. PMID:22577556

  18. Outcome from Complicated versus Uncomplicated Mild Traumatic Brain Injury

    Directory of Open Access Journals (Sweden)

    Grant L. Iverson

    2012-01-01

    Full Text Available Objective. To compare acute outcome following complicated versus uncomplicated mild traumatic brain injury (MTBI using neurocognitive and self-report measures. Method. Participants were 47 patients who presented to the emergency department of Tampere University Hospital, Finland. All completed MRI scanning, self-report measures, and neurocognitive testing at 3-4 weeks after injury. Participants were classified into the complicated MTBI or uncomplicated MTBI group based on the presence/absence of intracranial abnormality on day-of-injury CT scan or 3-4 week MRI scan. Results. There was a large statistically significant difference in time to return to work between groups. The patients with uncomplicated MTBIs had a median of 6.0 days (IQR = 0.75–14.75, range = 0–77 off work compared to a median of 36 days (IQR = 13.5–53, range = 3–315 for the complicated group. There were no significant differences between groups for any of the neurocognitive or self-report measures. There were no differences in the proportion of patients who (a met criteria for ICD-10 postconcussional disorder or (b had multiple low scores on the neurocognitive measures. Conclusion. Patients with complicated MTBIs took considerably longer to return to work. They did not perform more poorly on neurocognitive measures or report more symptoms, at 3-4 weeks after injury compared to patients with uncomplicated MTBIs.

  19. Traumatic brain injury impairs synaptic plasticity in hippocampus in rats

    Institute of Scientific and Technical Information of China (English)

    ZHANG Bao-liang; CHEN Xin; TAN Tao; YANG Zhuo; CARLOS Dayao; JIANG Rong-cai; ZHANG Jian-ning

    2011-01-01

    Background Traumatic brain injury (TBl) often causes cognitive deficits and remote symptomatic epilepsy.Hippocampal regional excitability is associated with the cognitive function. However, little is known about injury-induced neuronal loss and subsequent alterations of hippocampal regional excitability. The present study was designed to determine whether TBl may impair the cellular circuit in the hippocampus.Methods Forty male Wistar rats were randomized into control (n=20) and TBl groups (n=20). Long-term potentiation,extracellular input/output curves, and hippocampal parvalbumin-immunoreactive and cholecystokinin-immunoreactive interneurons were compared between the two groups.Results TBI resulted in a significantly increased excitability in the dentate gyrus (DG), but a significantly decreased excitability in the cornu ammonis 1 (CA1) area. Using design-based stereological injury procedures, we induced interneuronal loss in the DG and CA3 subregions in the hippocampus, but not in the CA1 area.Conclusions TBl leads to the impairment of hippocampus synaptic plasticity due to the changing of interneuronal interaction. The injury-induced disruption of synaptic efficacy within the hippocampal circuit may underlie the observed cognitive deficits and symptomatic epilepsy.

  20. Head motions while riding roller coasters: implications for brain injury.

    Science.gov (United States)

    Pfister, Bryan J; Chickola, Larry; Smith, Douglas H

    2009-12-01

    The risk of traumatic brain injury (TBI) while riding roller coasters has received substantial attention. Case reports of TBI around the time of riding roller coasters have led many medical professionals to assert that the high gravitational forces (G-forces) induced by roller coasters pose a significant TBI risk. Head injury research, however, has shown that G-forces alone cannot predict TBI. Established head injury criterions and procedures were employed to compare the potential of TBI between daily activities and roller coaster riding. Three-dimensional head motions were measured during 3 different roller coaster rides, a pillow fight, and car crash simulations. Data was analyzed and compared with published data, using similar analyses of head motions. An 8.05 m/s car crash lead to the largest head injury criterion measure of 28.1 and head impact power of 3.41, over 6 times larger than the roller coaster rides of 4.1 and 0.36. Notably, the linear and rotational components of head acceleration during roller coaster rides were milder than those induced by many common activities. As such, there appears to be an extremely low risk of TBI due to the head motions induced by roller coaster rides. PMID:19901817

  1. Treatments for traumatic brain injury with emphasis on transcranial near-infrared laser phototherapy

    Directory of Open Access Journals (Sweden)

    Morries LD

    2015-08-01

    Full Text Available Larry D Morries,1 Paolo Cassano,2 Theodore A Henderson1,3 1Neuro-Laser Foundation, Lakewood, CO, 2Harvard Medical School, Depression Clinical and Research Program, Massachusetts General Hospital, Boston, MA, 3The Synaptic Space, Centennial, CO, USA Abstract: Traumatic brain injury (TBI is a growing health concern affecting civilians and military personnel. In this review, treatments for the chronic TBI patient are discussed, including pharmaceuticals, nutraceuticals, cognitive therapy, and hyperbaric oxygen therapy. All available literature suggests a marginal benefit with prolonged treatment courses. An emerging modality of treatment is near-infrared (NIR light, which has benefit in animal models of stroke, spinal cord injury, optic nerve injury, and TBI, and in human trials for stroke and TBI. The extant literature is confounded by variable degrees of efficacy and a bewildering array of treatment parameters. Some data indicate that diodes emitting low-level NIR energy often have failed to demonstrate therapeutic efficacy, perhaps due to failing to deliver sufficient radiant energy to the necessary depth. As part of this review, we present a retrospective case series using high-power NIR laser phototherapy with a Class IV laser to treat TBI. We demonstrate greater clinical efficacy with higher fluence, in contrast to the bimodal model of efficacy previously proposed. In ten patients with chronic TBI (average time since injury 9.3 years given ten treatments over the course of 2 months using a high-power NIR laser (13.2 W/0.89 cm2 at 810 nm or 9 W/0.89 cm2 at 810 nm and 980 nm, symptoms of headache, sleep disturbance, cognition, mood dysregulation, anxiety, and irritability improved. Symptoms were monitored by depression scales and a novel patient diary system specifically designed for this study. NIR light in the power range of 10–15 W at 810 nm and 980 nm can safely and effectively treat chronic symptoms of TBI. The clinical

  2. Chronic traumatic encephalopathy: a spectrum of neuropathological changes following repetitive brain trauma in athletes and military personnel

    OpenAIRE

    Stein, Thor D.; Alvarez, Victor E.; McKee, Ann C.

    2014-01-01

    Chronic traumatic encephalopathy (CTE) is a progressive neurodegenerative disease that occurs in association with repetitive traumatic brain injury experienced in sport and military service. In most instances, the clinical symptoms of the disease begin after a long period of latency ranging from several years to several decades. The initial symptoms are typically insidious, consisting of irritability, impulsivity, aggression, depression, short-term memory loss and heightened suicidality. The ...

  3. Structural Neuroimaging Findings in Mild Traumatic Brain Injury.

    Science.gov (United States)

    Bigler, Erin D; Abildskov, Tracy J; Goodrich-Hunsaker, Naomi J; Black, Garrett; Christensen, Zachary P; Huff, Trevor; Wood, Dawn-Marie G; Hesselink, John R; Wilde, Elisabeth A; Max, Jeffrey E

    2016-09-01

    Common neuroimaging findings in mild traumatic brain injury (mTBI), including sport-related concussion (SRC), are reviewed based on computed tomography and magnetic resonance imaging (MRI). Common abnormalities radiologically identified on the day of injury, typically a computed tomographic scan, are in the form of contusions, small subarachnoid or intraparenchymal hemorrhages as well as subdural and epidural collections, edema, and skull fractures. Common follow-up neuroimaging findings with MRI include white matter hyperintensities, hypointense signal abnormalities that reflect prior hemorrhage, focal encephalomalacia, presence of atrophy and/or dilated Virchow-Robins perivascular space. The MRI findings from a large pediatric mTBI study show low frequency of positive MRI findings at 6 months postinjury. The review concludes with an examination of some of the advanced MRI-based image analysis methods that can be performed in the patient who has sustained an mTBI. PMID:27482782

  4. Structural changes in the brain according to CT findings in children with long-term consequences of closed brain injury

    International Nuclear Information System (INIS)

    Long-term structural changes in the brain substance after closed brain injury (CBI) in children using computerized tomography was studied. 30 patients aged 11-18 with CBI with favourable and unfavourable course was examined. The obtained findings suggest a complicated picture of the reaction of the involved brain. The degree of neurologic signs and the type of traumatic injuries depend on the degree of structural changes

  5. Etanercept Attenuates Traumatic Brain Injury in Rats by Reducing Brain TNF-α Contents and by Stimulating Newly Formed Neurogenesis

    OpenAIRE

    Chong-Un Cheong; Ching-Ping Chang; Chien-Ming Chao; Bor-Chih Cheng; Chung-Zhing Yang; Chung-Ching Chio

    2013-01-01

    It remains unclear whether etanercept penetrates directly into the contused brain and improves the outcomes of TBI by attenuating brain contents of TNF- α and/or stimulating newly formed neurogenesis. Rats that sustained TBI are immediately treated with etanercept. Acute neurological and motor injury is assessed in all rats the day prior to and 7 days after surgery. The numbers of the colocalizations of 5-bromodeoxyuridine and doublecortin specific markers in the contused brain injury that oc...

  6. Magnetic resonance imaging and cell-based neurorestorative therapy after brain injury

    Institute of Scientific and Technical Information of China (English)

    Quan Jiang

    2016-01-01

    Restorative cell-based therapies for experimental brain injury, such as stroke and traumatic brain injury, substantially improve functional outcome. We discuss and review state of the art magnetic resonance im-aging methodologies and their applications related to cell-based treatment after brain injury. We focus on the potential of magnetic resonance imaging technique and its associated challenges to obtain useful new information related to cell migration, distribution, and quantitation, as well as vascular and neuronal remodeling in response to cell-based therapy after brain injury. The noninvasive nature of imaging might more readily help with translation of cell-based therapy from the laboratory to the clinic.

  7. Magnetic resonance imaging and cell-based neurorestorative therapy after brain injury

    Directory of Open Access Journals (Sweden)

    Quan Jiang

    2016-01-01

    Full Text Available Restorative cell-based therapies for experimental brain injury, such as stroke and traumatic brain injury, substantially improve functional outcome. We discuss and review state of the art magnetic resonance imaging methodologies and their applications related to cell-based treatment after brain injury. We focus on the potential of magnetic resonance imaging technique and its associated challenges to obtain useful new information related to cell migration, distribution, and quantitation, as well as vascular and neuronal remodeling in response to cell-based therapy after brain injury. The noninvasive nature of imaging might more readily help with translation of cell-based therapy from the laboratory to the clinic.

  8. Correlation of cell apoptosis with brain edema and elevated intracranial pressure in traumatic brain injury

    Institute of Scientific and Technical Information of China (English)

    YANG Xiao-feng; LIU Wei-guo; SHEN Hong; GONG Jiang-biao; YU Jun; HU Wei-wei; L(U) Shi-ting; ZHENG Xiu-jue; FU Wei-ming

    2005-01-01

    Objective: To study the correlation between brain edema, elevated intracranial pressure (ICP) and cell apoptosis in traumatic brain injury (TBI). Methods: In this study, totally 42 rabbits in 7 groups were studied. Six of the animals were identified as a control group, and the remaining 36 animals were equally divided into 6 TBI groups. TBI models were produced by the modified method of Feeney. After the impact, ICP of each subject was recorded continuously by an ICP monitor until the animal was sacrificed at scheduled time. The apoptotic brain cells were detected by an terminal deoxynucleotide-transferase-mediated dUTP-digoxigenin nick end labeling (TUNEL) assay. Cerebral water content (CWC) was measured with a drying method and calculated according to the Elliott formula. Then, an analysis was conducted to determine the correlation between the count of apoptotic cells and the clinical pathological changes of the brain. Results: Apoptotic cell count began to increase 2 h after the impact, and reached its maximum about 3 days after the impact. The peak value of CWC and ICP appeared 1 day and 3 days after the impact, respectively. Apoptotic cell count had a positive correlation with CWC and ICP. Conclusions: In TBI, occurrence of brain edema and ICP increase might lead to apoptosis of brain cells. Any therapy which can relieve brain edema and/or decrease ICP would be able to reduce neuron apoptosis, thereby to attenuate the secondary brain damage.

  9. Gesture Based Educational Software for Children with Acquired Brain Injuries

    Directory of Open Access Journals (Sweden)

    Er. Zainab Pirani

    2010-05-01

    Full Text Available " GESBI” is gesture based audio visual teaching tool designed to help children with acquired brain injuries, providing hours of entertainment in a play-and-learn environment while introducing the foundation skills in basic arithmetic, spelling, reading and solving puzzles. These children communicate with the computer via gestures based on my previous research paper “KONCERN- Hand Gesture Recognition for Physically Impaired” in which gestures are captured by camera and processed without the need of wearing any sensor based gloves etc.

  10. Temporal-spatial feature of gait after traumatic brain injury.

    Science.gov (United States)

    Ochi, F; Esquenazi, A; Hirai, B; Talaty, M

    1999-04-01

    The temporal-spatial characteristics of the gait of patients with traumatic brain injury (TBI) were investigated and compared with those of normal gait and the gait of stroke survivors. A slower walking velocity is evident in the TBI population when compared with normal. The average walking speed of TBI survivors is faster than that of stroke patients and is mainly related to a longer step length. TBI survivors produce a gait pattern with a prolonged stance period for the unaffected limb, without prolonged stance period for the affected limb, and a shorter step length for the unaffected limb. PMID:10191370

  11. A patients perspective on eating difficulties following brain injury

    DEFF Research Database (Denmark)

    Kjaersgaard, Annette; Kristensen, Hanne Kaae; Borg, Tove

    Purpose: The aim of this study is to explore and interpret how persons with acquired brain injury (ABI) experience and adapt to reduced abilities to swallowing and eating - and clinical implications. Method: Explorative multiple-case study with qualitative interviews of six persons following ABI...... from the analysis: individual psychological assets, swallowing and ingestion, eating and drinking, communication and meals, rehabilitation of swallowing and eating. Three predominating sub-themes were: feeding by tube, difficulties in swallowing and meals with social interactions, and inpatient...

  12. 78 FR 28546 - Secondary Service Connection for Diagnosable Illnesses Associated With Traumatic Brain Injury

    Science.gov (United States)

    2013-05-15

    ... Traumatic Brain Injury Correction In proposed rule document 2012-29709 beginning on page 73366 in the issue...: Structural imaging of the brain. LOC--Loss of consciousness. AOC--Alteration of consciousness/mental...

  13. Sleep Doesn't Come Easy to Those with Brain Injuries

    Science.gov (United States)

    ... page: https://medlineplus.gov/news/fullstory_158527.html Sleep Doesn't Come Easy to Those With Brain ... who suffer a traumatic brain injury struggle with sleep problems they may not be aware of, Swiss ...

  14. Radiation-induced brain injury: low-hanging fruit for neuroregeneration.

    Science.gov (United States)

    Burns, Terry C; Awad, Ahmed J; Li, Matthew D; Grant, Gerald A

    2016-05-01

    Brain radiation is a fundamental tool in neurooncology to improve local tumor control, but it leads to profound and progressive impairments in cognitive function. Increased attention to quality of life in neurooncology has accelerated efforts to understand and ameliorate radiation-induced cognitive sequelae. Such progress has coincided with a new understanding of the role of CNS progenitor cell populations in normal cognition and in their potential utility for the treatment of neurological diseases. The irradiated brain exhibits a host of biochemical and cellular derangements, including loss of endogenous neurogenesis, demyelination, and ablation of endogenous oligodendrocyte progenitor cells. These changes, in combination with a state of chronic neuroinflammation, underlie impairments in memory, attention, executive function, and acquisition of motor and language skills. Animal models of radiation-induced brain injury have demonstrated a robust capacity of both neural stem cells and oligodendrocyte progenitor cells to restore cognitive function after brain irradiation, likely through a combination of cell replacement and trophic effects. Oligodendrocyte progenitor cells exhibit a remarkable capacity to migrate, integrate, and functionally remyelinate damaged white matter tracts in a variety of preclinical models. The authors here critically address the opportunities and challenges in translating regenerative cell therapies from rodents to humans. Although valiant attempts to translate neuroprotective therapies in recent decades have almost uniformly failed, the authors make the case that harnessing human radiation-induced brain injury as a scientific tool represents a unique opportunity to both successfully translate a neuroregenerative therapy and to acquire tools to facilitate future restorative therapies for human traumatic and degenerative diseases of the central nervous system. PMID:27132524

  15. Strongly compromised inflammatory response to brain injury in interleukin-6-deficient mice

    DEFF Research Database (Denmark)

    Penkowa, M; Moos, T; Carrasco, J;

    1999-01-01

    response in the brain following disruption of the blood-brain barrier (BBB), we examined the effects of a focal cryo injury to the fronto-parietal cortex in interleukin-6-deficient (IL-6-/-) and normal (IL-6+/+) mice. In IL-6+/+ mice, brain injury resulted in the appearance of brain macrophages and...... brain macrophages and reactive astrocytes was markedly depressed and the number of NSE positive neurons was reduced. Brain damage-induced GM-CSF and MT-I+II expression were also markedly depressed compared to IL-6+/+ mice. In contrast, MT-III immunoreactivity was markedly increased in brain macrophages...

  16. Assessing Neuro-Systemic & Behavioral Components in the Pathophysiology of Blast-Related Brain Injury

    OpenAIRE

    Kobeissy, Firas; Mondello, Stefania; Tümer, Nihal; Toklu, Hale Z.; Whidden, Melissa A; Kirichenko, Nataliya; Zhang, Zhiqun; Prima, Victor; Yassin, Walid; Anagli, John; Chandra, Namas; Svetlov, Stan; Wang, Kevin K. W.

    2013-01-01

    Among the U.S. military personnel, blast injury is among the leading causes of brain injury. During the past decade, it has become apparent that even blast injury as a form of mild traumatic brain injury (mTBI) may lead to multiple different adverse outcomes, such as neuropsychiatric symptoms and long-term cognitive disability. Blast injury is characterized by blast overpressure, blast duration, and blast impulse. While the blast injuries of a victim close to the explosion will be severe, maj...

  17. Assessing Neuro-Systemic & Behavioral Components in the Pathophysiology of Blast-Related Brain Injury

    OpenAIRE

    Firas H Kobeissy; Stefania eMondello; Nihal eTumer; Toklu, Hale Z.; Whidden, Melissa A; Nataliya eKirichenko; Zhiqun eZhang; Victor ePrima; Walid eYassin; Chandra eNamas; John eAnagli; Stanislav eSvetlov; Wang, Kevin K. W.

    2013-01-01

    Among the U.S. military personnel, blast injury is among the leading causes of brain injury. During the past decade, it has become apparent that even blast injury as a form of mild traumatic brain injury (mTBI) may lead to multiple different adverse outcomes, such as neuropsychiatric symptoms and long-term cognitive disability. Blast injury is characterized by blast overpressure (BOP), blast duration, and blast impulse. While the blast injuries of a victim close to the explosion will be sever...

  18. Resveratrol attenuates peripheral and brain inflammation and reduces ischemic brain injury in aged female mice.

    Science.gov (United States)

    Jeong, Sae Im; Shin, Jin A; Cho, Sunghee; Kim, Hye Won; Lee, Ji Yoon; Kang, Jihee Lee; Park, Eun-Mi

    2016-08-01

    Resveratrol is known to improve metabolic dysfunction associated with obesity. Visceral obesity is a sign of aging and is considered a risk factor for ischemic stroke. In this study, we investigated the effects of resveratrol on inflammation in visceral adipose tissue and the brain and its effects on ischemic brain injury in aged female mice. Mice treated with resveratrol (0.1 mg/kg, p.o.) for 10 days showed reduced levels of interleukin-1β and tumor necrosis factor-α, as well as a reduction in the size of adipocytes in visceral adipose tissue. Resveratrol also reduced interleukin-1β and tumor necrosis factor-α protein levels and immunoglobulin G extravasation in the brain. Mice treated with resveratrol demonstrated smaller infarct size, improved neurological function, and blunted peripheral inflammation at 3 days postischemic stroke. These results showed that resveratrol counteracted inflammation in visceral adipose tissue and in the brain and reduced stroke-induced brain injury and peripheral inflammation in aged female mice. Therefore, resveratrol administration can be a valuable strategy for the prevention of age-associated and disease-provoked inflammation in postmenopausal women. PMID:27318135

  19. How to Get Hyperbaric Oxygen Therapy for Children with Cerebral Palsy or Brain Injury: Navigating Insurance Denials, Red Tape, and Other Challenges

    Science.gov (United States)

    Console, Richard P., Jr.

    2010-01-01

    Medical professionals who use hyperbaric oxygen therapy (HBOT) say that recent studies, as well as anecdotal evidence, indicate that this treatment significantly improves the lives of many children with cerebral palsy and other types of chronic brain injury. So why do many children with these diagnoses not have access to this treatment? Simply…

  20. Recovery from Mild Traumatic Brain Injury in Previously Healthy Adults.

    Science.gov (United States)

    Losoi, Heidi; Silverberg, Noah D; Wäljas, Minna; Turunen, Senni; Rosti-Otajärvi, Eija; Helminen, Mika; Luoto, Teemu M; Julkunen, Juhani; Öhman, Juha; Iverson, Grant L

    2016-04-15

    This prospective longitudinal study reports recovery from mild traumatic brain injury (MTBI) across multiple domains in a carefully selected consecutive sample of 74 previously healthy adults. The patients with MTBI and 40 orthopedic controls (i.e., ankle injuries) completed assessments at 1, 6, and 12 months after injury. Outcome measures included cognition, post-concussion symptoms, depression, traumatic stress, quality of life, satisfaction with life, resilience, and return to work. Patients with MTBI reported more post-concussion symptoms and fatigue than the controls at the beginning of recovery, but by 6 months after injury, did not differ as a group from nonhead injury trauma controls on cognition, fatigue, or mental health, and by 12 months, their level of post-concussion symptoms and quality of life was similar to that of controls. Almost all (96%) patients with MTBI returned to work/normal activities (RTW) within the follow-up of 1 year. A subgroup of those with MTBIs and controls reported mild post-concussion-like symptoms at 1 year. A large percentage of the subgroup who had persistent symptoms had a modifiable psychological risk factor at 1 month (i.e., depression, traumatic stress, and/or low resilience), and at 6 months, they had greater post-concussion symptoms, fatigue, insomnia, traumatic stress, and depression, and worse quality of life. All of the control subjects who had mild post-concussion-like symptoms at 12 months also had a mental health problem (i.e., depression, traumatic stress, or both). This illustrates the importance of providing evidence-supported treatment and rehabilitation services early in the recovery period. PMID:26437675