Clinical significance of changes of serum NSE, TNF-α and IL-6 levels in patients with hypoxic ischemic encephalopathy

International Nuclear Information System (INIS)

Zhang Yuhong; Zhang Yujuan; Zhou Xiujuan; Shan Huali

2010-01-01

Objective: To study the clinical significance of changes of serum NSE, TNF-α and IL-6 levels in neonates with hypoxic ischemic encephalopathy. Methods: Serum NSE (with ELISA) and TNF-α, IL-6 (with RIA) levels were measured in 30 neonates with hypoxic ischemic encephalopathy and 30 controls. Results: Serum NSE, TNF-α and IL-6 levels were significantly higher in neonates with hypoxic-ischemic encephalopathy than those in controls (P<0.01). Serum NSE levels were positively correlated with those of TNF-α, IL-6 (r=0.5812, 0.6014, P<0.01). Conclusion: Serum NSE, TNF-α and IL-6 levels were closely related to the diseases process of hypoxic-ischemic encephalopathy. (authors)

Persistent lactic acidosis in neonatal hypoxic-ischaemic encephalopathy correlates with EEG grade and electrographic seizure burden.

LENUS (Irish Health Repository)

Murray, D M

2012-02-03

BACKGROUND: Predicting at birth which infants with perinatal hypoxic-ischaemic injury will progress to significant encephalopathy remains a challenge. OBJECTIVE: To determine whether lactic acidosis at birth in asphyxiated neonates could predict the grade of EEG encephalopathy by examining the relationship between time taken for the normalisation of lactate, severity of encephalopathy and seizure burden. METHODS: Continuous early video-EEG monitoring was performed in babies at risk for hypoxic-ischaemic encephalopathy. Encephalopathy was graded from the EEG data. Total seizure burden (seconds) was calculated for each baby. Initial blood gas measurements of pH, base deficit and lactate were taken within 30 minutes of delivery. Time to normal serum lactate was determined in hours from birth for each infant. RESULTS: All 50 term infants had raised initial serum lactate (median (lower, upper quartiles) 11.7 (10.2, 14.9)). There were no significant differences between the initial serum lactate, pH and base deficit in infants with normal\\/mildly abnormal (n = 24), moderately abnormal (n = 14), severely abnormal (n = 5) and inactive EEGs (n = 7). Time to normal lactate varied significantly with EEG grade (median (lower, upper quartile) 6.0 (4.1, 9.5) for mild\\/normal EEG, 13.5 (6.8, 23.5) moderate EEG, 41.5 (30.0, 55.5) severe group, 12.0 (8.1, 21.5) inactive group; p<0.001). Time to normal lactate correlated significantly with EEG seizure burden (seconds; R = 0.446, p = 0.002). Mean (SD) time to normal lactate was 10.0 (7.2) hours in infants who did not have seizures and 27.3 (19.0) hours in the 13 infants with electrographic seizures (p = 0.002). CONCLUSIONS: Serum lactate levels in the first 30 minutes of life do not predict the severity of the ensuing encephalopathy. In contrast, sustained lactic acidosis is associated with severe encephalopathy on EEG and correlates with seizure burden.

Early blood glucose profile and neurodevelopmental outcome at two years in neonatal hypoxic-ischaemic encephalopathy.

LENUS (Irish Health Repository)

Nadeem, Montasser

2012-01-31

BACKGROUND: To examine the blood glucose profile and the relationship between blood glucose levels and neurodevelopmental outcome in term infants with hypoxic-ischaemic encephalopathy. METHODS: Blood glucose values within 72 hours of birth were collected from 52 term infants with hypoxic-ischaemic encephalopathy. Hypoglycaemia [< 46.8 mg\\/dL (2.6 mmol\\/L)] and hyperglycaemia [> 150 mg\\/dL (8.3 mmol\\/L)] were correlated to neurodevelopmental outcome at 24 months of age. RESULTS: Four fifths of the 468 blood samples were in the normoglycaemic range (392\\/468:83.8%). Of the remaining 76 samples, 51.3% were in the hypoglycaemic range and (48.7%) were hyperglycaemic. A quarter of the hypoglycaemic samples (28.2%:11\\/39) and a third of the hyperglycaemic samples (32.4%:12\\/37) were recorded within the first 30 minutes of life. Mean (SD) blood glucose values did not differ between infants with normal and abnormal outcomes [4.89(2.28) mmol\\/L and 5.02(2.35) mmol\\/L, p value = 0.15] respectively. In term infants with hypoxic-ischaemic encephalopathy, early hypoglycaemia (between 0-6 hours of life) was associated with adverse outcome at 24 months of age [OR = 5.8, CI = 1.04-32)]. On multivariate analysis to adjust for grade of HIE this association was not statistically significant. Late hypoglycaemia (6-72 hours of life) was not associated with abnormal outcome [OR = 0.22, CI (0.04-1.14)]. The occurrence of hyperglycaemia was not associated with adverse outcome. CONCLUSION: During the first 72 hours of life, blood glucose profile in infants with hypoxic-ischaemic encephalopathy varies widely despite a management protocol. Early hypoglycaemia (0-6 hours of life) was associated with severe HIE, and thereby; adverse outcome.

Early blood glucose profile and neurodevelopmental outcome at two years in neonatal hypoxic-ischaemic encephalopathy

LENUS (Irish Health Repository)

Nadeem, Montasser

2011-02-04

Abstract Background To examine the blood glucose profile and the relationship between blood glucose levels and neurodevelopmental outcome in term infants with hypoxic-ischaemic encephalopathy. Methods Blood glucose values within 72 hours of birth were collected from 52 term infants with hypoxic-ischaemic encephalopathy. Hypoglycaemia [< 46.8 mg\\/dL (2.6 mmol\\/L)] and hyperglycaemia [> 150 mg\\/dL (8.3 mmol\\/L)] were correlated to neurodevelopmental outcome at 24 months of age. Results Four fifths of the 468 blood samples were in the normoglycaemic range (392\\/468:83.8%). Of the remaining 76 samples, 51.3% were in the hypoglycaemic range and (48.7%) were hyperglycaemic. A quarter of the hypoglycaemic samples (28.2%:11\\/39) and a third of the hyperglycaemic samples (32.4%:12\\/37) were recorded within the first 30 minutes of life. Mean (SD) blood glucose values did not differ between infants with normal and abnormal outcomes [4.89(2.28) mmol\\/L and 5.02(2.35) mmol\\/L, p value = 0.15] respectively. In term infants with hypoxic-ischaemic encephalopathy, early hypoglycaemia (between 0-6 hours of life) was associated with adverse outcome at 24 months of age [OR = 5.8, CI = 1.04-32)]. On multivariate analysis to adjust for grade of HIE this association was not statistically significant. Late hypoglycaemia (6-72 hours of life) was not associated with abnormal outcome [OR = 0.22, CI (0.04-1.14)]. The occurrence of hyperglycaemia was not associated with adverse outcome. Conclusion During the first 72 hours of life, blood glucose profile in infants with hypoxic-ischaemic encephalopathy varies widely despite a management protocol. Early hypoglycaemia (0-6 hours of life) was associated with severe HIE, and thereby; adverse outcome.

Apparent diffusion coefficient histogram analysis of neonatal hypoxic-ischemic encephalopathy

International Nuclear Information System (INIS)

Cauley, Keith A.; Filippi, Christopher G.

2014-01-01

Diffusion-weighted imaging is a valuable tool in the assessment of the neonatal brain, and changes in diffusion are seen in normal development as well as in pathological states such as hypoxic-ischemic encephalopathy (HIE). Various methods of quantitative assessment of diffusion values have been reported. Global ischemic injury occurring during the time of rapid developmental changes in brain myelination can complicate the imaging diagnosis of neonatal HIE. To compare a quantitative method of histographic analysis of brain apparent coefficient (ADC) maps to the qualitative interpretation of routine brain MR imaging studies. We correlate changes in diffusion values with gestational age in radiographically normal neonates, and we investigate the sensitivity of the method as a quantitative measure of hypoxic-ischemic encephalopathy. We reviewed all brain MRI studies from the neonatal intensive care unit (NICU) at our university medical center over a 4-year period to identify cases that were radiographically normal (23 cases) and those with diffuse, global hypoxic-ischemic encephalopathy (12 cases). We histographically displayed ADC values of a single brain slice at the level of the basal ganglia and correlated peak (s-sD av ) and lowest histogram values (s-sD lowest ) with gestational age. Normative s-sD av values correlated significantly with gestational age and declined linearly through the neonatal period (r 2 = 0.477, P av and s-sD lowest ADC values than were reflected in the normative distribution; several cases of HIE fell within a 95% confidence interval for normative studies, and one case demonstrated higher-than-normal s-sD av . Single-slice histographic display of ADC values is a rapid and clinically feasible method of quantitative analysis of diffusion. In this study normative values derived from consecutive neonates without radiographic evidence of ischemic injury are correlated with gestational age, declining linearly throughout the perinatal period. This

Hypoxic ischemic encephalopathy in children : CT findings related to prognosis

International Nuclear Information System (INIS)

Cho, Jae Min; Il, Yim Byung; Kim, Ok Hwa; Kang, Doo Kyoung; Suh, Jung Ho

1997-01-01

To evaluate prognosis-related CT findings in hypoxic ischemic encephalopathy. For the purpose of prognosis, 28 children with a clinical history and CT findings suggestive of hypoxic ischemic encephalopathy (HIE) were restrospectively reviewed. The diagnostic criteria for HIE, as seen on CT scanning, were as follows : 1, ventricular collapse;2, effacement of cortical sulci;3, prominent enhancement of cortical vessels;4, poor differentiation of gray and white matter;5, reversal sign;6, obliteration of perimesencephalic cistern;7, high density on tentorial edge, as seen on precontrast scans;and 8, low density in thalamus, brain stem and basal ganglia. On the basis of clinical outcome, we divided the patients into three groups, as follows:group I(good prognosis);group II(neurologic sequelae), and group III(vegetative state or expire), and among these, compared CT findings. There were thirteen patients in group I, six in group II, and nine in group III. Ventricular collapse, effacement of cortical sulci, and prominent enhancement of cortical vessels were noted in all groups, whereas poor differentiation of gray and white matter, reversal sign, obliteration of perimesencephalic cistern, high density on tentorial edge, on precontrast scan, and low density in brain stem and basal ganglia were observed only in groups II and III. CT findings showed distinct differences between groups in whom prognosis was good, and in whom it was poor. An awareness of poor prognostic CT findings may be clinically helpful in the evaluation of patients with hypoxic ischemic encephalopathy

Cooling for newborns with hypoxic ischaemic encephalopathy.

Science.gov (United States)

Jacobs, Susan E; Berg, Marie; Hunt, Rod; Tarnow-Mordi, William O; Inder, Terrie E; Davis, Peter G

2013-01-31

Newborn animal studies and pilot studies in humans suggest that mild hypothermia following peripartum hypoxia-ischaemia in newborn infants may reduce neurological sequelae without adverse effects. To determine the effect of therapeutic hypothermia in encephalopathic asphyxiated newborn infants on mortality, long-term neurodevelopmental disability and clinically important side effects. We used the standard search strategy of the Cochrane Neonatal Review Group as outlined in The Cochrane Library (Issue 2, 2007). Randomised controlled trials evaluating therapeutic hypothermia in term and late preterm newborns with hypoxic ischaemic encephalopathy were identified by searching the Oxford Database of Perinatal Trials, the Cochrane Central Register of Controlled Trials (CENTRAL, The Cochrane Library, 2007, Issue 2), MEDLINE (1966 to June 2007), previous reviews including cross-references, abstracts, conferences, symposia proceedings, expert informants and journal handsearching. We updated this search in May 2012. We included randomised controlled trials comparing the use of therapeutic hypothermia with standard care in encephalopathic term or late preterm infants with evidence of peripartum asphyxia and without recognisable major congenital anomalies. The primary outcome measure was death or long-term major neurodevelopmental disability. Other outcomes included adverse effects of cooling and 'early' indicators of neurodevelopmental outcome. Four review authors independently selected, assessed the quality of and extracted data from the included studies. Study authors were contacted for further information. Meta-analyses were performed using risk ratios (RR) and risk differences (RD) for dichotomous data, and weighted mean difference for continuous data with 95% confidence intervals (CI). We included 11 randomised controlled trials in this updated review, comprising 1505 term and late preterm infants with moderate/severe encephalopathy and evidence of intrapartum asphyxia

Clinical significance of determination of changes of plasma ET and SS contents in neonates with hypoxic-ischemic encephalopathy (HIE)

International Nuclear Information System (INIS)

Zhang Yuhong; Chen Chuanbing; Li Hua

2008-01-01

Objective: To explore the clinical significance of changes of plasma ET and somatostatin (SS) levels in neonates with hypoxic-ischemic encephalopathy (HIE). Methods: Plasma ET and SS contents were determined with RIA in 63 neonates with hypoxic-ischemic encephalopathy and 35 controls. Results: In neonates with HIE, the plasma ET levels were significantly higher than those in the controls (P<0.01), while the plasma SS levels were significantly lower (P<0.01). Conclusion: Development of hypoxic-ischemic encephalopathy in newborn infants was closely associated with increase of plasma ET and SS levels. (authors)

Rewarming affects EEG background in term newborns with hypoxic-ischemic encephalopathy undergoing therapeutic hypothermia.

Science.gov (United States)

Birca, Ala; Lortie, Anne; Birca, Veronica; Decarie, Jean-Claude; Veilleux, Annie; Gallagher, Anne; Dehaes, Mathieu; Lodygensky, Gregory A; Carmant, Lionel

2016-04-01

To investigate how rewarming impacts the evolution of EEG background in neonates with hypoxic-ischemic encephalopathy (HIE) undergoing therapeutic hypothermia (TH). We recruited a retrospective cohort of 15 consecutive newborns with moderate (9) and severe (6) HIE monitored with a continuous EEG during TH and at least 12h after its end. EEG background was analyzed using conventional visual and quantitative EEG analysis methods including EEG discontinuity, absolute and relative spectral magnitudes. One patient with seizures on rewarming was excluded from analyses. Visual and quantitative analyses demonstrated significant changes in EEG background from pre- to post-rewarming, characterized by an increased EEG discontinuity, more pronounced in newborns with severe compared to moderate HIE. Neonates with moderate HIE also had an increase in the relative magnitude of slower delta and a decrease in higher frequency theta and alpha waves with rewarming. Rewarming affects EEG background in HIE newborns undergoing TH, which may represent a transient adaptive response or reflect an evolving brain injury. EEG background impairment induced by rewarming may represent a biomarker of evolving encephalopathy in HIE newborns undergoing TH and underscores the importance of continuously monitoring the brain health in critically ill neonates. Copyright © 2015 International Federation of Clinical Neurophysiology. Published by Elsevier Ireland Ltd. All rights reserved.

Evolving Understanding of Hypoxic-Ischemic Encephalopathy in the Term Infant

NARCIS (Netherlands)

de Vries, Linda S.; Cowan, Frances M.

2009-01-01

Our aim was to document changes in the evaluation and prognosis of term-born infants with neonatal encephalopathy of hypoxic-ischemic origin, with particular reference to our own experiences and influences, and to summarize the debate on causation and the relative importance of antenatal and

Apparent diffusion coefficient histogram analysis of neonatal hypoxic-ischemic encephalopathy

Energy Technology Data Exchange (ETDEWEB)

Cauley, Keith A. [University of Massachusetts Medical School, Department of Radiology, Worcester, MA (United States); New York Presbyterian Hospital, Columbia University Medical Center, Department of Radiology, New York, NY (United States); Filippi, Christopher G. [New York Presbyterian Hospital, Columbia University Medical Center, Department of Radiology, New York, NY (United States)

2014-06-15

Diffusion-weighted imaging is a valuable tool in the assessment of the neonatal brain, and changes in diffusion are seen in normal development as well as in pathological states such as hypoxic-ischemic encephalopathy (HIE). Various methods of quantitative assessment of diffusion values have been reported. Global ischemic injury occurring during the time of rapid developmental changes in brain myelination can complicate the imaging diagnosis of neonatal HIE. To compare a quantitative method of histographic analysis of brain apparent coefficient (ADC) maps to the qualitative interpretation of routine brain MR imaging studies. We correlate changes in diffusion values with gestational age in radiographically normal neonates, and we investigate the sensitivity of the method as a quantitative measure of hypoxic-ischemic encephalopathy. We reviewed all brain MRI studies from the neonatal intensive care unit (NICU) at our university medical center over a 4-year period to identify cases that were radiographically normal (23 cases) and those with diffuse, global hypoxic-ischemic encephalopathy (12 cases). We histographically displayed ADC values of a single brain slice at the level of the basal ganglia and correlated peak (s-sD{sub av}) and lowest histogram values (s-sD{sub lowest}) with gestational age. Normative s-sD{sub av} values correlated significantly with gestational age and declined linearly through the neonatal period (r {sup 2} = 0.477, P < 0.01). Six of 12 cases of known HIE demonstrated significantly lower s-sD{sub av} and s-sD{sub lowest} ADC values than were reflected in the normative distribution; several cases of HIE fell within a 95% confidence interval for normative studies, and one case demonstrated higher-than-normal s-sD{sub av}. Single-slice histographic display of ADC values is a rapid and clinically feasible method of quantitative analysis of diffusion. In this study normative values derived from consecutive neonates without radiographic evidence of

Effect of Neonatal Seizures on Cognitive Outcome of Hypoxic-Ischemic Encephalopathy

Directory of Open Access Journals (Sweden)

J Gordon Millichap

2009-10-01

Full Text Available The independent effect of clinical neonatal seizures and their treatment on longterm neurodevelopmental outcome in 77 term newborns at risk for hypoxic-ischemic encephalopathy (HIE was determined in a study at University of California San Francisco.

Early MR detection of cortical and subcortical hypoxic-ischemic encephalopathy in full-term-infants

International Nuclear Information System (INIS)

Christophe, C.; Clercx, A.; Blum, D.; Hasaerts, D.; Segebarth, C.; Perlmutter, N.

1994-01-01

Four observations illustrate the potential of MR imaging in the early depiction of multiple types of neuropathologic lesions which may coexist in the full-term newborn, upon severe hypoxic-ischemic encephalopathy (HIE). In particular, diffuse, postnatal involvement of cerebral cortex and subcortical white matter (WM) is demonstrated. Cortical hyperintensity on both proton-density- and T1-weighted images is probably related to cellular necrosis which is distributed diffusely or parasigattally. Hyperintense, frontal, subcortical WM edging on proton-density-weighted images results from the increase of water concentration, induced either by infract or by edema. Diffuse WM areas of low intensity on T1-weighted images and of high intensity on T2-weighted images are presumably related to cytotoxic and/or vasogenic edema, proportional to the underlying damaged tissues. On follow-up MR examinations, several months later, the importance of cortical atrophy and of the myelination delay appeared related to the importance of the lesions detected during the post-natal period. (orig.)

Clinical significance of determination of changes of plasma ET and CGRP contents in neonates with hypoxic-ischemic encephalopathy

International Nuclear Information System (INIS)

Liu Hui; Wang Haifeng; Zhu Hongyan; Chou Weimin; Chen Jing

2007-01-01

Objective: To investigate the clinical significance of changes of plasma ET and CGRP levels in neonates with hypoxic-ischemic encephalopathy (HIE). Methods: Plasma ET and CGRP contents were determined with RIA in 68 neonates with hypoxic -ischemic encephalopathy and 30 controls. Results: In neonates with HIE, the plasma ET levels were significantly higher than those in the controls (P<0.01), while the plasma CGRP levels were significantly lower(P <0.01). Conclusion: Development of hypoxie -isehemic encephalopathy in newborn infants was closely related to the plasma ET and CGRP levels. (authors)

Hypoxic encephalopathy after heart valve replacement: etiology and pathogenesis, diagnostic criteria and treatment

Directory of Open Access Journals (Sweden)

В. Г. Постнов

2015-10-01

Full Text Available Reviewed in this paper are modern approaches in the intensive therapy of acute hypoxic encephalopathy developing in a number of occasions after the heart valve replacement surgery. The study is based on the results of neurological, neuropsychological and neurophysiological (EEG examinations of 240 patients who underwent heart valve replacement surgery under cardiopulmonary bypass conditions complicated later by the development of hypoxic encephalopathies of varying severity and who received complex intensive care. Relying on many years of experience in the treatment of heart surgery patients in whom manifestations of encephalopathy developed in the early postoperative period, or were delayed, we have formulated the following algorithms of therapy. (1 Maintenance of normal blood gas: Hb>100 g/L, pH 7.45, PaCO2 35 mmHg. (2 Maintenance of hemodynamics: ABPsystolic>90 mmHg. (3 Supplying fluids and electrolytes: isoosmolar infusion solutions, adding of KCl and MgSO4 to the infusion. (4 Antiedemic therapy: 15% mannitol or 40% glycerol solution. (5 If necessary (in case of psychomotor agitation, seizures, short-acting barbiturates (sodium thiopental, neuroleptics (haloperidol, propofol. No benzodiazepines in case of psychoses (6 Cerebral metabolism stimulation (not earlier than 48 hours after surgery with cholinomimetics, nootropics, cerebral blood flow protectors. Cholinomimetics are allowed on the first day after surgery. This algorithm and the above-mentioned groups of drugs, especially central cholinomimetics, allow for correcting the neurocognitive impairment in the discussed group of patients quickly and effectively.

Hypothermia broadens the therapeutic time window of mesenchymal stem cell transplantation for severe neonatal hypoxic ischemic encephalopathy.

Science.gov (United States)

Ahn, So Yoon; Chang, Yun Sil; Sung, Dong Kyung; Sung, Se In; Park, Won Soon

2018-05-16

Recently, we have demonstrated that concurrent hypothermia and mesenchymal stem cells (MSCs) transplantation synergistically improved severe neonatal hypoxic ischemic encephalopathy (HIE). The current study was designed to determine whether hypothermia could extend the therapeutic time window of MSC transplantation for severe neonatal HIE. To induce HIE, newborn rat pups were exposed to 8% oxygen for 2 h following unilateral carotid artery ligation on postnatal day (P) 7. After approving severe HIE involving >50% of the ipsilateral hemisphere volume, hypothermia (32 °C) for 2 days was started. MSCs were transplanted 2 days after HIE modeling. Follow-up brain MRI, sensorimotor function tests, assessment of inflammatory cytokines in the cerebrospinal fluid (CSF), and histological evaluation of peri-infarction area were performed. HIE induced progressively increasing brain infarction area over time, increased cell death, reactive gliosis and brain inflammation, and impaired sensorimotor function. All these damages observed in severe HIE showed better, robust improvement with a combination treatment of hypothermia and delayed MSC transplantation than with either stand-alone therapy. Hypothermia itself did not significantly reduce brain injury, but broadened the therapeutic time window of MSC transplantation for severe newborn HIE.

Hypoxic-ischemic encephalopathy in neonates and infants: an evaluation with spiral CT

International Nuclear Information System (INIS)

Zhu Linghua

2006-01-01

Objective: To evaluate spiral CT imaging in the diagnosis of hypoxic-ischemic encephalopathy (HIE) in the neonates and infants. Methods: 112 children with history of asphyxia in peri-natal period and evident clinical symptoms were evaluated with Spiral CT. CT findings were studied. Results: 46 minor cases, 57 moderate cases and 9 severe cases were found out of 112 patients. Intracranial hemorrhage was revealed in 38 cases. Mortality occurred in 1 case. Conclusion: Spiral CT is helpful for evaluating brain damage and predicting prognosis in neonates with HIE. (authors)

Clinical significance of determination of plasma endothelin (ET), thromboxane A2(TXA2) and prostacyclin (PGI2) contents in neonates with hypoxic-ischemic encephalopathy

International Nuclear Information System (INIS)

Liu Hui; Chen Jing; Wang Haifeng; Zhu Hongyan

2008-01-01

Objective: To explore the role of plasma ET, TXA 2 , PGI 2 in the intensification of neonates hypoxic-ischemic encephalopathy. Methods: The concentrations of plasma ET, TXB 2 , 6-keto-PGF 1α were detected with radioimmunoassay in 33 neonates with hypoxic-ischemic encephalopathy and 30 controls. Results: The plasma ET, TXB 2 levels in neonates with hypoxic-ischemic encephalopathy were significantly higher than those in controls (P 1α levels were significantly lower (P 2 but negatively correlated with those of 6-keto-PGF 1α (both P 2 with disturbance of the normal feedback modulation mechanism might play an important role in the pathogenesis of neonates hypoxic-ischemic encephalopathy. (authors)

EEG and MR Spectroscopy in Hypoxic-Ischemic Encephalopathy in Term Newborns

OpenAIRE

J Gordon Millichap

2010-01-01

Researchers from the University of Bologna, Italy, studied the relation of amplitude integrated EEG findings in the first 24 hrs of life to brain metabolic changes, detected by proton MR spectroscopy (H-MRS) at 7-10 days of life, in 32 term newborns with hypoxic-ischemic encephalopathy (HIE).

Features of the Early Adaptation Period of Newborns with Hypoxic-Ischemic Encephalopathy Depending on Birth Weight

Directory of Open Access Journals (Sweden)

Ye.P. Ortemenka

2015-04-01

Full Text Available In the department of neonatal pathology of Chernivtsi regional children’s clinical hospital, 41 full-term newborns with hypoxic-ischemic encephalopathy have been exa­mined in order to study the features of early period of their adaptation depending on birth weight. It was found that the early adaptation period of full-term newborns with hypoxi­­c-ischemic encephalopathy and body weight adequate in terms of gestational age was characterized by: pathological deli­very in one third (32.1 % of cases and the birth of one fourth (25 % of infants with tight nuchal cord that three times more often (22.2 % of neonates led to severe asphyxia, associated with the development of the multiple organ failure (14.3 % of cases and seizures (17.9 % of observations. Full-term children with hypoxic-ischemic encephalopathy and body weight low in terms of gestational age are characterized by: lower gestational age (37–39 weeks at birth (84.6 % of children, which has been associated with young (under 20 years age of mothers in 15.4 % of cases, and twice as likely (61.5 % of children led to respiratory disorders at birth, requiring artificial lung ventilation.

Preferential cephalic redistribution of left ventricular cardiac output during therapeutic hypothermia for perinatal hypoxic-ischemic encephalopathy.

Science.gov (United States)

Hochwald, Ori; Jabr, Mohammad; Osiovich, Horacio; Miller, Steven P; McNamara, Patrick J; Lavoie, Pascal M

2014-05-01

To determine the relationship between left ventricular cardiac output (LVCO), superior vena cava (SVC) flow, and brain injury during whole-body therapeutic hypothermia. Sixteen newborns with moderate or severe hypoxic-ischemic encephalopathy were studied using echocardiography during and immediately after therapeutic hypothermia. Measures were also compared with 12 healthy newborns of similar postnatal age. Newborns undergoing therapeutic hypothermia also had cerebral magnetic resonance imaging as part of routine clinical care on postnatal day 3-4. LVCO was markedly reduced (mean ± SD 126 ± 38 mL/kg/min) during therapeutic hypothermia, whereas SVC flow was maintained within expected normal values (88 ± 27 mL/kg/min) such that SVC flow represented 70% of the LVCO. The reduction in LVCO during therapeutic hypothermia was mainly accounted by a reduction in heart rate (99 ± 13 vs 123 ± 17 beats/min; P newborns without brain injury (P = .013). Newborns with perinatal hypoxic-ischemic encephalopathy showed a preferential systemic-to-cerebral redistribution of cardiac blood flow during whole-body therapeutic hypothermia, which may reflect a lack of cerebral vascular adaptation in newborns with more severe brain injury. Copyright © 2014 Elsevier Inc. All rights reserved.

Prevalence and etiology of false normal aEEG recordings in neonatal hypoxic-ischaemic encephalopathy

OpenAIRE

Marics, Gábor; Csekő, Anna; Vásárhelyi, Barna; Zakariás, Dávid; Schuster, György; Szabó, Miklós

2013-01-01

Background Amplitude-integrated electroencephalography (aEEG) is a useful tool to determine the severity of neonatal hypoxic-ischemic encephalopathy (HIE). Our aim was to assess the prevalence and study the origin of false normal aEEG recordings based on 85 aEEG recordings registered before six hours of age. Methods Raw EEG recordings were reevaluated retrospectively with Fourier analysis to identify and describe the frequency patterns of the raw EEG signal, in cases with inconsistent aEEG re...

Curved reformat of the paediatric brain MRI into a 'flat-earth map' - standardised method for demonstrating cortical surface atrophy resulting from hypoxic-ischaemic encephalopathy.

Science.gov (United States)

Simpson, Ewan; Andronikou, Savvas; Vedajallam, Schadie; Chacko, Anith; Thai, Ngoc Jade

2016-09-01

Hypoxic-ischaemic encephalopathy is optimally imaged with brain MRI in the neonatal period. However neuroimaging is often also performed later in childhood (e.g., when parents seek compensation in cases of alleged birth asphyxia). We describe a standardised technique for creating two curved reconstructions of the cortical surface to show the characteristic surface changes of hypoxic-ischaemic encephalopathy in children imaged after the neonatal period. The technique was applied for 10 cases of hypoxic-ischaemic encephalopathy and also for age-matched healthy children to assess the visibility of characteristic features of hypoxic-ischaemic encephalopathy. In the abnormal brains, fissural or sulcal widening was seen in all cases and ulegyria was identifiable in 7/10. These images could be used as a visual aid for communicating MRI findings to clinicians and other interested parties.

The metabolomic profile of umbilical cord blood in neonatal hypoxic ischaemic encephalopathy.

Directory of Open Access Journals (Sweden)

Brian H Walsh

Full Text Available Hypoxic ischaemic encephalopathy (HIE in newborns can cause significant long-term neurological disability. The insult is a complex injury characterised by energy failure and disruption of cellular homeostasis, leading to mitochondrial damage. The importance of individual metabolic pathways, and their interaction in the disease process is not fully understood. The aim of this study was to describe and quantify the metabolomic profile of umbilical cord blood samples in a carefully defined population of full-term infants with HIE.The injury severity was defined using both the modified Sarnat score and continuous multichannel electroencephalogram. Using these classification systems, our population was divided into those with confirmed HIE (n = 31, asphyxiated infants without encephalopathy (n = 40 and matched controls (n = 71. All had umbilical cord blood drawn and biobanked at -80 °C within 3 hours of delivery. A combined direct injection and LC-MS/MS assay (AbsolutIDQ p180 kit, Biocrates Life Sciences AG, Innsbruck, Austria was used for the metabolomic analyses of the samples. Targeted metabolomic analysis showed a significant alteration between study groups in 29 metabolites from 3 distinct classes (Amino Acids, Acylcarnitines, and Glycerophospholipids. 9 of these metabolites were only significantly altered between neonates with Hypoxic ischaemic encephalopathy and matched controls, while 14 were significantly altered in both study groups. Multivariate Discriminant Analysis models developed showed clear multifactorial metabolite associations with both asphyxia and HIE. A logistic regression model using 5 metabolites clearly delineates severity of asphyxia and classifies HIE infants with AUC = 0.92. These data describe wide-spread disruption to not only energy pathways, but also nitrogen and lipid metabolism in both asphyxia and HIE.This study shows that a multi-platform targeted approach to metabolomic analyses using accurately phenotyped and

Neuroprotective effects of ginsenoside Rg1-induced neural stem cell transplantation on hypoxic-ischemic encephalopathy

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Ying-bo Li

2015-01-01

Full Text Available Ginsenoside Rg1 is the major pharmacologically active component of ginseng, and is reported to have various therapeutic actions. To determine whether it induces the differentiation of neural stem cells, and whether neural stem cell transplantation after induction has therapeutic effects on hypoxic-ischemic encephalopathy, we cultured neural stem cells in 10-80 µM ginsenoside Rg1. Immunohistochemistry revealed that of the concentrations tested, 20 mM ginsenoside Rg1 had the greatest differentiation-inducing effect and was the concentration used for subsequent experiments. Whole-cell patch clamp showed that neural stem cells induced by 20 µM ginsenoside Rg1 were more mature than non-induced cells. We then established neonatal rat models of hypoxic-ischemic encephalopathy using the suture method, and ginsenoside Rg1-induced neural stem cells were transplanted via intracerebroventricular injection. These tests confirmed that neural stem cells induced by ginsenoside had fewer pathological lesions and had a significantly better behavioral capacity than model rats that received saline. Transplanted neural stem cells expressed neuron-specific enolase, and were mainly distributed in the hippocampus and cerebral cortex. The present data suggest that ginsenoside Rg1-induced neural stem cells can promote the partial recovery of complicated brain functions in models of hypoxic-ischemic encephalopathy.

Evaluation of 80 Term Neonates with Hypoxic Ischemic Encephalopathy

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Selahattin Katar

2007-01-01

Full Text Available This study aimed to review the etiology, clinical - laboratory features and mortality rate of term 80 neonates with perinatal asphyxia admitted to our neonatal unit between January 2005-April 2006. The sex distribution was 24 (%30 female and 56 (% 70 male. The mean gestational age was 38.6±1.3 weeks and weight 3156±561 gram. Of the patients % 46.25 were delivered with a cesarean section and % 53.75 with spontaneous vaginal delivery. The etiologic factors for hypoxic ischemic encephalopathy were % 31.25 force delivery, meconium aspiration, and % 66.25 preeclampsia, eclampsia and diabetic mother’s infant. The distribution of patients according to HIE statging system (Sarnat&Sarnat were as follows: 33 patients (% 41.25 in stage 1, 20 (% 25 in stage 2 and 27 (% 33.75 in stage 3. Seizures were observed in % 33.75 of patients. The mean duration of hospital stay was 10.6±7.7 days for the surviving patients and 4.2±3.4 days for patients who died. Except from central nervous system, liver and kidney were the most involved organs.Perinatal asphyxia remains to be leading cause of neonatal mortality. Hypoxic ischemic encephalopathy is a common newborn problem and cause important mortality and morbidity where low-social –cultural –education conditions with in regions.

Detection of butane gas inhalation at 16days after hypoxic encephalopathy: A case report.

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Sato, Takako; Nishioka, Hiroshi; Tsuboi, Kento; Katagi, Munehiro; Miki, Akihiro; Saito, Takashi; Abe, Shuntaro; Nomura, Masakatsu; Kitagawa, Misa; Tsuchihashi, Hitoshi; Suzuki, Koichi

2017-11-01

In Japan, there are increasing reports of death by poisoning following butane abuse. To determine the specific cause of death in such cases, it is important to confirm the presence of fuel gas components in the body, although careful analysis is required because of their volatile properties. In most reported cases, the subject died suddenly during or immediately after butane aspiration. Thus, the butane concentration in the samples from the deceased should be relatively high. Herein, we present a case of an 18-year-old man found with cardiopulmonary arrest, who then exhibited hypoxic encephalopathy for 16days in a hospital. At autopsy, we detected hypoxic encephalopathy, pneumonia, and ischemia-reperfusion injury of the myocardium, while the cause of cardiac arrest remained unclear. Toxicological analysis was then performed for fuel gas components in several specimens collected at autopsy. Results showed that n-butane and isobutane were detected in the adipose tissue at 16days after inhalation, indicating a role of butane gas inhalation as the cause of death. These data suggest that adipose tissue may be the most appropriate analysis sample to be collected at postmortem in cases where involvement of volatile and fat-soluble gas inhalation is suspected. Copyright © 2017 Elsevier B.V. All rights reserved.

Multimodal predictor of neurodevelopmental outcome in newborns with hypoxic-ischaemic encephalopathy.

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Temko, Andriy; Doyle, Orla; Murray, Deirdre; Lightbody, Gordon; Boylan, Geraldine; Marnane, William

2015-08-01

Automated multimodal prediction of outcome in newborns with hypoxic-ischaemic encephalopathy is investigated in this work. Routine clinical measures and 1h EEG and ECG recordings 24h after birth were obtained from 38 newborns with different grades of HIE. Each newborn was reassessed at 24 months to establish their neurodevelopmental outcome. A set of multimodal features is extracted from the clinical, heart rate and EEG measures and is fed into a support vector machine classifier. The performance is reported with the statistically most unbiased leave-one-patient-out performance assessment routine. A subset of informative features, whose rankings are consistent across all patients, is identified. The best performance is obtained using a subset of 9 EEG, 2h and 1 clinical feature, leading to an area under the ROC curve of 87% and accuracy of 84% which compares favourably to the EEG-based clinical outcome prediction, previously reported on the same data. The work presents a promising step towards the use of multimodal data in building an objective decision support tool for clinical prediction of neurodevelopmental outcome in newborns with hypoxic-ischaemic encephalopathy. Copyright © 2015 Elsevier Ltd. All rights reserved.

Curved reformat of the paediatric brain MRI into a 'flat-earth map' - standardised method for demonstrating cortical surface atrophy resulting from hypoxic-ischaemic encephalopathy

International Nuclear Information System (INIS)

Simpson, Ewan; Andronikou, Savvas; Vedajallam, Schadie; Chacko, Anith; Thai, Ngoc Jade

2016-01-01

Hypoxic-ischaemic encephalopathy is optimally imaged with brain MRI in the neonatal period. However neuroimaging is often also performed later in childhood (e.g., when parents seek compensation in cases of alleged birth asphyxia). We describe a standardised technique for creating two curved reconstructions of the cortical surface to show the characteristic surface changes of hypoxic-ischaemic encephalopathy in children imaged after the neonatal period. The technique was applied for 10 cases of hypoxic-ischaemic encephalopathy and also for age-matched healthy children to assess the visibility of characteristic features of hypoxic-ischaemic encephalopathy. In the abnormal brains, fissural or sulcal widening was seen in all cases and ulegyria was identifiable in 7/10. These images could be used as a visual aid for communicating MRI findings to clinicians and other interested parties. (orig.)

Curved reformat of the paediatric brain MRI into a 'flat-earth map' - standardised method for demonstrating cortical surface atrophy resulting from hypoxic-ischaemic encephalopathy

Energy Technology Data Exchange (ETDEWEB)

Simpson, Ewan [Bristol Royal Hospital for Children, Department of Pediatric Radiology, Bristol (United Kingdom); Andronikou, Savvas [Bristol Royal Hospital for Children, Department of Pediatric Radiology, Bristol (United Kingdom); University of Bristol, CRICBristol, Bristol (United Kingdom); Vedajallam, Schadie; Chacko, Anith; Thai, Ngoc Jade [University of Bristol, CRICBristol, Bristol (United Kingdom)

2016-09-15

Hypoxic-ischaemic encephalopathy is optimally imaged with brain MRI in the neonatal period. However neuroimaging is often also performed later in childhood (e.g., when parents seek compensation in cases of alleged birth asphyxia). We describe a standardised technique for creating two curved reconstructions of the cortical surface to show the characteristic surface changes of hypoxic-ischaemic encephalopathy in children imaged after the neonatal period. The technique was applied for 10 cases of hypoxic-ischaemic encephalopathy and also for age-matched healthy children to assess the visibility of characteristic features of hypoxic-ischaemic encephalopathy. In the abnormal brains, fissural or sulcal widening was seen in all cases and ulegyria was identifiable in 7/10. These images could be used as a visual aid for communicating MRI findings to clinicians and other interested parties. (orig.)

Medial Occipital Lobe Hyperperfusion Identified by Arterial Spin-Labeling: A Poor Prognostic Sign in Patients with Hypoxic-Ischemic Encephalopathy.

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de Havenon, A; Sultan-Qurraie, A; Tirschwell, D; Cohen, W; Majersik, J; Andre, J B

2015-12-01

Hypoxic-ischemic encephalopathy carries an uncertain prognosis. We sought to retrospectively assess the prognostic value of arterial spin-labeling MR imaging in 22 adult patients diagnosed with hypoxic-ischemic encephalopathy. Quantitative CBF maps were generated from the M0 map, and arterial spin-labeling data on a per-voxel basis were regionally interrogated via visual inspection and ROI placement. Hyperperfusion was defined as regional increases in CBF of >20% (relative to global CBF) and/or >100 mL/100 g/min. Eleven of 22 patients had prominent bilateral medial occipital lobe hyperperfusion, all of whom died before hospital discharge. One patient who had nondistinct arterial spin-labeling hyperperfusion and restricted diffusion survived. Medial occipital lobe hyperperfusion is a distinctive pattern that merits prospective investigation in a cohort of patients with moderate hypoxic-ischemic encephalopathy to determine its predictive ability in patients with a higher likelihood of survival. © 2015 by American Journal of Neuroradiology.

Term Neonate with Atypical Hypoxic-Ischemic Encephalopathy Presentation: A Case Report.

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Townley, Nick; McNellis, Emily; Sampath, Venkatesh

2017-07-01

We describe a case of atypical hypoxic-ischemic encephalopathy (HIE) in a neonate following a normal pregnancy and delivery who was found to have an umbilical vein thrombosis. The infant arrived to our center with continuous bicycling movement of her lower extremities. She had a continuous electroencephalogram that showed burst suppression and magnetic resonance imaging of the brain showed diffusely abnormal cerebral cortical/subcortical diffusion restriction which may be secondary hypoxic-ischemic injury. Interestingly, a pathology report noted a focal umbilical vein thrombosis appearing to have compressed an umbilical artery with associated arterial dissection and hematoma. Our case illustrates how umbilical venous or arterial thrombosis may be associated with HIE and refractory seizures.

The research of melatonin in hypoxic-ischemic encephalopathy

International Nuclear Information System (INIS)

Sun Bin; Feng Xing; Qian Zhihong; Shi Ming

2006-01-01

Objective: To elucidate the function of melatonin in the pathogenesis and the prognosis of hypoxic-ischemic encephalopathy (HIE) and provide the pathophysiology basis for therapying HIE with melatonin. Methods: The level of plasma melatonin of twenty normal term infants and twenty modest HIE and twenty middle-severity HIE in their acute phase and recovery phase were assayed respectively with radioimmunoassay (RIA). Then compare the difference of the melatonin level among these neonates. Results: (1) For modest HIE, the melatonin level was higher than that in the normal in the acute phase and there was no difference to the normal in the recovery phase. (2) There was no difference between the melatonin level in middle-severity HIE in the acute phase and that in the normal, but in the recovery phase it was higher than that in the normal. (3) For modest HIE, the melatonin level in acute phase was higher than that in the recovery phase, but for middle-severity HIE, it was adverse. (4) In the acute phase, the level in modest HIE was higher than that in the middle-severity HIE, but on the contrary in the recovery phase. Conclusion: Melatonin have protection action on HIE. The prognosis of modest HIE neonates with rising melatonin level in the acute phase is better than that with lower melatonin level of middle-severity HIE. (authors)

The Correlation Between a Short-term Conventional Electroencephalography in the First Day of Life and Brain Magnetic Resonance Imaging in Newborns Undergoing Hypothermia for Hypoxic-Ischemic Encephalopathy.

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Obeid, Rawad; Sogawa, Yoshimi; Gedela, Satyanarayana; Naik, Monica; Lee, Vince; Telesco, Richard; Wisnowski, Jessica; Magill, Christine; Painter, Michael J; Panigrahy, Ashok

2017-02-01

Electroencephalograph recorded in the first day of life in newborns treated with hypothermia for hypoxic-ischemic encephalopathy could be utilized as a predictive tool for the severity of brain injury on magnetic resonance imaging and mortality. We analyzed newborns who were admitted for therapeutic hypothermia due to hypoxic-ischemic encephalopathy. All enrolled infants underwent encephalography within the first 24 hours of life and underwent brain magnetic resonance imaging after rewarming. All encephalographs were independently reviewed for background amplitude, continuity, and variability. Brain injury determined by magnetic resonance imaging was scored using methods described by Bonifacio et al. Forty-one newborns were included in the study. Each encephalograph variable correlated significantly with the severity of injury on brain magnetic resonance imaging (P encephalopathy correlated with the extent of injury on brain magnetic resonance imaging. This information may be useful for families and aid guide clinical decision making. Copyright © 2017 Elsevier Inc. All rights reserved.

Safety and efficacy of topiramate in neonates with hypoxic ischemic encephalopathy treated with hypothermia (NeoNATI)

Science.gov (United States)

2012-01-01

Background Despite progresses in neonatal care, the mortality and the incidence of neuro-motor disability after perinatal asphyxia have failed to show substantial improvements. In countries with a high level of perinatal care, the incidence of asphyxia responsible for moderate or severe encephalopathy is still 2–3 per 1000 term newborns. Recent trials have demonstrated that moderate hypothermia, started within 6 hours after birth and protracted for 72 hours, can significantly improve survival and reduce neurologic impairment in neonates with hypoxic-ischemic encephalopathy. It is not currently known whether neuroprotective drugs can further improve the beneficial effects of hypothermia. Topiramate has been proven to reduce brain injury in animal models of neonatal hypoxic ischemic encephalopathy. However, the association of mild hypothermia and topiramate treatment has never been studied in human newborns. The objective of this research project is to evaluate, through a multicenter randomized controlled trial, whether the efficacy of moderate hypothermia can be increased by concomitant topiramate treatment. Methods/Design Term newborns (gestational age ≥ 36 weeks and birth weight ≥ 1800 g) with precocious metabolic, clinical and electroencephalographic (EEG) signs of hypoxic-ischemic encephalopathy will be randomized, according to their EEG pattern, to receive topiramate added to standard treatment with moderate hypothermia or standard treatment alone. Topiramate will be administered at 10 mg/kg once a day for the first 3 days of life. Topiramate concentrations will be measured on serial dried blood spots. 64 participants will be recruited in the study. To evaluate the safety of topiramate administration, cardiac and respiratory parameters will be continuously monitored. Blood samplings will be performed to check renal, liver and metabolic balance. To evaluate the efficacy of topiramate, the neurologic outcome of enrolled newborns will be evaluated by serial

Safety and efficacy of topiramate in neonates with hypoxic ischemic encephalopathy treated with hypothermia (NeoNATI

Directory of Open Access Journals (Sweden)

Filippi Luca

2012-09-01

Full Text Available Abstract Background Despite progresses in neonatal care, the mortality and the incidence of neuro-motor disability after perinatal asphyxia have failed to show substantial improvements. In countries with a high level of perinatal care, the incidence of asphyxia responsible for moderate or severe encephalopathy is still 2–3 per 1000 term newborns. Recent trials have demonstrated that moderate hypothermia, started within 6 hours after birth and protracted for 72 hours, can significantly improve survival and reduce neurologic impairment in neonates with hypoxic-ischemic encephalopathy. It is not currently known whether neuroprotective drugs can further improve the beneficial effects of hypothermia. Topiramate has been proven to reduce brain injury in animal models of neonatal hypoxic ischemic encephalopathy. However, the association of mild hypothermia and topiramate treatment has never been studied in human newborns. The objective of this research project is to evaluate, through a multicenter randomized controlled trial, whether the efficacy of moderate hypothermia can be increased by concomitant topiramate treatment. Methods/Design Term newborns (gestational age ≥ 36 weeks and birth weight ≥ 1800 g with precocious metabolic, clinical and electroencephalographic (EEG signs of hypoxic-ischemic encephalopathy will be randomized, according to their EEG pattern, to receive topiramate added to standard treatment with moderate hypothermia or standard treatment alone. Topiramate will be administered at 10 mg/kg once a day for the first 3 days of life. Topiramate concentrations will be measured on serial dried blood spots. 64 participants will be recruited in the study. To evaluate the safety of topiramate administration, cardiac and respiratory parameters will be continuously monitored. Blood samplings will be performed to check renal, liver and metabolic balance. To evaluate the efficacy of topiramate, the neurologic outcome of enrolled newborns

Effect of Therapeutic Hypothermia Initiated After 6 Hours of Age on Death or Disability Among Newborns With Hypoxic-Ischemic Encephalopathy

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Laptook, Abbot R.; Shankaran, Seetha; Tyson, Jon E.; Munoz, Breda; Bell, Edward F.; Goldberg, Ronald N.; Parikh, Nehal A.; Ambalavanan, Namasivayam; Pedroza, Claudia; Pappas, Athina; Das, Abhik; Chaudhary, Aasma S.; Ehrenkranz, Richard A.; Hensman, Angelita M.; Van Meurs, Krisa P.; Chalak, Lina F.; Hamrick, Shannon E. G.; Sokol, Gregory M.; Walsh, Michele C.; Poindexter, Brenda B.; Faix, Roger G.; Watterberg, Kristi L.; Frantz, Ivan D.; Guillet, Ronnie; Devaskar, Uday; Truog, William E.; Chock, Valerie Y.; Wyckoff, Myra H.; McGowan, Elisabeth C.; Carlton, David P.; Harmon, Heidi M.; Brumbaugh, Jane E.; Cotten, C. Michael; Sánchez, Pablo J.; Hibbs, Anna Maria; Higgins, Rosemary D.

2018-01-01

IMPORTANCE Hypothermia initiated at less than 6 hours after birth reduces death or disability for infants with hypoxic-ischemic encephalopathy at 36 weeks’ or later gestation. To our knowledge, hypothermia trials have not been performed in infants presenting after 6 hours. OBJECTIVE To estimate the probability that hypothermia initiated at 6 to 24 hours after birth reduces the risk of death or disability at 18 months among infants with hypoxic-ischemic encephalopathy. DESIGN, SETTING, AND PARTICIPANTS A randomized clinical trial was conducted between April 2008 and June 2016 among infants at 36 weeks’ or later gestation with moderate or severe hypoxic-ischemic encephalopathy enrolled at 6 to 24 hours after birth. Twenty-one US Neonatal Research Network centers participated. Bayesian analyses were prespecified given the anticipated limited sample size. INTERVENTIONS Targeted esophageal temperature was used in 168 infants. Eighty-three hypothermic infants were maintained at 33.5°C (acceptable range, 33°C–34°C) for 96 hours and then rewarmed. Eighty-five noncooled infants were maintained at 37.0°C (acceptable range, 36.5°C–37.3°C). MAIN OUTCOMES AND MEASURES The composite of death or disability (moderate or severe) at 18 to 22 months adjusted for level of encephalopathy and age at randomization. RESULTS Hypothermic and noncooled infants were term (mean [SD], 39 [2] and 39 [1] weeks’ gestation, respectively), and 47 of 83 (57%) and 55 of 85 (65%) were male, respectively. Both groups were acidemic at birth, predominantly transferred to the treating center with moderate encephalopathy, and were randomized at a mean (SD) of 16 (5) and 15 (5) hours for hypothermic and noncooled groups, respectively. The primary outcome occurred in 19 of 78 hypothermic infants (24.4%) and 22 of 79 noncooled infants (27.9%) (absolute difference, 3.5%; 95% CI, −1% to 17%). Bayesian analysis using a neutral prior indicated a 76% posterior probability of reduced death or

Therapeutic hypothermia in the prevention of hypoxic-ischaemic encephalopathy: new categories to be enrolled.

Science.gov (United States)

Gancia, Paolo; Pomero, Giulia

2012-10-01

Therapeutic hypothermia is now the standard of care for brain injury control in term infants with perinatal hypoxic ischemic encephalopathy (HIE). Accumulated evidence shows a reduction in mortality and long-term neurodevelopmental disability at 12-24 months of age, with more favourable effects in the less severe forms of HIE. Only few trials recruited newborns encephalopathy with base deficit (BD) newborns with stroke. Preterm HIE: Therapeutic hypothermia shows a good safety profile in clinical studies, and no adverse effects were noted in the preterm fetal animal model. Recently, it has been shown that mild hypothermia in preterm newborns with necrotizing enterocolitis (NEC) and multiple organ dysfunction syndrome (MODS) does not increase mortality, bleeding, infection, or need for inotropes in cooled newborns. A pilot study (NCT00620711) is currently recruiting newborns of > 32 but newborn. In a systematic review and meta-analysis of animal studies of focal cerebral ischemia, hypothermia reduced the infarct size by 44%. No specific neuroprotective interventions are available for the management of acute perinatal stroke. Hypothermia may decrease seizures in newborns with encephalopathy and a focal infarct, potentially improving the long-term outcome for these infants. Future studies of therapeutic hypothermia should include the categories of newborns excluded from the published clinical trials, that is infants encephalopathy not imputable to HIE. New entry criteria will allow significant number of newborns to benefit from the treatment.

[Magnesium sulphate in the treatment of ischemic-hypoxic neonatal encephalopathy].

Science.gov (United States)

Kornacka, M K

2001-01-01

Hypoxic-ischaemic encephalopathy (HIE) remains one of the most important neurological complications in full and near full term newborns. During HIE glutamate and other excitatory neurotransmitters are released and progressive energy failure in brain is observed. Toxicity of glutamate plays the main role in brain injury. Glutamate activates the specific receptors that, in turn, mediate an overwhelming influx of calcium into the postsynaptic neuron. The pathological changes are located particularly in hippocampus. Magnesium sulfate has been used safely for years to treat preclampsia. The animal experimental evidence support a neuroprotective role for magnesium in HIE.

[Isolated severe neurologic disorders in post-partum: posterior reversible encephalopathy syndrome].

Science.gov (United States)

Wernet, A; Benayoun, L; Yver, C; Bruno, O; Mantz, J

2007-01-01

Just after Caesarean section for twin pregnancy and feto-pelvic dysproportion, a woman presented severe headaches and arterial hypertension, then blurred vision, then generalised seizures. There were no oedematous syndrome, proteinuria was negative, ASAT were 1.5 N and platelet count was 120,000/mm(3). Cerebral CT-scan was normal. Posterior reversible encephalopathy syndrome (PRES) was diagnosed on MRI. A second MRI performed at day 9 showed complete regression of cerebral lesions, while patient was taking anti-hypertensive and antiepileptic drugs. PRES has to be evoked in post-partum central neurological symptoms, even in absence of classical sign of pre-eclampsia, like proteinuria. PRES and eclampsia share probably common physiopathological pathways. There management and prognosis seems identical.

An unusual cause of anemia and encephalopathy

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Sanjeev Kumar Sharma

2015-04-01

Full Text Available The authors present here an interesting case of recent onset anemia that was associated with an encephalopathy of the unusual cause.Although severe anemia can theoretically result in anemic hypoxia and can then lead to hypoxic encephalopathy, it is not a primary cause of encephalopathy. More frequently anemia can contribute together with other multiple causes of encephalopathy, such as infections, metabolic abnormalities, trauma, hepatic dysfunction, hypertension, toxins.

Pathophysiology of perinatal hypoxic-ischemic encephalopathy – biomarkers, animal models and treatment perspectives

Czech Academy of Sciences Publication Activity Database

Riljak, V.; Kraf, J.; Daryanani, A.; Jiruška, Přemysl; Otáhal, Jakub

2016-01-01

Roč. 65, Suppl.5 (2016), S533-S545 ISSN 0862-8408 R&D Projects: GA MZd(CZ) NV15-33115A; GA ČR(CZ) GA15-08565S; GA ČR(CZ) GA14-02634S; GA MŠk LM2015062 Institutional support: RVO:67985823 Keywords : hypoxic-ischemic encephalopathy * excitotoxicity * oxidative stress * inflammation * biomarkers Subject RIV: FH - Neurology Impact factor: 1.461, year: 2016

Induced hypothermia for infants with hypoxic- ischemic encephalopathy using a servo-controlled fan: an exploratory pilot study.

Science.gov (United States)

Horn, Alan; Thompson, Clare; Woods, David; Nel, Alida; Bekker, Adrie; Rhoda, Natasha; Pieper, Clarissa

2009-06-01

Several trials suggest that hypothermia is beneficial in selected infants with hypoxic-ischemic encephalopathy. However, the cooling methods used required repeated interventions and were either expensive or reported significant temperature variation. The objective of this pilot study was to describe the use, efficacy, and physiologic impact of an inexpensive servo-controlled cooling fan blowing room-temperature air. A servo-controlled fan was manufactured and used to cool 10 infants with hypoxic-ischemic encephalopathy to a rectal temperature of 33 degrees C to 34 degrees C. The infants were sedated with phenobarbital, but clonidine was administered to some infants if shivering or discomfort occurred. A servo-controlled radiant warmer was used simultaneously with the fan to prevent overcooling. The settings used on the fan and radiant warmer differed slightly between some infants as the technique evolved. A rectal temperature of 34 degrees C was achieved in a median time of 58 minutes. Overcooling did not occur, and the mean temperature during cooling was 33.6 degrees C +/- 0.2 degrees C. Inspired oxygen requirements increased in 6 infants, and 5 infants required inotropic support during cooling, but this was progressively reduced after 1 to 2 days. Dehydration did not occur. Five infants shivered when faster fan speeds were used, but 4 of the 5 infants had hypomagnesemia. Shivering was controlled with clonidine in 4 infants, but 1 infant required morphine. Servo-controlled fan cooling with room-temperature air, combined with servo-controlled radiant warming, was an effective, simple, and safe method of inducing and maintaining rectal temperatures of 33 degrees C to 34 degrees C in sedated infants with hypoxic-ischemic encephalopathy. After induction of hypothermia, a low fan speed facilitated accurate temperature control, and warmer-controlled rewarming at 0.2 degrees C increments every 30 minutes resulted in more appropriate rewarming than when 0.5 degrees C

Melatonin in the management of perinatal hypoxic-ischemic encephalopathy: light at the end of the tunnel?

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Hendaus MA

2016-09-01

Full Text Available Mohamed A Hendaus,1,2 Fatima A Jomha,3 Ahmed H Alhammadi1,2 1Department of Pediatrics, Section of Academic General Pediatrics, Hamad Medical Corporation, 2Department of Clinical Pediatrics, Weill-Cornell Medical College, Doha, Qatar; 3School of Pharmacy, Lebanese International University, Khiara, Lebanon Abstract: Perinatal hypoxic-ischemic encephalopathy (HIE affects one to three per 1,000 live full-term births and can lead to severe and permanent neuropsychological sequelae, such as cerebral palsy, epilepsy, mental retardation, and visual motor or visual perceptive dysfunction. Melatonin has begun to be contemplated as a good choice in order to diminish the neurological sequelae from hypoxic-ischemic brain injury. Melatonin emerges as a very interesting medication, because of its capacity to cross all physiological barriers extending to subcellular compartments and its safety and effectiveness. The purpose of this commentary is to detail the evidence on the use of melatonin as a neuroprotection agent. The pharmacologic aspects of the drug as well as its potential neuroprotective characteristics in human and animal studies are described in this study. Melatonin seems to be safe and beneficial in protecting neonatal brains from perinatal HIE. Larger randomized controlled trials in humans are required, to implement a long-awaited feasible treatment in order to avoid the dreaded sequelae of HIE. Keywords: melatonin, hypoxia, use, encephalopathy

Effect of Therapeutic Hypothermia Initiated After 6 Hours of Age on Death or Disability Among Newborns With Hypoxic-Ischemic Encephalopathy: A Randomized Clinical Trial.

Science.gov (United States)

Laptook, Abbot R; Shankaran, Seetha; Tyson, Jon E; Munoz, Breda; Bell, Edward F; Goldberg, Ronald N; Parikh, Nehal A; Ambalavanan, Namasivayam; Pedroza, Claudia; Pappas, Athina; Das, Abhik; Chaudhary, Aasma S; Ehrenkranz, Richard A; Hensman, Angelita M; Van Meurs, Krisa P; Chalak, Lina F; Khan, Amir M; Hamrick, Shannon E G; Sokol, Gregory M; Walsh, Michele C; Poindexter, Brenda B; Faix, Roger G; Watterberg, Kristi L; Frantz, Ivan D; Guillet, Ronnie; Devaskar, Uday; Truog, William E; Chock, Valerie Y; Wyckoff, Myra H; McGowan, Elisabeth C; Carlton, David P; Harmon, Heidi M; Brumbaugh, Jane E; Cotten, C Michael; Sánchez, Pablo J; Hibbs, Anna Maria; Higgins, Rosemary D

2017-10-24

Hypothermia initiated at less than 6 hours after birth reduces death or disability for infants with hypoxic-ischemic encephalopathy at 36 weeks' or later gestation. To our knowledge, hypothermia trials have not been performed in infants presenting after 6 hours. To estimate the probability that hypothermia initiated at 6 to 24 hours after birth reduces the risk of death or disability at 18 months among infants with hypoxic-ischemic encephalopathy. A randomized clinical trial was conducted between April 2008 and June 2016 among infants at 36 weeks' or later gestation with moderate or severe hypoxic-ischemic encephalopathy enrolled at 6 to 24 hours after birth. Twenty-one US Neonatal Research Network centers participated. Bayesian analyses were prespecified given the anticipated limited sample size. Targeted esophageal temperature was used in 168 infants. Eighty-three hypothermic infants were maintained at 33.5°C (acceptable range, 33°C-34°C) for 96 hours and then rewarmed. Eighty-five noncooled infants were maintained at 37.0°C (acceptable range, 36.5°C-37.3°C). The composite of death or disability (moderate or severe) at 18 to 22 months adjusted for level of encephalopathy and age at randomization. Hypothermic and noncooled infants were term (mean [SD], 39 [2] and 39 [1] weeks' gestation, respectively), and 47 of 83 (57%) and 55 of 85 (65%) were male, respectively. Both groups were acidemic at birth, predominantly transferred to the treating center with moderate encephalopathy, and were randomized at a mean (SD) of 16 (5) and 15 (5) hours for hypothermic and noncooled groups, respectively. The primary outcome occurred in 19 of 78 hypothermic infants (24.4%) and 22 of 79 noncooled infants (27.9%) (absolute difference, 3.5%; 95% CI, -1% to 17%). Bayesian analysis using a neutral prior indicated a 76% posterior probability of reduced death or disability with hypothermia relative to the noncooled group (adjusted posterior risk ratio, 0.86; 95% credible interval

Hypoxic ischemic encephalopathy in newborns linked to placental and umbilical cord abnormalities.

Science.gov (United States)

Nasiell, Josefine; Papadogiannakis, Nikos; Löf, Erika; Elofsson, Fanny; Hallberg, Boubou

2016-03-01

Birth asphyxia and hypoxic ischemic encephalopathy (HIE) of the newborn remain serious complications. We present a study investigating if placental or umbilical cord abnormalities in newborns at term are associated with HIE. A prospective cohort study of the placenta and umbilical cord of infants treated with hypothermia (HT) due to hypoxic brain injury and follow-up at 12 months of age has been carried out. The study population included 41 infants treated for HT whose placentas were submitted for histopathological analysis. Main outcome measures were infant development at 12 months, classified as normal, cerebral palsy, or death. A healthy group of 100 infants without HIE and normal follow-up at 12 months of age were used as controls. A velamentous or marginal umbilical cord insertion and histological abruption was associated with the risk of severe HIE, OR = 5.63, p = 0.006, respectively, OR = 20.3, p = 0.01 (multiple-logistic regression). Velamentous or marginal umbilical cord insertion was found in 39% among HIE cases compared to 7% in controls. Placental and umbilical cord abnormalities have a profound association with HIE. A prompt examination of the placentas of newborns suffering from asphyxia can provide important information on the pathogenesis behind the incident and contribute to make a better early prognosis.

Hypothermia for neonatal hypoxic-ischemic encephalopathy: NICHD Neonatal Research Network contribution to the field.

Science.gov (United States)

Shankaran, Seetha; Natarajan, Girija; Chalak, Lina; Pappas, Athina; McDonald, Scott A; Laptook, Abbot R

2016-10-01

In this article, we summarize the NICHD Neonatal Research Network (NRN) trial of whole-body hypothermia for neonates with hypoxic-ischemic encephalopathy in relation to other randomized controlled trials (RCTs) of hypothermia neuroprotection. We describe the NRN secondary studies that have been published in the past 10 years evaluating clinical, genetic, biochemical, and imaging biomarkers of outcome. Copyright © 2016 Elsevier Inc. All rights reserved.

Early predictors of brain damage in full-term newborns with hypoxic ischemic encephalopathy

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Alkholy UM

2017-08-01

Full Text Available Usama M Alkholy,1 Nermin Abdalmonem,1 Ahmed Zaki,2 Yasser F Ali,1 Soma Abdalla Mohamed,3 Nasser I Abdelsalam,1 Mustafa Ismail Abu Hashim,1 Mohamed Abou Sekkien,3 Yasser Makram Elsherbiny4 1Pediatric Department, Zagazig University, Egypt; 2Pediatric Department, Mansoura University, Egypt; 3Pediatric Department, Al Azhar University, Egypt; 4Clinical Pathology Department, Menoufia University, Egypt Objective of the study: To evaluate the value of serum creatine phosphokinase-brain specific (CK-BB and urinary lactate/creatinine (L/C ratio as early indicators of brain damage in full-term newborns with hypoxic ischemic encephalopathy (HIE.Patients and methods: A case–control study including 25 full-term new-born infants with perinatal asphyxia who were admitted to neonatal intensive care unit (NICU with a proven diagnosis of HIE, compared to 20 healthy age- and sex-matched full-term newborns. All newborn infants were subjected to full history taking, clinical examination, routine investigations (cord blood gases and complete blood picture, and assessment of serum CK-BB (cord blood, 6 and 24 hours after birth and urinary L/C ratio (collected within the first 6 hours, on the 2nd and 3rd day after birth.Results: The serum CK-BB and urinary L/C ratio in infants with HIE were significantly higher in samples collected throughout the monitoring period when compared with the control group (all P<0.001. The cord CK-BB and urinary L/C ratio within the first 6 hours were significantly higher in infants with severe HIE than in infants with mild and moderate HIE (P<0.001. Cord CK-BB level at 12.5 U/L had 100% sensitivity and 84% specificity in the detection of severe HIE infants. Urinary L/C ratio of more than 10.5 collected within the first 6 hours after birth had 100% sensitivity and 78% specificity for the detection of severe HIE infants.Conclusion: The serum CK-BB and urinary L/C ratio in HIE infants were significantly increased early in the course of the

[Neuroprotection with hypothermia in the newborn with hypoxic-ischaemic encephalopathy. Standard guidelines for its clinical application].

Science.gov (United States)

Blanco, D; García-Alix, A; Valverde, E; Tenorio, V; Vento, M; Cabañas, F

2011-11-01

Standardisation of hypothermia as a treatment for perinatal hypoxic-ischaemic encephalopathy is supported by current scientific evidence. The following document was prepared by the authors on request of the Spanish Society of Neonatology and is intended to be a guide for the proper implementation of this therapy. We discuss the difficulties that may arise when moving from the strict framework of clinical trials to clinical daily care: early recognition of clinical encephalopathy, inclusion and exclusion criteria, hypothermia during transport, type of hypothermia (selective head or systemic cooling) and side effects of therapy. The availability of hypothermia therapy has changed the prognosis of children with hypoxic-ischaemic encephalopathy and our choices of therapeutic support. In this sense, it is especially important to be aware of the changes in the predictive value of the neurological examination and the electroencephalographic recording in cooled infants. In order to improve neuroprotection with hypothermia we need earlier recognition of to recognise earlier the infants that may benefit from cooling. Biomarkers of brain injury could help us in the selection of these patients. Every single infant treated with hypothermia must be included in a follow up program in order to assess neurodevelopmental outcome. Copyright © 2011 Asociación Española de Pediatría. Published by Elsevier Espana. All rights reserved.

The clinical significance of determining the plasma superoxide dismutase and neuropeptide Y in newborn hypoxic-ischemic encephalopathy

International Nuclear Information System (INIS)

Xu Xuezhong; Cui Zhenxing

2002-01-01

Objective: To investigate the contents of plasma superoxide dismutase (SOD) and neuropeptide Y (NPY) in newborn hypoxic-ischemic encephalopathy (HIE) babies in various clinic stages and their clinical significance. Methods: The plasma levels of SOD and NPY of 63 HIE babies and controls were determined by radioimmunoassay (RIA) and the values were studied for different clinical stages (severe 22, moderate 7 and mild 24). Results: The contents of plasma SOD and NPY of HIE babies of various stages were different and there existed remarkable contrast between those in patients and controls (p<0.05 or p<0.01). Conclusion: The contents of plasma SOD and NPY in HIE neonates were correlated to the clinic stage and severeness of the disease process

Prevalence, severity and early outcomes of hypoxic ischemic encephalopathy among newborns at a tertiary hospital, in northern Tanzania.

Science.gov (United States)

Simiyu, Irene N; Mchaile, Deborah N; Katsongeri, Kahindo; Philemon, Rune N; Msuya, Sia E

2017-05-25

Hypoxic Ischemic Encephalopathy (HIE) remains a problem of great concern worldwide especially in developing countries. The occurrence of a neurological syndrome can be an indicator of insult to the brain. We aimed to determine the prevalence, HIE proportions, neurological signs and early outcomes of newborns that developed birth asphyxia at KCMC Tanzania. A prospective study was conducted at KCMC from November 2014 to April 2015 among newborns with birth asphyxia. Sarnat and Sarnat score was used to assess newborns immediately after birth to classify HIE and were later followed daily for 7 days or until discharge. Of the 1752 deliveries during the study period, 11.5% (n = 201) had birth asphyxia. Of the 201 newborns, 187 had HIE. Of these 187 with HIE; 39.0% had moderate HIE and 10.2% had severe HIE according to the Sarnat and Sarnat classification. Neurological signs that were observed during the study period were; weak/absent reflexes (46.0%), hypotonia (43.3%) and lethargy (42.2%). Mortality was 9.1% among the 187 newborns with HIE. Mortality was higher among newborns with severe HIE 84.2% (16/19) compared to those with moderate HIE 1.4% (1/73). On the 7th day after delivery, 17.1% (32/187) of the newborns did not show any change from the initial score at delivery. Prevalence of birth asphyxia is high in our setting and most of the newborns (49%) end up with moderate/severe HIE. Good obstetric care and immediate resuscitation of newborns are vital in reducing the occurrence of HIE and improving the general outcome of newborns.

Impact of perinatal systemic hypoxic-ischemic injury on the brain of male offspring rats: an improved model of neonatal hypoxic-ischemic encephalopathy in early preterm newborns.

Directory of Open Access Journals (Sweden)

Yuejun Huang

Full Text Available In this study, we attempted to design a model using Sprague-Dawley rats to better reproduce perinatal systemic hypoxic-ischemic encephalopathy (HIE in early preterm newborns. On day 21 of gestation, the uterus of pregnant rats were exposed and the blood supply to the fetuses of neonatal HIE groups were thoroughly abscised by hemostatic clamp for 5, 10 or 15 min. Thereafter, fetuses were moved from the uterus and manually stimulated to initiate breathing in an incubator at 37 °C for 1 hr in air. We showed that survival rates of offspring rats were decreased with longer hypoxic time. TUNEL staining showed that apoptotic cells were significant increased in the brains of offspring rats from the 10 min and 15 min HIE groups as compared to the offspring rats in the control group at postnatal day (PND 1, but there was no statistical difference between the offspring rats in the 5 min HIE and control groups. The perinatal hypoxic treatment resulted in decreased neurons and increased cleaved caspase-3 protein levels in the offspring rats from all HIE groups at PND 1. Platform crossing times and the percentage of the time spent in the target quadrant of Morris Water Maze test were significantly reduced in the offspring rats of all HIE groups at PND 30, which were associated with decreased brain-derived neurotrophic factor levels and neuronal cells in the hippocampus of offspring rats at PND 35. These data demonstrated that perinatal ischemic injury led to the death of neuronal cells and long-lasting impairment of memory. This model reproduced hypoxic ischemic encephalopathy in early preterm newborns and may be appropriate for investigating therapeutic interventions.

Fetal heart rate patterns in neonatal hypoxic-ischemic encephalopathy: relationship with early cerebral activity and neurodevelopmental outcome.

LENUS (Irish Health Repository)

Murray, Deirdre M

2009-09-01

Despite widespread use of fetal heart rate monitoring, the timing of injury in hypoxic-ischemic encephalopathy (HIE) remains unclear. Our aim was to examine fetal heart rate patterns during labor in infants with clinical and electroencephalographic (EEG) evidence of HIE and to relate these findings to neurodevelopmental outcome. Timing of onset of pathological cardiotocographs (CTGs) was determined in each case by two blinded reviewers and related to EEG grade at birth and neurological outcome at 24 months. CTGs were available in 35 infants with HIE (17 mild, 12 moderate, 6 severe on EEG). Admission CTGs were normal in 24\\/35 (69%), suspicious in 8\\/35 (23%), and pathological in 3\\/35 (8%). All CTGs developed nonreassuring features prior to delivery. Three patterns of fetal heart rate abnormalities were seen: group 1, abnormal CTGs on admission in 11\\/35 (31%); group 2, normal CTGs on admission with gradual deterioration to pathological in 20\\/35 cases (57%); and group 3, normal CTGs on admission with acute sentinel events in 4\\/35 (11.5%). The median (interquartile range) duration between the development of pathological CTGs and delivery was 145 (81, 221) minutes in group 2 and 22 (12, 28) minutes in group 3. There was no correlation between duration of pathological CTG trace and grade of encephalopathy (R = 0.09, P = 0.63) or neurological outcome (P = 0.75). However, the grade of encephalopathy was significantly worse in group 3 (P = 0.001), with a trend to worse outcomes. The majority of infants with HIE have normal CTG traces on admission but develop pathological CTG patterns within hours of delivery. More severe encephalopathy was associated with normal admission CTG and acute sentinel events shortly before delivery.

Fetal heart rate patterns in neonatal hypoxic-ischemic encephalopathy: relationship with early cerebral activity and neurodevelopmental outcome.

LENUS (Irish Health Repository)

Murray, Deirdre M

2012-01-31

Despite widespread use of fetal heart rate monitoring, the timing of injury in hypoxic-ischemic encephalopathy (HIE) remains unclear. Our aim was to examine fetal heart rate patterns during labor in infants with clinical and electroencephalographic (EEG) evidence of HIE and to relate these findings to neurodevelopmental outcome. Timing of onset of pathological cardiotocographs (CTGs) was determined in each case by two blinded reviewers and related to EEG grade at birth and neurological outcome at 24 months. CTGs were available in 35 infants with HIE (17 mild, 12 moderate, 6 severe on EEG). Admission CTGs were normal in 24\\/35 (69%), suspicious in 8\\/35 (23%), and pathological in 3\\/35 (8%). All CTGs developed nonreassuring features prior to delivery. Three patterns of fetal heart rate abnormalities were seen: group 1, abnormal CTGs on admission in 11\\/35 (31%); group 2, normal CTGs on admission with gradual deterioration to pathological in 20\\/35 cases (57%); and group 3, normal CTGs on admission with acute sentinel events in 4\\/35 (11.5%). The median (interquartile range) duration between the development of pathological CTGs and delivery was 145 (81, 221) minutes in group 2 and 22 (12, 28) minutes in group 3. There was no correlation between duration of pathological CTG trace and grade of encephalopathy (R = 0.09, P = 0.63) or neurological outcome (P = 0.75). However, the grade of encephalopathy was significantly worse in group 3 (P = 0.001), with a trend to worse outcomes. The majority of infants with HIE have normal CTG traces on admission but develop pathological CTG patterns within hours of delivery. More severe encephalopathy was associated with normal admission CTG and acute sentinel events shortly before delivery.

MRI of neonatal encephalopathy

International Nuclear Information System (INIS)

Khong, P.L.; Lam, B.C.C.; Tung, H.K.S.; Wong, V.; Chan, F.L.; Ooi, G.C.

2003-01-01

We present the magnetic resonance imaging (MRI) findings in neonatal encephalopathy, including hypoxic-ischaemic encephalopathy, perinatal/neonatal stroke, metabolic encephalopathy from inborn errors of metabolism, congenital central nervous system infections and birth trauma. The applications of advanced MRI techniques, such as diffusion-weighted imaging and magnetic resonance spectroscopy are emphasized

CT and MR in non-neonatal hypoxic-ischemic encephalopathy: radiological findings with pathophysiological correlations

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Gutierrez, Leonardo Guilhermino; Portela, Luiz Antonio Pezzi [Hospital Alemao Oswaldo Cruz and Hospital do Coracao, Diagnostic Imaging Division, Sao Paulo (Brazil); Rovira, Alex [University Hospital Vall d' Hebron, MR Unit, Department of Radiology, Barcelona (Spain); Costa Leite, Claudia da [Clinics Hospital of the University of Sao Paulo, School of Medicine, Department of Radiology, Sao Paulo (Brazil); Lucato, Leandro Tavares [Hospital Alemao Oswaldo Cruz and Hospital do Coracao, Diagnostic Imaging Division, Sao Paulo (Brazil); Clinics Hospital of the University of Sao Paulo, School of Medicine, Department of Radiology, Sao Paulo (Brazil)

2010-11-15

Non-neonatal hypoxic-ischemic encephalopathy is a clinical condition often related to cardiopulmonary arrest that demands critical management and treatment decisions. Management depends mainly on the degree of neurological impairment and prognostic considerations. Computed tomography (CT) is often used to exclude associated or mimicking pathology. If any, only nonspecific signs such as cerebral edema, sulci effacement, and decreased gray matter (GM)/white matter (WM) differentiation are evident. Pseudosubarachnoid hemorrhage, a GM/WM attenuation ratio <1.18, and inverted GM attenuation are associated with a poor prognosis. Magnetic resonance (MR) imaging is more sensitive than CT in assessing brain damage in hypoxic-ischemic encephalopathy. Some MR findings have similarities to those seen pathologically, based on spatial distribution and time scale, such as lesions distributed in watershed regions and selective injury to GM structures. In the acute phase, lesions are better depicted using diffusion-weighted imaging (DWI) because of the presence of cytotoxic edema, which, on T2-weighted images, only become apparent later in the early subacute phase. In the late subacute phase, postanoxic leukoencephalopathy and contrast enhancement could be observed. In the chronic phase, atrophic changes predominate over tissue signal changes. MR can be useful for estimating prognosis when other tests are inconclusive. Some findings, such as the extent of lesions on DWI and presence of a lactate peak and depleted N-acetyl aspartate peak on MR spectroscopy, seem to have prognostic value. (orig.)

CT and MR in non-neonatal hypoxic-ischemic encephalopathy: radiological findings with pathophysiological correlations

International Nuclear Information System (INIS)

Gutierrez, Leonardo Guilhermino; Portela, Luiz Antonio Pezzi; Rovira, Alex; Costa Leite, Claudia da; Lucato, Leandro Tavares

2010-01-01

Non-neonatal hypoxic-ischemic encephalopathy is a clinical condition often related to cardiopulmonary arrest that demands critical management and treatment decisions. Management depends mainly on the degree of neurological impairment and prognostic considerations. Computed tomography (CT) is often used to exclude associated or mimicking pathology. If any, only nonspecific signs such as cerebral edema, sulci effacement, and decreased gray matter (GM)/white matter (WM) differentiation are evident. Pseudosubarachnoid hemorrhage, a GM/WM attenuation ratio <1.18, and inverted GM attenuation are associated with a poor prognosis. Magnetic resonance (MR) imaging is more sensitive than CT in assessing brain damage in hypoxic-ischemic encephalopathy. Some MR findings have similarities to those seen pathologically, based on spatial distribution and time scale, such as lesions distributed in watershed regions and selective injury to GM structures. In the acute phase, lesions are better depicted using diffusion-weighted imaging (DWI) because of the presence of cytotoxic edema, which, on T2-weighted images, only become apparent later in the early subacute phase. In the late subacute phase, postanoxic leukoencephalopathy and contrast enhancement could be observed. In the chronic phase, atrophic changes predominate over tissue signal changes. MR can be useful for estimating prognosis when other tests are inconclusive. Some findings, such as the extent of lesions on DWI and presence of a lactate peak and depleted N-acetyl aspartate peak on MR spectroscopy, seem to have prognostic value. (orig.)

Therapeutic hypothermia for neonatal hypoxic-ischemic encephalopathy - where to from here?

Directory of Open Access Journals (Sweden)

Joanne O. Davidson

2015-09-01

Full Text Available Hypoxia-ischemia before or around the time of birth occurs in approximately 2/1000 live births and is associated with a high risk of death or lifelong disability. Therapeutic hypothermia is now well established as standard treatment for infants with moderate to severe hypoxic-ischemic encephalopathy but is only partially effective. There is compelling preclinical and clinical evidence that hypothermia is most protective when it is started as early as possible after hypoxia-ischemia. Further improvements in outcome from therapeutic hypothermia are very likely to arise from strategies to reduce the delay before starting treatment of affected infants. In this review we examine evidence that current protocols are reasonably close to the optimal depth and duration of cooling, but that the optimal rate of rewarming after hypothermia is unclear. The potential for combination treatments to augment hypothermic neuroprotection has considerable promise, particularly with endogenous targets such as melatonin and erythropoietin and noble gases such as xenon. We dissect the critical importance of preclinical studies using realistic delays in treatment and clinically relevant cooling protocols when examining combination treatment, and that for many strategies overlapping mechanisms of action can substantially attenuate any effects.

[Assessment of therapeutic passive hypothermia in newborns with hypoxic-ischemic encephalopathy that need interhospital transport].

Science.gov (United States)

Fuentes-Ruiz, José A; Lagares-Franco, Carolina; Rodríguez-Molina, Óscar; Cordero-Cañas, Enrique; Benavente-Fernández, Isabel

2015-04-01

Induced hypothermia for the first hours of life in a newborn is an effective treatment to reduce mortality and serious effects in neonates that had suffered a hypoxia episode. This method needs an universal attendance independently of the place of birth being usually necessary a transfer to the reference hospital. To analyze the efficacy of the newborn with hypoxic-ischemic encephalopathy transfer in passive hypothermia. Descriptive study of series of cases with retrospective character of newborn from Cadiz's province that need induced hypothermia. 46 newborn were included in the study: 33 of them (71.74%) needed being transfer by the Critical Patients Transport service (CPT group), the rest (28.26%) were born into the reference hospital. Both groups are similar in age gestational at birth, sex, weight and hypoxic-ischemic encephalopathy degree. It analyzed variables related to hypothermia therapy and in addition in CPT group transfer specific variables. At discharge, it does not exist significant differences between groups in the efficiency-consequence of neuroprotection therapy with hypothermia (p = 0.159). It does not find complications derived from the interhospital move. Neonatal inter-hospital transfer in passive therapeutic hypothermia is effective, safe and necessary for the therapy compliance. It is required reach an agreement between the attendance and the reference service, setting up guides for the support and suitable range of temperature.

Post-partum posterior reversible encephalopathy syndrome

OpenAIRE

B. V. Triveni; Salman Mohammed Sheikh; Deepak Shedde

2014-01-01

Posterior Reversible Encephalopathy Syndrome (PRES) is a clinicopathological syndrome associated with various clinical conditions presenting with headache, encephalopathy, seizure and cortical visual disturbances. Radiological findings in PRES are thought to be due to vasogenic edema predominantly in posterior cerebral hemispheres and are reversible with appropriate management. We present a case of post partum PRES,A 29 year old primigravida of 33 weeks 3 days period of gestation who prese...

Actualities on molecular pathogenesis and repairing processes of cerebral damage in perinatal hypoxic-ischemic encephalopathy

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Praticò Andrea D

2010-09-01

Full Text Available Abstract Hypoxic-ischemic encephalopathy (HIE is the most important cause of cerebral damage and long-term neurological sequelae in the perinatal period both in term and preterm infant. Hypoxic-ischemic (H-I injuries develop in two phases: the ischemic phase, dominated by necrotic processes, and the reperfusion phase, dominated by apoptotic processes extending beyond ischemic areas. Due to selective ischemic vulnerability, cerebral damage affects gray matter in term newborns and white matter in preterm newborns with the typical neuropathological aspects of laminar cortical necrosis in the former and periventricular leukomalacia in the latter. This article summarises the principal physiopathological and biochemical processes leading to necrosis and/or apoptosis of neuronal and glial cells and reports recent insights into some endogenous and exogenous cellular and molecular mechanisms aimed at repairing H-I cerebral damage.

Research Progress of Mechanism and Treatment of Neonatal Hypoxic-ischemic Encephalopathy

Directory of Open Access Journals (Sweden)

Yu-fei NI

2017-09-01

Full Text Available Neonatal hypoxic-ischemic encephalopathy (HIE is a hypoxic-ischemic brain injury caused by hypoxia after perinatal asphyxia in neonates, and one of the major causes of neonatal death, lifelong neurological disability and cognitive dysfunction. Although the mechanisms of HIE are complex and still unclear, it generally holds that HIE has a relationship with acute inflammatory reaction and is regulated by multiple cytokines and neuromodulators. Presently, therapeutic hypothermia, in the light of the lower mortality and improvement of prognosis, becomes a standard of care in many medical institutes, but there are still neonates dead or disabled after treatment. Therefore, it is necessary to use hypothermia in combination with other new adjuvant therapies (such as anti-inflammatory cytokine to improve the prognosis of neonatal HIE. Besides, glutamate receptor antagonist, calcium channel blockers, erythropoietin, and nerve growth factors also have certain therapeutic effects on neonatal HIE. Therefore, this review mainly focused on the mechanisms and treatments of HIE. Based on this, we hold that the future studies should concentrate on how to attenuate early brain injury and to improve the growth and differentiation of neuronal cells and non-neuronal cells, which is of great signifcance to prolong the therapeutic window of neuroprotection, promote long-term neural restoration and improve the prognosis.

[Therapeutic effect of early applying hydrotherapy with Chinese drugs on children hypoxic ischemic encephalopathy].

Science.gov (United States)

Ma, Yun-Zhi; Zhai, Hong-Yin; Su, Chun-Ya

2009-02-01

To observe the therapeutic effect of hydrotherapy with Chinese drugs (HT-C) in early intervention on children hypoxic ischemic encephalopathy (HIE). HIE children were assigned to the treatment group and the control group, 50 in each, at random depending on the willingness of patients' parents. Both groups received the conventional functional training, according to the "0 -3-year-old early intervention outline", but for the treatment group, HT-C was applied additionally. Indexes for quality of sleep, gross motor function, severity of spasm and intellectual development were observed and compared before and after treatment to assess the therapeutic effects. Therapeutic effect in the treatment group was better than that in the control group in all the indexes observed, showing statistical significance (all P <0.05). Early intervention of HT-C could improve clinical symptom, promote the functional recovery and intellectual development in children HIE, and also could reduce or prevent the sequelae occurrence of the nervous system in them.

Lack of evidence for a causal relationship between hypoxic-ischemic encephalopathy and subdural hemorrhage in fetal life, infancy, and early childhood

DEFF Research Database (Denmark)

Byard, Roger W; Blumbergs, Peter; Rutty, Guy

2013-01-01

It has been asserted that hypoxic-ischemic encephalopathy (HIE) with cerebral swelling in the absence of marked trauma may be responsible for subural hemorrhage in the young. As this may have considerable implications in determining both the mechanism of death and the degree of force required to ...

Stem Cell Therapy for Neonatal Hypoxic-Ischemic Encephalopathy

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Gabriel eGonzales-Portillo

2014-08-01

Full Text Available Treatments for neonatal hypoxic ischemic encephalopathy (HIE have been limited. The aim of this paper is to offer translational research guidance on stem cell therapy for neonatal HIE by examining clinically relevant animal models, practical stem cell sources, safety and efficacy of endpoint assays, as well as a general understanding of modes of action of this cellular therapy. In order to do so, we discuss the clinical manifestations of HIE, highlighting its overlapping pathologies with stroke providing insights on the potential of cell therapy, currently investigated in stroke, for HIE. To this end, we draw guidance from recommendations outlined in Stem cell Therapeutics as an Emerging Paradigm for Stroke or STEPS, which have been recently modified to Baby STEPS to cater for the neonatal symptoms of HIE. These guidelines recognized that neonatal HIE exhibits distinct disease symptoms from adult stroke in need of an innovative translational approach that facilitates the entry of cell therapy in the clinic. Finally, new information about recent clinical trials, and insights into combination therapy are provided with the vision that stem cell therapy may benefit from available treatments, such as hypothermia, already being tested in children diagnosed with HIE.

Acute hepatic encephalopathy with diffuse cortical lesions

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Arnold, S.M.; Spreer, J.; Schumacher, M. [Section of Neuroradiology, Univ. of Freiburg (Germany); Els, T. [Dept. of Neurology, University of Freiburg (Germany)

2001-07-01

Acute hepatic encephalopathy is a poorly defined syndrome of heterogeneous aetiology. We report a 49-year-old woman with alcoholic cirrhosis and hereditary haemorrhagic telangiectasia who developed acute hepatic coma induced by severe gastrointestinal bleeding. Laboratory analysis revealed excessively elevated blood ammonia. MRI showed lesions compatible with chronic hepatic encephalopathy and widespread cortical signal change sparing the perirolandic and occipital cortex. The cortical lesions resembled those of hypoxic brain damage and were interpreted as acute toxic cortical laminar necrosis. (orig.)

Acute hepatic encephalopathy with diffuse cortical lesions

International Nuclear Information System (INIS)

Arnold, S.M.; Spreer, J.; Schumacher, M.; Els, T.

2001-01-01

Acute hepatic encephalopathy is a poorly defined syndrome of heterogeneous aetiology. We report a 49-year-old woman with alcoholic cirrhosis and hereditary haemorrhagic telangiectasia who developed acute hepatic coma induced by severe gastrointestinal bleeding. Laboratory analysis revealed excessively elevated blood ammonia. MRI showed lesions compatible with chronic hepatic encephalopathy and widespread cortical signal change sparing the perirolandic and occipital cortex. The cortical lesions resembled those of hypoxic brain damage and were interpreted as acute toxic cortical laminar necrosis. (orig.)

Hypoxic ischemia encephalopathy leading to external hydrocephalus and the cerebral atrophy: mechanism and differential diagnosis

International Nuclear Information System (INIS)

Huang Zhenglin; Mo Xiaorong

2002-01-01

Objective: It is a study of the mechanism and differential diagnosis of the infant external hydrocephalus and cerebral atrophy. Methods: In total 84 cases of neonatal hypoxic ischemia encephalopathy followed by infant external hydrocephalus were investigated, among which 26 patients gradually were found having developed cerebral atrophy in follow up. Results: Characteristic dilation of the frontal-parietal subarachnoid space and the adjacent cistern was noted on the CT images of the external hydrocephalus. CT revealed the enlarged ventricle besides the dilated subarachnoid space in the cases of cerebral atrophy, while these two entities were indistinguishable on CT in the early stage. Conclusion: Clinical manifestations make a major differential diagnosis of the external hydrocephalus and cerebral atrophy: tic and mild delayed development of locomotion over major presentation of external hydrocephalus, while cerebral atrophy is featured by remarkable dysnoesia and severe delayed development of locomotion. In addition, hemiplegia and increased muscular tension are presented in a few cases of cerebral atrophy

Passive hypothermia (≥35 - newborns with hypoxic-ischaemic encephalopathy.

Science.gov (United States)

Sellam, Aurélie; Lode, Noëlla; Ayachi, Azzedine; Jourdain, Gilles; Dauger, Stéphane; Jones, Peter

2017-01-01

Hypothermia initiated in the first six hours of life in term infants with hypoxic ischemic encephalopathy reduces the risk of death and severe neurological sequelae. Our study's principal objective was to evaluate transport predictors potentially influencing arrival in NICU (Neonatal Intensive Care Unit) at a temperature ≥35-Newborns were selected for inclusion according to biological and clinical criteria before transport using passive hypothermia using a target temperature of ≥35-<36°C. Data on 120 of 126 inclusions were available for analysis. Thirty-three percent of the children arrived in NICU with the target temperature of ≥35-<36°C. The mean temperature for the whole group of infants on arrival in NICU was 35.4°C (34.3-36.5). The median age of all infants on arrival in NICU was 3h03min [2h25min-3h56min]. Three infants arrived in NICU with a temperature of <33°C and eleven with a temperature ≥37°C. Adrenaline during resuscitation was associated with a lower mean temperature on arrival in NICU. Our strategy using ≥35-<36°C passive hypothermia combined with short transport times had little effect on temperature after the arrival of Neonatal Transport Team although did reduce numbers of infants arriving in NICU in deep hypothermia. For those infants where hypothermia was discontinued in NICU our strategy facilitated re-warming. Re-adjustment to a lower target temperature to ≥34.5-<35.5°C may reduce the proportion of infants with high/normothermic temperatures.

Computed tomography diagnosis of neonatal hypoxic ischemic encephalopathy combined with intracranial hemorrhage and clinical nursing treatment.

Science.gov (United States)

Zhang, Y; Zhang, J L; Li, Y

2016-01-01

Hypoxic ischemic encephalopathy (HIE), one of the common causes of newborn invalidism, is likely to induce nervous system-associated sequelae and even intracranial hemorrhage in severe cases. The incidence rate of HIE has been rising in recent years. In order to study the clinical nursing effect for HIE combined with intracranial hemorrhage, 76 newborns diagnosed with HIE combined with intracranial hemorrhage by spiral computed tomography (CT) from the of Binzhou People’s Hospital, Shandong, China were selected. They were divided into a control group and an intervention group. The control group received routine nursing, while the intervention group received comprehensive nursing intervention. The experimental results suggested that the mental developmental index (MDI) value and the psychomotor developmental index (PDI) value of patients in the intervention group were much higher than those of the control group and the difference was significant (phemorrhage recover more effectively, therefore is worth applying.

Population pharmacokinetics of phenobarbital in infants with neonatal encephalopathy treated with therapeutic hypothermia.

Science.gov (United States)

Shellhaas, Renée A; Ng, Chee M; Dillon, Christina H; Barks, John D E; Bhatt-Mehta, Varsha

2013-02-01

Phenobarbital is the first-line treatment for neonatal seizures. Many neonates with hypoxic ischemic encephalopathy are treated with therapeutic hypothermia, and about 40% have clinical seizures. Little is known about the pharmacokinetics of phenobarbital in infants with hypoxic ischemic encephalopathy who undergo therapeutic hypothermia. The objective of this study was to determine the effect of therapeutic hypothermia on phenobarbital pharmacokinetics, taking into account maturational changes. Level 3 neonatal ICU. Infants with hypoxic ischemic encephalopathy and suspected seizures, all treated with phenobarbital. Some of these infants also received treatment with therapeutic hypothermia. None. A retrospective cohort study of 39 infants with hypoxic ischemic encephalopathy treated with phenobarbital (20 were treated with therapeutic hypothermia and 19 were not). Data on phenobarbital plasma concentrations were collected in 39 subjects with hypoxic ischemic encephalopathy with or without therapeutic hypothermia. Using nonlinear mixed-effects modeling, population pharmacokinetics of phenobarbital were developed with a total of 164 plasma concentrations. A one-compartment model best described the pharmacokinetics. The clearance of phenobarbital was linearly related to body weight and matured with increasing age with a maturation half-life of 22.1 days. Therapeutic hypothermia did not influence the pharmacokinetic parameters of phenobarbital. Therapeutic hypothermia does not influence the clearance of phenobarbital after accounting for weight and age. Standard phenobarbital dosing is appropriate for the initial treatment of seizures in neonates with hypoxic ischemic encephalopathy treated with therapeutic hypothermia.

Motor Testing at 1 Year Improves the Prediction of Motor and Mental Outcome at 2 Years after Perinatal Hypoxic-Ischaemic Encephalopathy

Science.gov (United States)

van Schie, Petra Em; Becher, Jules G.; Dallmeijer, Annet J.; Barkhof, Frederik; van Weissenbruch, Mirjam M.; Vermeulen, R. Jeroen

2010-01-01

Aim: To investigate the predictive value of motor testing at 1 year for motor and mental outcome at 2 years after perinatal hypoxic-ischaemic encephalopathy (HIE) in term neonates. Method: Motor and mental outcome at 2 years was assessed with the Bayley Scales of Infant Development, 2nd edition (BSID-II) in 32 surviving children (20 males, 12…

Clinical utility of high b-value diffusion-weighted magnetic resonance imaging in post-resuscitative encephalopathy

International Nuclear Information System (INIS)

Kano, Hitoshi; Danjou, Wataru; Yamazaki, Kei

2002-01-01

increasing b value in the first DW-MRI study. The latter areas were thought to be viable. Moreover, high b-values did not reverse the gray-white matter contrast in patients with severe post-resuscitative encephalopathy did so in healthy controls at 2000s/mm 2 . In patients with severe post-resuscitative encephalopathy, the high signal intensity areas enlarged progressively in follow-up DW-MRI; this phenomenon was thought to reveal progressive neuronal necrosis. DW-MRI with high b value (2000s/mm 2 ) appeared to distinguish irreversibly damaged areas from viable regions of the cerebral cortex. Therefore, we conclude that DW-MRI with high b value immediately after successful cardiopulmonary resuscitation is a very useful tool to evaluate the brain function and to elucidate the pathophysiology of post-resuscitative encephalopathy. (author)

Clinical utility of high b-value diffusion-weighted magnetic resonance imaging in post-resuscitative encephalopathy

Energy Technology Data Exchange (ETDEWEB)

Kano, Hitoshi; Danjou, Wataru; Yamazaki, Kei [Sapporo City General Hospital (Japan)] (and others)

2002-03-01

increasing b value in the first DW-MRI study. The latter areas were thought to be viable. Moreover, high b-values did not reverse the gray-white matter contrast in patients with severe post-resuscitative encephalopathy did so in healthy controls at 2000s/mm{sup 2}. In patients with severe post-resuscitative encephalopathy, the high signal intensity areas enlarged progressively in follow-up DW-MRI; this phenomenon was thought to reveal progressive neuronal necrosis. DW-MRI with high b value (2000s/mm{sup 2}) appeared to distinguish irreversibly damaged areas from viable regions of the cerebral cortex. Therefore, we conclude that DW-MRI with high b value immediately after successful cardiopulmonary resuscitation is a very useful tool to evaluate the brain function and to elucidate the pathophysiology of post-resuscitative encephalopathy. (author)

Post-hypoxic recovery of respiratory rhythm generation is gender dependent.

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Alfredo J Garcia

Full Text Available The preBötzinger complex (preBötC is a critical neuronal network for the generation of breathing. Lesioning the preBötC abolishes respiration, while when isolated in vitro, the preBötC continues to generate respiratory rhythmic activity. Although several factors influence rhythmogenesis from this network, little is known about how gender may affect preBötC function. This study examines the influence of gender on respiratory activity and in vitro rhythmogenesis from the preBötC. Recordings of respiratory activity from neonatal mice (P10-13 show that sustained post-hypoxic depression occurs with greater frequency in males compared to females. Moreover, extracellular population recordings from the preBötC in neonatal brainstem slices (P10-13 reveal that the time to the first inspiratory burst following reoxygenation (TTFB is significantly delayed in male rhythmogenesis when compared to the female rhythms. Altering activity of ATP sensitive potassium channels (KATP with either the agonist, diazoxide, or the antagonist, tolbutamide, eliminates differences in TTFB. By contrast, glucose supplementation improves post-hypoxic recovery of female but not male rhythmogenesis. We conclude that post-hypoxic recovery of respiration is gender dependent, which is, in part, centrally manifested at the level of the preBötC. Moreover, these findings provide potential insight into the basis of increased male vulnerability in a variety of conditions such as Sudden Infant Death Syndrome (SIDS.

Cytokine changes in newborns with therapeutic hypothermia after hypoxic ischemic encephalopathy.

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Moon, C J; Youn, Y A; Yum, S K; Sung, I K

2016-12-01

This study aimed to examine changes in cytokines according to therapeutic hypothermia (TH) for newborn hypoxic ischemic encephalopathy (HIE). We studied 20 neonates who were admitted with a diagnosis of HIE in the neonatal intensive care unit. Cytokine concentration assay was carried out for neonates (n=12) who received TH and neonates (n=8) who were not treated with hypothermia by collecting blood sample at 12, 48 and 120 h after birth. At 48 h after birth, interleukin (IL)-6 in the normothermia group was higher than that in the hypothermia group (P=0.010). At 48 h after birth, IL-10 was higher in the hypothermia group than in the normothermia group (P=0.038). This study confirmed that TH performs a role in the prevention of inflammatory process by way of maintaining proinflammatory cytokine IL-6 at low levels and anti-inflammatory cytokines IL-10 at high levels.

High glucose variability is associated with poor neurodevelopmental outcomes in neonatal hypoxic ischemic encephalopathy.

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Al Shafouri, N; Narvey, M; Srinivasan, G; Vallance, J; Hansen, G

2015-01-01

In neonatal hypoxic ischemic encephalopathy (HIE), hypo- and hyperglycemia have been associated with poor outcomes. However, glucose variability has not been reported in this population. To examine the association between serum glucose variability within the first 24 hours and two-year neurodevelopmental outcomes in neonates cooled for HIE. In this retrospective cohort study, glucose, clinical and demographic data were documented from 23 term newborns treated with whole body therapeutic hypothermia. Severe neurodevelopmental outcomes from planned two-year assessments were defined as the presence of any one of the following: Gross Motor Function Classification System levels 3 to 5, Bayley III Motor Standard Score neurodevelopmental outcomes from 8 of 23 patients were considered severe, and this group demonstrated a significant increase of mean absolute glucose (MAG) change (-0.28 to -0.03, 95% CI, p = 0.032). There were no significant differences between outcome groups with regards to number of patients with hyperglycemic means, one or multiple hypo- or hyperglycemic measurement(s). There were also no differences between both groups with mean glucose, although mean glucose standard deviation was approaching significance. Poor neurodevelopmental outcomes in whole body cooled HIE neonates are significantly associated with MAG changes. This information may be relevant for prognostication and potential management strategies.

Neuroprotective strategies for patients with acute myocardial infarction combined with hypoxic ischemic encephalopathy in the ICU

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Weiwei Hu

2017-11-01

Full Text Available Background: We investigated neuroprotective treatment strategies for patients with acute myocardial infarction (AMI complicated with hypoxic ischemic encephalopathy (HIE in the ICU. Methods: The 83 cases diagnosed with secondary AMI were, for the first time, divided into an observation group (n = 43 and control group (n = 40. All of the patients underwent emergency or elective PCI. Patients in the control group were treated with mannitol to reduce intracranial pressure and cinepazide maleate to improve microcirculation in the brain as well as given a comprehensive treatment with oxygen inhalation, fluid infusion, acid-base imbalance correction and electrolyte disturbance. Patients in the observation group underwent conventional treatment combined with neuroprotective therapeutic strategies. The effects of the different treatment strategies were compared. Results: Consciousness recovery time, reflex recovery time, muscle tension recovery time and duration of ICU stay were significantly shorter in the observation group compared with the control group (P < 0.05. After treatment, the jugular vein oxygen saturation (SjvO2 and blood lactate (JB-LA levels of both groups were lower than before treatment and the cerebral oxygen utilization rate (O2UC increased, with a significantly higher increase in the observation group (P < 0.05. After treatment, the activities of daily living (ADL score was higher for both groups and the neural function defect (NIHS score was lower. Conclusion: The neuroprotective strategies of hypothermia and ganglioside administration assisted with hyperbaric oxygen was effective for treating AMI patients with HIE and may be worth clinical promotion. Keywords: ICU, Acute myocardial infarction, Hypoxic ischemic encephalopathy, Neural protection

Preliminary study on hypoxic-ischemic encephalopathy in neonates with diffusion-weighted MR imaging

International Nuclear Information System (INIS)

Wang Xiaoming; Chen Liying; Lin Nan; Guo Qiyong

2005-01-01

Objective: To evaluate hypoxic-ischemic encephalopathy (HIE) in neonates with diffusion-weighted MR imaging, and to explore the value and limitation of diffusion-weighted imaging (DWI) compared with conventional magnetic resonance imaging. Methods: Conventional magnetic resonance T 1 -weighted imaging (T 1 WI) and DWI (b=700 s/mm 2 ) were performed in 36 neonates with HIE (average age, 8.44 days; range, 3 hours to 22 days), and the cortex and subcortical white matter, deep white matter, basal ganglia and thalamus, cerebral ventricle, and extra-cerebral interspace etc were observed. Results: Signal abnormalities were shown on DWI with hypoxic-ischemic insults, which included diffuse brain damage (19.4%, 7/36): extensive high signals in the regional cortex, subcortical and deep white matter; localized brain damage: high signals along lateral ventricular wall and triangular part (27.8%, 10/36 ), and punctate high signals in the frontal deep white matter (5.6%, 2/36). On T 1 WI, the incidence of the corresponding changes were 16.7% (6/36), 36.1% (13/36), and 30.6%(11/36), respectively. Hemorrhagic lesions demonstrated high signals on T 1 WI and no signals on DWI. Conclusion: DWI was applicable for acute HIE, and T 1 WI was suitable for subacute and chronic HIE. (authors)

Systemic hypothermia after neonatal encephalopathy: outcomes of neo.nEURO.network RCT

DEFF Research Database (Denmark)

Simbruner, Georg; Mittal, Rashmi A; Rohlmann, Friederike

2010-01-01

Mild hypothermia after perinatal hypoxic-ischemic encephalopathy (HIE) reduces neurologic sequelae without significant adverse effects, but studies are needed to determine the most-efficacious methods.......Mild hypothermia after perinatal hypoxic-ischemic encephalopathy (HIE) reduces neurologic sequelae without significant adverse effects, but studies are needed to determine the most-efficacious methods....

[Sensitivity and specificity of the cerebral blood flow reactions to acupuncture in the newborn infants presenting with hypoxic ischemic encephalopathy].

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Filonenko, A V; Vasilenko, A M; Khan, M A

2015-01-01

To evaluate the effects of acupuncture integrated into the standard therapy, the condition of cerebral blood flow, and other syndromes associated with cerebral ischemia in the newborn infants. MATERIAL AND METHODS. A total of 131 pairs of puerperae and newborns with hypoxic ischemic encephalopathy were divided into four treatment groups. 34 children of the first group were given standard therapy (control), in the second group comprised of 33 mothers and children the standard treatment was supplemented by acupuncture, the third group included only 32 mothers given the acupuncture treatment alone, and the fourth group contained only 32 newborn infants treated by acupuncture. Each course of acupuncture treatment consisted of five sessions. Sensitivity and specificity of cerebral blood flow reactions were determined based on the results of the ROC-analysis and the area under the curve before and after the treatment. The treatment with the use of acupuncture greatly improved the cerebrospinal hemodynamics (p newborn babies. The high level of sensitivity (84.4-94.8%) associated with good specificity makes it possible to distinguish between the true positive and true negative cases. Acupuncture integrated into the treatment of "mother-baby" pairs presenting with hypoxic ischemic encephalopathy can be used to improve the initially low level of cerebral blood flow in neonates presenting with this condition.

Changes in lactate dehydrogenase are associated with central gray matter lesions in newborns with hypoxic-ischemic encephalopathy.

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Yum, Sook Kyung; Moon, Cheong-Jun; Youn, Young-Ah; Sung, In Kyung

2017-05-01

Biomarkers may predict neurological prognosis in infants with hypoxic-ischemic encephalopathy (HIE). We evaluated the relationship between serum lactate dehydrogenase (LDH) and brain magnetic resonance imaging (MRI), which predicts neurodevelopmental outcomes, in order to assess whether LDH levels are similarly predictive. Medical records were reviewed for infants with HIE and LDH levels were assessed on the first (LDH 1 ) and third (LDH 3 ) days following birth. Receiver operating characteristic curves were obtained in relation to central gray matter hypoxic-ischemic lesions. Of 92 patients, 52 (56.5%) had hypoxic-ischemic lesions on brain MRI, and 21 of these infants (40.4%) had central gray matter lesions. LDH 1 and LDH 3 did not differ; however, the percentage change (ΔLDH%) was significantly higher in infants with central gray matter lesions (36.9% versus 6.6%, p = 0.006). With cutoffs of 187 (IU/L, ΔLDH) and 19.4 (%, ΔLDH%), the sensitivity, specificity, positive predictive value and negative predictive value were 71.4, 69.0, 40.5 and 89.1%, respectively. The relative risk was 5.57 (p = 0.001). Changes in serum LDH may be a useful biomarker for predicting future neurodevelopmental prognosis in infants with HIE.

Electroencephalogram and magnetic resonance imaging comparison as a predicting factor for neurodevelopmental outcome in hypoxic ischemic encephalopathy infant treated with hypothermia

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Francesca Del Balzo

2014-10-01

Full Text Available Hypoxic-ischemic encephalopathy (HIE is an important cause of acute neurological damage in newborns at (or near term. Several trials in recent years have shown that moderate hypothermia by total body cooling or selective head is an effective intervention to reduce mortality and major disability in infants survived a perinatal hypoxic-ischemic attack. Follow-up in these patients is very important to establish neurodevelopmental outcome, and specific markers can lead us to detect predicting sign for good or poor outcome. We reported a few cases of newborn with HIE treated with hypothermia, in whom the comparison between electroencephalogram (EEG and magnetic resonance imaging (MRI represents the first marker for neurodevelopment outcome prediction. The continuous EEG monitoring showed a depressed EEG activity with diffuse burst depression in 7 patients. No epileptic abnormalities were registered. In 10 out of 20 patients no abnormalities of the background activity and no epileptic abnormalities were observed. We found that a depressed EEG activity during the first 72 h of life and a diffused alteration of basal ganglia at MRI were correlated with a poor neurodevelopmental outcome at 18 months of follow-up.

Biomarkers of Hypoxic Ischemic Encephalopathy in Newborns

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Martha V. Douglas-Escobar

2012-11-01

Full Text Available As neonatal intensive care has evolved, the focus has shifted from improving mortality alone to an effort to improve both mortality and morbidity. The most frequent source of neonatal brain injury occurs as a result of hypoxic-ischemic injury. Hypoxic-ischemic injury occurs in about 2 of 1,000 full-term infants and severe injured infants will have lifetime disabilities and neurodevelopmental delays. Most recently, remarkable efforts toward neuroprotection have been started with the advent of therapeutic hypothermia and a key step in the evolution of neonatal neuroprotection is the discovery of biomarkers that enable the clinician-scientist to screen infants for brain injury, monitor progression of disease, identify injured brain regions, and assess efficacy of neuroprotective clinical trials. Lastly, biomarkers offer great hope identifying when an injury occurred shedding light on the potential pathophysiology and the most effective therapy. In this article, we will review biomarkers of HIE including S100b, neuron specific enolase, umbilical cord IL-6, CK-BB, GFAP, myelin basic protein, UCHL-1, and pNF-H. We hope to contribute to the awareness, validation and clinical use of established as well as novel neonatal brain injury biomarkers.

Seizure Severity Is Correlated With Severity of Hypoxic-Ischemic Injury in Abusive Head Trauma.

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Dingman, Andra L; Stence, Nicholas V; O'Neill, Brent R; Sillau, Stefan H; Chapman, Kevin E

2017-12-12

The objective of this study was to characterize hypoxic-ischemic injury and seizures in abusive head trauma. We performed a retrospective study of 58 children with moderate or severe traumatic brain injury due to abusive head trauma. Continuous electroencephalograms and magnetic resonance images were scored. Electrographic seizures (51.2%) and hypoxic-ischemic injury (77.4%) were common in our cohort. Younger age was associated with electrographic seizures (no seizures: median age 13.5 months, interquartile range five to 25 months, versus seizures: 4.5 months, interquartile range 3 to 9.5 months; P = 0.001). Severity of hypoxic-ischemic injury was also associated with seizures (no seizures: median injury score 1.0, interquartile range 0 to 3, versus seizures: 4.5, interquartile range 3 to 8; P = 0.01), but traumatic injury severity was not associated with seizures (no seizures: mean injury score 3.78 ± 1.68 versus seizures: mean injury score 3.83 ± 0.95, P = 0.89). There was a correlation between hypoxic-ischemic injury severity and seizure burden when controlling for patient age (r s =0.61, P interquartile range 0 to 0.23 on magnetic resonance imaging done within two days versus median restricted diffusion ratio 0.13, interquartile range 0.01 to 0.43 on magnetic resonance imaging done after two days, P = 0.03). Electrographic seizures are common in children with moderate to severe traumatic brain injury from abusive head trauma, and therefore children with suspected abusive head trauma should be monitored with continuous electroencephalogram. Severity of hypoxic-ischemic brain injury is correlated with severity of seizures, and evidence of hypoxic-ischemic injury on magnetic resonance imaging may evolve over time. Therefore children with a high seizure burden should be reimaged to evaluate for evolving hypoxic-ischemic injury. Published by Elsevier Inc.

Evolution of the Therapeutic Effects of Induced Local Hypothermia in Neonates with Hypoxic-Ischemic Encephalopathy

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B. Basiri

2011-04-01

Full Text Available Introduction & Objective: Hypoxic-ischemic encephalopathy is one of the most important causes of permanent damage to brain tissue that redound to mortality and/or late sequelae such as cerebral palsy or delayed neural development. 15-20 percent of Hypoxic-ischemic encephalopathy (HIE cases die during neonatal period and 25-30 percent of those who survive suffer from neural development problems such as cerebral palsy and mental retardation. Hypothermia or lowering temperature of brain or total body is a new and promising treatment. The present study was done to assess therapeutic effects of induced local hypothermia in hypoxic-ischemic encephalopathy (HIE among neonates admitted to Fatemieh and Beset hospitals of Hamadan city.Materials & Method: The present study was performed as a randomized clinical trial upon 36 neonates who had inclusion criteria to be imported into the study. In the first 6 hours after birth, the neonates were randomly classified into two 18 person groups. In the control group the neonates were managed with routine treatments consisted of preservative measures and anti-convulsive treatments, if necessary. In the case group the neonates received induced local hypothermia for 6 hours in addition to routine therapeutic managements. The data were analyzed using SPSS Version 13.Results: 72.7% of the neonates of the case and control groups were male. There was no significant difference between the case and control groups in sex, birth weight, gestational age and perinatal obstetric complications. The mean duration of admission was 7.72±4.23 days in the case group and 10.06±5.99 days in the control group with no significant difference between the two groups (P=0.199. The mean time of starting oral feeding was 3.44±3.11 days and 4.53±2.74 days in the control and case groups respectively and this difference was not statistically significant either (P=0.737.The mean time of regaining consciousness was 3.72±3.19 days in the case

Cost-effective therapeutic hypothermia treatment device for hypoxic ischemic encephalopathy

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Allen RH

2013-01-01

Full Text Available John J Kim,1,2 Nathan Buchbinder,1,† Simon Ammanuel,1,4,5,† Robert Kim,1,† Erika Moore,1 Neil O'Donnell,1 Jennifer K Lee,3 Ewa Kulikowicz,3 Soumyadipta Acharya,1 Robert H Allen,1,9 Ryan W Lee,6,7 Michael V Johnston4–81Department of Biomedical Engineering, Whiting School of Engineering, The Johns Hopkins University, 2The James Buchanan Brady Urological Institute, Department of Urology, The Johns Hopkins University School of Medicine, 3Department of Anesthesia and Critical Care Medicine, Johns Hopkins University, 4Kennedy Krieger Institute, 5Hugo W Moser Research Institute, 6Department of Neurology, 7Department of Pediatrics, 8Department of Physical Medicine and Rehabilitation Johns Hopkins University School of Medicine, Baltimore, MD; 9Department of Gynecology and Obstetrics, Johns Hopkins University School of Medicine, Baltimore, MD, USA†These authors contributed equally to this workAbstract: Despite recent advances in neonatal care and monitoring, asphyxia globally accounts for 23% of the 4 million annual deaths of newborns, and leads to hypoxic-ischemic encephalopathy (HIE. Occurring in five of 1000 live-born infants globally and even more in developing countries, HIE is a serious problem that causes death in 25%–50% of affected neonates and neurological disability to at least 25% of survivors. In order to prevent the damage caused by HIE, our invention provides an effective whole-body cooling of the neonates by utilizing evaporation and an endothermic reaction. Our device is composed of basic electronics, clay pots, sand, and urea-based instant cold pack powder. A larger clay pot, lined with nearly 5 cm of sand, contains a smaller pot, where the neonate will be placed for therapeutic treatment. When the sand is mixed with instant cold pack urea powder and wetted with water, the device can extract heat from inside to outside and maintain the inner pot at 17°C for more than 24 hours with monitoring by LED lights and thermistors

Stimulus induced bursts in severe postanoxic encephalopathy.

Science.gov (United States)

Tjepkema-Cloostermans, Marleen C; Wijers, Elisabeth T; van Putten, Michel J A M

2016-11-01

To report on a distinct effect of auditory and sensory stimuli on the EEG in comatose patients with severe postanoxic encephalopathy. In two comatose patients admitted to the Intensive Care Unit (ICU) with severe postanoxic encephalopathy and burst-suppression EEG, we studied the effect of external stimuli (sound and touch) on the occurrence of bursts. In patient A bursts could be induced by either auditory or sensory stimuli. In patient B bursts could only be induced by touching different facial regions (forehead, nose and chin). When stimuli were presented with relatively long intervals, bursts persistently followed the stimuli, while stimuli with short intervals (encephalopathy can be induced by external stimuli, resulting in stimulus-dependent burst-suppression. Stimulus induced bursts should not be interpreted as prognostic favourable EEG reactivity. Copyright © 2016 International Federation of Clinical Neurophysiology. Published by Elsevier Ireland Ltd. All rights reserved.

The Frequency and Severity of Magnetic Resonance Imaging Abnormalities in Infants with Mild Neonatal Encephalopathy.

Science.gov (United States)

Walsh, Brian H; Neil, Jeffrey; Morey, JoAnn; Yang, Edward; Silvera, Michelle V; Inder, Terrie E; Ortinau, Cynthia

2017-08-01

To assess and contrast the incidence and severity of abnormalities on cerebral magnetic resonance imaging (MRI) between infants with mild, moderate, and severe neonatal encephalopathy who received therapeutic hypothermia. This retrospective cohort studied infants with mild, moderate, and severe neonatal encephalopathy who received therapeutic hypothermia at a single tertiary neonatal intensive care unit between 2013 and 2015. Two neuroradiologists masked to the clinical condition evaluated brain MRIs for cerebral injury after therapeutic hypothermia using the Barkovich classification system. Additional abnormalities not included in this classification system were also noted. The rate, pattern, and severity of abnormalities/injury were compared across the grades of neonatal encephalopathy. Eighty-nine infants received therapeutic hypothermia and met study criteria, 48 with mild neonatal encephalopathy, 35 with moderate neonatal encephalopathy, and 6 with severe neonatal encephalopathy. Forty-eight infants (54%) had an abnormality on MRI. There was no difference in the rate of overall MRI abnormalities by grade of neonatal encephalopathy (mild neonatal encephalopathy 54%, moderate neonatal encephalopathy 54%, and severe neonatal encephalopathy 50%; P= .89). Basal ganglia/thalamic injury was more common in those with severe neonatal encephalopathy (mild neonatal encephalopathy 4%, moderate neonatal encephalopathy 9%, severe neonatal encephalopathy 34%; P = .03). In contrast, watershed injury did not differ between neonatal encephalopathy grades (mild neonatal encephalopathy 36%, moderate neonatal encephalopathy 32%, severe neonatal encephalopathy 50%; P = .3). Mild neonatal encephalopathy is commonly associated with MRI abnormalities after therapeutic hypothermia. The grade of neonatal encephalopathy during the first hours of life may not discriminate adequately between infants with and without cerebral injury noted on MRI after therapeutic hypothermia

Hypoxic-Ischemic Encephalopathy-Associated Liver Fatty Degeneration and the Effects of Therapeutic Hypothermia in Newborn Piglets.

Science.gov (United States)

Kubo, Hiroyuki; Shimono, Ryuichi; Nakamura, Shinji; Koyano, Kosuke; Jinnai, Wataru; Yamato, Satoshi; Yasuda, Saneyuki; Nakamura, Makoto; Tanaka, Aya; Fujii, Takayuki; Kanenishi, Kenji; Chiba, Yoichi; Miki, Takanori; Kusaka, Takashi; Ueno, Masaki

2017-01-01

Although liver can be injured under the hypoxic-ischemic encephalopathy (HIE) condition, there is currently no histopathological evidence. Therapeutic hypothermia is used to protect the brain; however, the therapeutic potential for concomitant liver injury is unknown. This study aimed to histopathologically prove HIE-associated liver injury and to investigate the influence of therapeutic hypothermia in a newborn piglet HIE model. Eighteen newborn piglets were divided into 3 groups: control (n = 4), HIE (n = 8), and therapeutic hypothermia (n = 6) groups. The hypoxic insult was induced by decreasing the fraction of inspiratory oxygen from 21 to 2-4% over 40 min while monitoring cerebral blood volume and cerebral hemoglobin oxygen saturation. For therapeutic hypothermia, whole-body cooling at 33-34°C was administered for 24 h after the hypoxic insult. We hematologically and histopathologically investigated the liver injury in all groups. Alanine transaminase and lactate dehydrogenase levels in the HIE group were significantly elevated compared with those in the control group. Micro-lipid droplet accumulation in the periportal zone, but not in the perivenous zone, was significantly greater in the HIE group than in the control group and significantly smaller in the therapeutic hypothermia group than in the HIE group. We demonstrated that micro-lipid droplet accumulation in the cytoplasm of hepatocytes in the periportal zone occurs under the HIE condition and that this accumulation is suppressed by therapeutic hypothermia. © 2016 S. Karger AG, Basel.

Clinical hypoxic-ischemic encephalopathy score of the Iberoamerican Society of Neonatology (Siben: A new proposal for diagnosis and management

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José Maria Rodriguez Perez

Full Text Available Summary Hypoxic ischemic encephalopathy is a major complication of perinatal asphyxia, with high morbidity, mortality and neurologic sequelae as cerebral palsy, mostly in poor or developing countries. The difficulty in the diagnosis and management of newborns in these countries is astonishing, thus resulting in unreliable data on this pathology and bad outcomes regarding mortality and incidence of neurologic sequelae. The objective of this article is to present a new clinical diagnostic score to be started in the delivery room and to guide the therapeutic approach, in order to improve these results.

Clinical hypoxic-ischemic encephalopathy score of the Iberoamerican Society of Neonatology (Siben): A new proposal for diagnosis and management.

Science.gov (United States)

Perez, José Maria Rodriguez; Golombek, Sergio G; Sola, Augusto

2017-01-01

Hypoxic ischemic encephalopathy is a major complication of perinatal asphyxia, with high morbidity, mortality and neurologic sequelae as cerebral palsy, mostly in poor or developing countries. The difficulty in the diagnosis and management of newborns in these countries is astonishing, thus resulting in unreliable data on this pathology and bad outcomes regarding mortality and incidence of neurologic sequelae. The objective of this article is to present a new clinical diagnostic score to be started in the delivery room and to guide the therapeutic approach, in order to improve these results.

Protein S100B in umbilical cord blood as a potential biomarker of hypoxic-ischemic encephalopathy in asphyxiated newborns.

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Zaigham, Mehreen; Lundberg, Fredrik; Olofsson, Per

2017-09-01

Neonatal hypoxic ischemic encephalopathy (HIE) is a devastating condition resulting from a sustained lack of oxygen during birth. The interest in identifying a relevant biomarker of HIE has thrown into limelight the role of protein S100B as a clinical diagnostic marker of hypoxic brain damage in neonates. To evaluate the diagnostic value of protein S100B, measured in umbilical cord blood immediately after birth, as a useful biomarker in the diagnosis of HIE Sarnat stages II-III as well as a marker for long-term mortality and morbidity. Protein S100B was analyzed in cord blood sampled at birth from 13 newborns later diagnosed with stage II-III HIE and compared with 21 healthy controls. S100B concentrations were related to cord artery pH, amplitude-integrated electroencephalography (aEEG), stage of HIE, and death/sequelae up to an age of 6years. Both parametric and non-parametric statistics were used with a two-sided P<0.05 considered significant. The difference in S100B concentration was marginally statistically significant between HIE cases and controls (P=0.056). Cord blood acidosis (P=0.046), aEEG pattern severity (P=0.030), HIE severity (P=0.027), and condition at 6-year follow-up (healthy/permanent sequelae/death; P=0.027) were all related to an increase in S100B concentration. Protein S100B in neonates suffering from HIE stages II-III appeared elevated in umbilical cord blood at birth. The S100B concentrations were positively associated to the severity of disease and the risk of suffering from neurodevelopmental sequelae and even death. Copyright © 2017. Published by Elsevier B.V.

Important hypercalcemia due to subcutaneous fat necrosis treated with pamidronate in an infant with severe hypoxic-ischemic encephalopathy

OpenAIRE

Pasqua Anna Quitadamo; Antonio Villani; Piero Paolo Cristalli; Marina Marinelli; Anita Riganti; Michele Bisceglia; Alberto Gatta

2016-01-01

Subcutaneous fat necrosis (SCFN) of the newborn is an uncommon form of panniculitis that occurs after fetal distress and involves fatty areas during the first weeks of life. This rare disorder is generally self-limiting and undergoes complete regression. However, it can be complicated with a potentially life-threatening hypercalcemia. We report a case of severe hypercalcemia due to SCFN occurring after serious perinatal hypoxic injury, which resolved by intravenous administration of pamidrona...

Management and investigation of neonatal encephalopathy: 2017 update

Science.gov (United States)

Martinello, Kathryn; Hart, Anthony R; Yap, Sufin; Mitra, Subhabrata

2017-01-01

This review discusses an approach to determining the cause of neonatal encephalopathy, as well as current evidence on resuscitation and subsequent management of hypoxic-ischaemic encephalopathy (HIE). Encephalopathy in neonates can be due to varied aetiologies in addition to hypoxic-ischaemia. A combination of careful history, examination and the judicious use of investigations can help determine the cause. Over the last 7 years, infants with moderate to severe HIE have benefited from the introduction of routine therapeutic hypothermia; the number needed to treat for an additional beneficial outcome is 7 (95% CI 5 to 10). More recent research has focused on optimal resuscitation practices for babies with cardiorespiratory depression, such as delayed cord clamping after establishment of ventilation and resuscitation in air. Around a quarter of infants with asystole at 10 min after birth who are subsequently cooled have normal outcomes, suggesting that individualised decision making on stopping resuscitation is needed, based on access to intensive treatment unit and early cooling. The full benefit of cooling appears to have been exploited in our current treatment protocols of 72 hours at 33.5°C; deeper and longer cooling showed adverse outcome. The challenge over the next 5–10 years will be to assess which adjunct therapies are safe and optimise hypothermic brain protection in phase I and phase II trials. Optimal care may require tailoring treatments according to gender, genetic risk, injury severity and inflammatory status. PMID:28389438

Important hypercalcemia due to subcutaneous fat necrosis treated with pamidronate in an infant with severe hypoxic-ischemic encephalopathy

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Pasqua Anna Quitadamo

2016-08-01

Full Text Available Subcutaneous fat necrosis (SCFN of the newborn is an uncommon form of panniculitis that occurs after fetal distress and involves fatty areas during the first weeks of life. This rare disorder is generally self-limiting and undergoes complete regression. However, it can be complicated with a potentially life-threatening hypercalcemia. We report a case of severe hypercalcemia due to SCFN occurring after serious perinatal hypoxic injury, which resolved by intravenous administration of pamidronate. This treatment was rapidly effective and well tolerated. We suggest that pamidronate could be the first-line therapy for severe hypercalcemia in SCFN.

A validated clinical MRI injury scoring system in neonatal hypoxic-ischemic encephalopathy

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Trivedi, Shamik B.; Vesoulis, Zachary A.; Rao, Rakesh; Liao, Steve M.; Mathur, Amit M. [Washington University School of Medicine, Division of Newborn Medicine, Edward Mallinckrodt Department of Pediatrics, St. Louis, MO (United States); Shimony, Joshua S.; McKinstry, Robert C. [Washington University School of Medicine, Mallinckrodt Institute of Radiology, St. Louis, MO (United States)

2017-10-15

Deep nuclear gray matter injury in neonatal hypoxic-ischemic encephalopathy (HIE) is associated with worse neurodevelopmental outcomes. We previously published a qualitative MRI injury scoring system utilizing serial T1-weighted, T2-weighted and diffusion-weighted imaging (DWI), weighted for deep nuclear gray matter injury. To establish the validity of the MRI scoring system with neurodevelopmental outcome at 18-24 months. MRI scans from neonates with moderate to severe HIE treated with therapeutic hypothermia were evaluated. Signal abnormality was scored on T1-weighted, T2-weighted and DWI sequences and assessed using an established system in five regions: (a) subcortical: caudate nucleus, globus pallidus and putamen, thalamus and the posterior limb of the internal capsule; (b) white matter; (c) cortex, (d) cerebellum and (e) brainstem. MRI injury was graded as none, mild, moderate or severe. Inter-rater reliability was tested on a subset of scans by two independent and blinded neuroradiologists. Surviving infants underwent the Bayley Scales of Infant and Toddler Development-III (Bayley-III) at 18-24 months. Data were analyzed using univariate and multivariate linear and logistic regression. Fifty-seven eligible neonates underwent at least one MRI scan in the first 2 weeks of life. Mean postnatal age at scan 1 was 4±2 days in 50/57 (88%) neonates and 48/54 (89%) surviving infants underwent scan 2 at 10±2 days. In 54/57 (95%) survivors, higher MRI injury grades were significantly associated with worse outcomes in the cognitive, motor and language domains of the Bayley-III. A qualitative MRI injury scoring system weighted for deep nuclear gray matter injury is a significant predictor of neurodevelopmental outcome at 18-24 months in neonates with HIE. (orig.)

A validated clinical MRI injury scoring system in neonatal hypoxic-ischemic encephalopathy

International Nuclear Information System (INIS)

Trivedi, Shamik B.; Vesoulis, Zachary A.; Rao, Rakesh; Liao, Steve M.; Mathur, Amit M.; Shimony, Joshua S.; McKinstry, Robert C.

2017-01-01

Deep nuclear gray matter injury in neonatal hypoxic-ischemic encephalopathy (HIE) is associated with worse neurodevelopmental outcomes. We previously published a qualitative MRI injury scoring system utilizing serial T1-weighted, T2-weighted and diffusion-weighted imaging (DWI), weighted for deep nuclear gray matter injury. To establish the validity of the MRI scoring system with neurodevelopmental outcome at 18-24 months. MRI scans from neonates with moderate to severe HIE treated with therapeutic hypothermia were evaluated. Signal abnormality was scored on T1-weighted, T2-weighted and DWI sequences and assessed using an established system in five regions: (a) subcortical: caudate nucleus, globus pallidus and putamen, thalamus and the posterior limb of the internal capsule; (b) white matter; (c) cortex, (d) cerebellum and (e) brainstem. MRI injury was graded as none, mild, moderate or severe. Inter-rater reliability was tested on a subset of scans by two independent and blinded neuroradiologists. Surviving infants underwent the Bayley Scales of Infant and Toddler Development-III (Bayley-III) at 18-24 months. Data were analyzed using univariate and multivariate linear and logistic regression. Fifty-seven eligible neonates underwent at least one MRI scan in the first 2 weeks of life. Mean postnatal age at scan 1 was 4±2 days in 50/57 (88%) neonates and 48/54 (89%) surviving infants underwent scan 2 at 10±2 days. In 54/57 (95%) survivors, higher MRI injury grades were significantly associated with worse outcomes in the cognitive, motor and language domains of the Bayley-III. A qualitative MRI injury scoring system weighted for deep nuclear gray matter injury is a significant predictor of neurodevelopmental outcome at 18-24 months in neonates with HIE. (orig.)

Comparison of early and late MRI in neonatal hypoxic-ischemic encephalopathy using three assessment methods

International Nuclear Information System (INIS)

Charon, Valerie; Proisy, Maia; Bruneau, Bertrand; Treguier, Catherine; Rozel, Celine; Ferre, Jean-Christophe; Beuchee, Alain; Chauvel, Jennifer

2015-01-01

There is no consensus on the optimum timing of MRI in neonates with hypoxic-ischemic encephalopathy treated with hypothermia. Reliable early imaging assessment might help managing treatment. To assess non-random differences between early and late MRI that might influence intensive-care decisions. This single-center retrospective study included all asphyxiated term neonates eligible for hypothermia treatment November 2009-July 2012. MRI scans were systematically performed at day 4 (early MRI) and day 11 of life as part of routine protocol. Two experienced pediatric radiologists reviewed both scans according to three assessment methods: a pattern classification, a scoring system and a simplified classification. Agreement between early and late imaging findings was assessed using Cohen's kappa coefficients. Thirty-three neonates were included. Interobserver agreement was excellent. Early MRI detected all severe injuries. Agreement between early and late MRI was excellent for the simplified classification (κ = 0.82), good for the pattern classification (κ = 0.64), and good to excellent for 3 scores out of 4 in the scoring system (κ = 0.70-0.89). Early MRI may provide valuable information about brain injury to help parents and neonatologists in intensive-care decisions at the end of hypothermia treatment. (orig.)

Comparison of early and late MRI in neonatal hypoxic-ischemic encephalopathy using three assessment methods

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Charon, Valerie; Proisy, Maia; Bruneau, Bertrand; Treguier, Catherine; Rozel, Celine [University Hospital, Department of Imaging, Hopital Sud, Rennes, Cedex 2 (France); Ferre, Jean-Christophe [University Hospital, Department of Neuroradiology, Hopital Pontchaillou, Rennes (France); Beuchee, Alain [University Hospital, Department of Neonatology, Hopital Sud, Rennes (France); Chauvel, Jennifer [Saint Brieuc Hospital, Department of Neonatology, Saint-Brieuc (France)

2015-12-15

There is no consensus on the optimum timing of MRI in neonates with hypoxic-ischemic encephalopathy treated with hypothermia. Reliable early imaging assessment might help managing treatment. To assess non-random differences between early and late MRI that might influence intensive-care decisions. This single-center retrospective study included all asphyxiated term neonates eligible for hypothermia treatment November 2009-July 2012. MRI scans were systematically performed at day 4 (early MRI) and day 11 of life as part of routine protocol. Two experienced pediatric radiologists reviewed both scans according to three assessment methods: a pattern classification, a scoring system and a simplified classification. Agreement between early and late imaging findings was assessed using Cohen's kappa coefficients. Thirty-three neonates were included. Interobserver agreement was excellent. Early MRI detected all severe injuries. Agreement between early and late MRI was excellent for the simplified classification (κ = 0.82), good for the pattern classification (κ = 0.64), and good to excellent for 3 scores out of 4 in the scoring system (κ = 0.70-0.89). Early MRI may provide valuable information about brain injury to help parents and neonatologists in intensive-care decisions at the end of hypothermia treatment. (orig.)

Investigation of the effect and mechanism of hyperbaric oxygenation therapy on neonatal hypoxic-ischemic encephalopathy with SPECT

International Nuclear Information System (INIS)

Jia Shaowei; Yi Zhi; Liao Jianxiang

2001-01-01

Objective: To evaluate the effect of HBO on neonatal hypoxic-ischemic encephalopathy with SPECT, and to explore the mechanisms. Methods: The research subjects were totally 34 newborn babies, including 3 normal neonates. The group treated with HBO included 20 babies with HIE, and the control group contained 11 HIE babies. All babies in both groups received SPECT exams before and after the treatments. Results: SPECT before treatment showed 46 foci of low perfusion and functional defect or insufficiencies in 31 HIE babies. SPECT after 1-2 period of treatments of HBO therapy in HIE babies showed disappeared or reduced low perfusion and functional defect or insufficiency in the brains. The HIE babies in the control group showed improvement with less degree than HBO treated babies. There were significant differences (P<0.01) between two groups. Conclusion: The effect of HBO on HIE babies were prominent. The treatment can improve the hypoxic status of brain cell through increase the regional cerebral blood flow perfusion and oxygen content of the brain tissue, then provoked the brain cells activities, and at last, enhance the repair of the injured brain cells

Predicting outcome in term neonates with hypoxic-ischaemic encephalopathy using simplified MR criteria

International Nuclear Information System (INIS)

Jyoti, Rajeev; O'Neil, Ross

2006-01-01

MRI is an established investigation in the evaluation of neonates with suspected hypoxic-ischaemic encephalopathy (HIE). However, its role as a predictor of neurodevelopmental outcome remains complex. To establish reproducible simplified MR criteria and evaluate their role in predicting neurodevelopmental outcome in term neonates with HIE. Term neonates with suspected HIE had MRI at 7-10 days of age. MR scans were interpreted according to new simplified criteria by two radiologists blinded to the clinical course and outcome. The new simplified criteria allocated grade 1 to cases with no central and less than 10% peripheral change, grade 2 to those with less than 30% central and/or 10-30% peripheral area change, and grade 3 to those with more than 30% central or peripheral change. MRI changes were compared with clinical neurodevelopmental outcome evaluated prospectively at 1 year of age. Neurodevelopmental outcome was based upon the DQ score (revised Griffith's) and cerebral palsy on neurological assessment. Of 20 subjects, all those showing severe (grade 3) MR changes (35%) died or had poor neurodevelopmental outcome. Subjects with a normal MR scan or with scans showing only mild (grade 1) MR changes (55%) had normal outcomes. One subject showing moderate (grade 2) changes on MRI had a moderate outcome (5%), while another had an atypical pattern of MR changes with a normal outcome (5%). Assessment of full-term neonates with suspected HIE using the simplified MR criteria is highly predictive of neurodevelopmental outcome. (orig.)

Predicting outcome in term neonates with hypoxic-ischaemic encephalopathy using simplified MR criteria

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Jyoti, Rajeev; O' Neil, Ross [Canberra Hospital, Medical Imaging, Canberra, ACT (Australia)

2006-01-01

MRI is an established investigation in the evaluation of neonates with suspected hypoxic-ischaemic encephalopathy (HIE). However, its role as a predictor of neurodevelopmental outcome remains complex. To establish reproducible simplified MR criteria and evaluate their role in predicting neurodevelopmental outcome in term neonates with HIE. Term neonates with suspected HIE had MRI at 7-10 days of age. MR scans were interpreted according to new simplified criteria by two radiologists blinded to the clinical course and outcome. The new simplified criteria allocated grade 1 to cases with no central and less than 10% peripheral change, grade 2 to those with less than 30% central and/or 10-30% peripheral area change, and grade 3 to those with more than 30% central or peripheral change. MRI changes were compared with clinical neurodevelopmental outcome evaluated prospectively at 1 year of age. Neurodevelopmental outcome was based upon the DQ score (revised Griffith's) and cerebral palsy on neurological assessment. Of 20 subjects, all those showing severe (grade 3) MR changes (35%) died or had poor neurodevelopmental outcome. Subjects with a normal MR scan or with scans showing only mild (grade 1) MR changes (55%) had normal outcomes. One subject showing moderate (grade 2) changes on MRI had a moderate outcome (5%), while another had an atypical pattern of MR changes with a normal outcome (5%). Assessment of full-term neonates with suspected HIE using the simplified MR criteria is highly predictive of neurodevelopmental outcome. (orig.)

BLOOD BIOMARKERS FOR EVALUATION OF PERINATAL ENCEPHALOPATHY

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Ernest Marshall Graham

2016-07-01

Full Text Available Recent research in identification of brain injury after trauma shows many possible blood biomarkers that may help identify the fetus and neonate with encephalopathy. Traumatic brain injury shares many common features with perinatal hypoxic-ischemic encephalopathy. Trauma has a hypoxic component, and one of the 1st physiologic consequences of moderate-severe traumatic brain injury is apnea. Trauma and hypoxia-ischemia initiate an excitotoxic cascade and free radical injury followed by the inflammatory cascade, producing injury in neurons, glial cells and white matter. Increased excitatory amino acids, lipid peroxidation products and alteration in microRNAs and inflammatory markers are common to both traumatic brain injury and perinatal encephalopathy. The blood-brain barrier is disrupted in both leading to egress of substances normally only found in the central nervous system. Brain exosomes may represent ideal biomarker containers, as RNA and protein transported within the vesicles are protected from enzymatic degradation. Evaluation of fetal or neonatal brain derived exosomes that cross the blood-brain barrier and circulate peripherally has been referred to as the liquid brain biopsy. A multiplex of serum biomarkers could improve upon the current imprecise methods of identifying fetal and neonatal brain injury such as fetal heart rate abnormalities, meconium, cord gases at delivery, and Apgar scores. Quantitative biomarker measurements of perinatal brain injury and recovery could lead to operative delivery only in the presence of significant fetal risk, triage to appropriate therapy after birth and measure the effectiveness of treatment.

Ammonia levels and the severity of hepatic encephalopathy

International Nuclear Information System (INIS)

Qureshi, M.O.; Khokhar, N.; Shafqat, F.

2014-01-01

Objective: To evaluate the correlation between ammonia levels with the severity of HE in patients coming to the tertiary care hospital with liver cirrhosis and hepatic encephalopathy (HE). Study Design: Descriptive, analytical study. Place and Duration of Study: Shifa International Hospital, Islamabad, from January 2011 to February 2012. Methodology: A total of 135 patients with liver cirrhosis and HE had serum ammonia levels measured on admission. The diagnosis of HE was based on clinical criteria, and its severity was graded according to the West Haven Criteria for grading of mental status. Ammonia levels were correlated with the severity of HE using Spearman rank correlation. Results: Out of 20 patients with normal ammonia levels, 13 (65%) were in HE I-II, 6 (30%) were in grade-III, while 1 (5%) patient was in grade-IV HE. Out of 45 patients with mild hyperammonemia, 27 (60%) were in grade I-II, 12 (26%) were in grade-III and 6 (13%) were in grade-IV HE. Out of 34 patients with moderate hyperammonemia, 9 (26%) were in grade I-II, 18 (53%) were in grade-III, and 7 (20%) were in grade-IV HE. Out of 36 patients with severe hyperammonemia, 31 (86%) patients were in grade-IV HE (p < 0.001). Conclusion: Ammonia levels correlated with the severity of hepatic encephalopathy. Greater the ammonia level, severe is the grade of hepatic encephalopathy. (author)

Glucocorticoids Protect Neonatal Rat Brain in Model of Hypoxic-Ischemic Encephalopathy (HIE

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Benjamin Harding

2016-12-01

Full Text Available Hypoxic-ischemic encephalopathy (HIE resulting from asphyxia in the peripartum period is the most common cause of neonatal brain damage and can result in significant neurologic sequelae, including cerebral palsy. Currently therapeutic hypothermia is the only accepted treatment in addition to supportive care for infants with HIE, however, many additional neuroprotective therapies have been investigated. Of these, glucocorticoids have previously been shown to have neuroprotective effects. HIE is also frequently compounded by infectious inflammatory processes (sepsis and as such, the infants may be more amenable to treatment with an anti-inflammatory agent. Thus, the present study investigated dexamethasone and hydrocortisone treatment given after hypoxic-ischemic (HI insult in neonatal rats via intracerebroventricular (ICV injection and intranasal administration. In addition, we examined the effects of hydrocortisone treatment in HIE after lipopolysaccharide (LPS sensitization in a model of HIE and sepsis. We found that dexamethasone significantly reduced rat brain infarction size when given after HI treatment via ICV injection; however it did not demonstrate any neuroprotective effects when given intranasally. Hydrocortisone after HI insult also significantly reduced brain infarction size when given via ICV injection; and the intranasal administration showed to be protective of brain injury in male rats at a dose of 300 µg. LPS sensitization did significantly increase the brain infarction size compared to controls, and hydrocortisone treatment after LPS sensitization showed a significant decrease in brain infarction size when given via ICV injection, as well as intranasal administration in both genders at a dose of 300 µg. To conclude, these results show that glucocorticoids have significant neuroprotective effects when given after HI injury and that these effects may be even more pronounced when given in circumstances of additional

Role of magnetic resonance imaging in biometric evaluation of corpus callosum in hypoxic ischemic encephalopathy patients

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Amit Garhwal

2017-01-01

Full Text Available Background: Corpus callosum (CC has an important role in establishing hemispheric lateralization of function. Significance of this structure which is the primary white matter commissure of the brain lies in the fact that damage to the CC during development has been found to be associated with poor neurological outcome and neuropsychological performance. Magnetic resonance imaging (MRI can precisely detect, localize, and evaluate damage to CC in hypoxic-ischemic encephalopathy (HIE patients and assist in reaching to at an accurate anatomical diagnosis, thus heeling in further management of the patient. Objectives: The objective of this study is to analyze the effect of HIE on CC morphometry by assessing various diameters of CC. Materials and Methods: Fifty-four patients with history of hypoxic-ischemic injury referred to the Department of Radiodiagnosis were included in the study. All the patients were made to undergo MRI of the brain using Siemens Symphony Magnetom 1.5 Tesla scanner after taking informed consent for the same. The findings of MRI brain were assessed and analyzed. Data analysis was done using percentages of different diagnosis and outcomes made by MRI brain were computed and compiled. Results: In the present study, male predominance is seen, 77.78% patients were male and 22.22% were female. In the present study, maximum numbers of patients were <1 year of age (37.04%. In the present study, we see that the isthmus was the most commonly affected portion of CC. Children who did not cry at birth, born with low birth weight, low Apgar score were positively correlated with severity of damage to CC. Conclusion: From the present study, it was noted that MRI is very efficient tool in evaluating morphometry of CC in HIE. Its noninvasiveness and no exposure to ionizing radiation is an added advantage. However, experience and understanding of the principles are essential for accurate diagnosis.

Sodium Pyruvate Reduced Hypoxic-Ischemic Injury to Neonatal Rat Brain

OpenAIRE

Pan, Rui; Rong, Zhihui; She, Yun; Cao, Yuan; Chang, Li-Wen; Lee, Wei-Hua

2012-01-01

Background Neonatal hypoxia-ischemia (HI) remains a major cause of severe brain damage and is often associated with high mortality and lifelong disability. Immature brains are extremely sensitive to hypoxia-ischemia, shown as prolonged mitochondrial neuronal death. Sodium pyruvate (SP), a substrate of the tricarboxylic acid cycle and an extracellular antioxidant, has been considered as a potential treatment for hypoxic-ischemic encephalopathy (HIE), but its effects have not been evaluated in ...

Hypoxic-Ischemic Encephalopathy With Clinical and Imaging Abnormalities Limited to Occipital Lobe.

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Parmar, Hemant A; Trobe, Jonathan D

2016-09-01

The vulnerable brain areas in hypoxic-ischemic encephalopathy (HIE) following systemic hypotension are typically the neocortex, deep cerebral gray nuclei, hippocampus, cerebellum, and the parieto-occipital arterial border zone region. The visual cortex is not commonly recognized as a target in this setting. Single-institution review from 2007 to 2015 of patients who suffered cortical visual loss as an isolated clinical manifestation following systemic hypotension and whose brain imaging showed abnormalities limited to the occipital lobe. Nine patients met inclusion criteria. Visual loss at outset ranged from hand movements to 20/20, but all patients had homonymous field loss at best. In 1 patient, imaging was initially normal but 4 months later showed encephalomalacia. In 2 patients, imaging was initially subtle enough to be recognized as abnormal only when radiologists were advised that cortical visual loss was present. The occipital lobe may be an isolated target in HIE with cortical visual loss as the only clinical manifestation. Imaging performed in the acute period may appear normal or disclose abnormalities subtle enough to be overlooked. Radiologists informed of the clinical manifestations may be more attune to these abnormalities, which will become more apparent months later when occipital volume loss develops.

Arterial spin-labelling perfusion MRI and outcome in neonates with hypoxic-ischemic encephalopathy

International Nuclear Information System (INIS)

Vis, Jill B. de; Hendrikse, Jeroen; Petersen, Esben T.; Vries, Linda S. de; Bel, Frank van; Alderliesten, Thomas; Negro, Simona; Groenendaal, Floris; Benders, Manon J.N.L.

2015-01-01

Hyperperfusion may be related to outcome in neonates with hypoxic-ischemic encephalopathy (HIE). The purpose of this study was to evaluate whether arterial spin labelling (ASL) perfusion is associated with outcome in neonates with HIE and to compare the predictive value of ASL MRI to known MRI predictive markers. Twenty-eight neonates diagnosed with HIE and assessed with MR imaging (conventional MRI, diffusion-weighted MRI, MR spectroscopy [MRS], and ASL MRI) were included. Perfusion in the basal ganglia and thalami was measured. Outcome at 9 or 18 months of age was scored as either adverse (death or cerebral palsy) or favourable. The median (range) perfusion in the basal ganglia and thalami (BGT) was 63 (28-108) ml/100 g/min in the neonates with adverse outcome and 28 (12-51) ml/100 g/min in the infants with favourable outcome (p 2 = 0.86, p < 0.001). Higher ASL perfusion values in neonates with HIE are associated with a worse neurodevelopmental outcome. A combination of the MRS and ASL MRI information is the best predictor of outcome. (orig.)

Neuroprotective body hypothermia among newborns with hypoxic ischemic encephalopathy: three-year experience in a tertiary university hospital. A retrospective observational study.

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Magalhães, Mauricio; Rodrigues, Francisco Paulo Martins; Chopard, Maria Renata Tollio; Melo, Victoria Catarina de Albuquerque; Melhado, Amanda; Oliveira, Inez; Gallacci, Clery Bernardi; Pachi, Paulo Roberto; Lima Neto, Tabajara Barbosa

2015-01-01

Neonatal hypoxic-ischemic encephalopathy is associated with high morbidity and mortality. Studies have shown that therapeutic hypothermia decreases neurological sequelae and death. Our aim was therefore to report on a three-year experience of therapeutic hypothermia among asphyxiated newborns. Retrospective study, conducted in a university hospital. Thirty-five patients with perinatal asphyxia undergoing body cooling between May 2009 and November 2012 were evaluated. Thirty-nine infants fulfilled the hypothermia protocol criteria. Four newborns were removed from study due to refractory septic shock, non-maintenance of temperature and severe coagulopathy. The median Apgar scores at 1 and 5 minutes were 2 and 5. The main complication was infection, diagnosed in seven mothers (20%) and 14 newborns (40%). Convulsions occurred in 15 infants (43%). Thirty-one patients (88.6%) required mechanical ventilation and 14 of them (45%) were extubated within 24 hours. The duration of mechanical ventilation among the others was 7.7 days. The cooling protocol was started 1.8 hours after birth. All patients showed elevated levels of creatine phosphokinase, creatine phosphokinase- MB and lactate dehydrogenase. There was no severe arrhythmia; one newborn (2.9%) presented controlled coagulopathy. Four patients (11.4%) presented controlled hypotension. Twenty-nine patients (82.9%) underwent cerebral ultrasonography and 10 of them (34.5%) presented white matter hyper-echogenicity. Brain magnetic resonance imaging was performed on 33 infants (94.3%) and 11 of them (33.3%) presented hypoxic-ischemic changes. The hospital stay was 23 days. All newborns were discharged. Two patients (5.8%) needed gastrostomy. Hypothermia as therapy for asphyxiated newborns was shown to be safe.

Impaired cerebral autoregulation and brain injury in newborns with hypoxic-ischemic encephalopathy treated with hypothermia.

Science.gov (United States)

Massaro, An N; Govindan, R B; Vezina, Gilbert; Chang, Taeun; Andescavage, Nickie N; Wang, Yunfei; Al-Shargabi, Tareq; Metzler, Marina; Harris, Kari; du Plessis, Adre J

2015-08-01

Impaired cerebral autoregulation may contribute to secondary injury in newborns with hypoxic-ischemic encephalopathy (HIE). Continuous, noninvasive assessment of cerebral pressure autoregulation can be achieved with bedside near-infrared spectroscopy (NIRS) and systemic mean arterial blood pressure (MAP) monitoring. This study aimed to evaluate whether impaired cerebral autoregulation measured by NIRS-MAP monitoring during therapeutic hypothermia and rewarming relates to outcome in 36 newborns with HIE. Spectral coherence analysis between NIRS and MAP was used to quantify changes in the duration [pressure passivity index (PPI)] and magnitude (gain) of cerebral autoregulatory impairment. Higher PPI in both cerebral hemispheres and gain in the right hemisphere were associated with neonatal adverse outcomes [death or detectable brain injury by magnetic resonance imaging (MRI), P < 0.001]. NIRS-MAP monitoring of cerebral autoregulation can provide an ongoing physiological biomarker that may help direct care in perinatal brain injury. Copyright © 2015 the American Physiological Society.

Sodium bicarbonate supplementation improves severe-intensity intermittent exercise under moderate acute hypoxic conditions.

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Deb, Sanjoy K; Gough, Lewis A; Sparks, S Andy; McNaughton, Lars R

2018-03-01

Acute moderate hypoxic exposure can substantially impair exercise performance, which occurs with a concurrent exacerbated rise in hydrogen cation (H + ) production. The purpose of this study was therefore, to alleviate this acidic stress through sodium bicarbonate (NaHCO 3 ) supplementation and determine the corresponding effects on severe-intensity intermittent exercise performance. Eleven recreationally active individuals participated in this randomised, double-blind, crossover study performed under acute normobaric hypoxic conditions (FiO 2 % = 14.5%). Pre-experimental trials involved the determination of time to attain peak bicarbonate anion concentrations ([HCO 3 - ]) following NaHCO 3 ingestion. The intermittent exercise tests involved repeated 60-s work in their severe-intensity domain and 30-s recovery at 20 W to exhaustion. Participants ingested either 0.3 g kg bm -1 of NaHCO 3 or a matched placebo of 0.21 g kg bm -1 of sodium chloride prior to exercise. Exercise tolerance (+ 110.9 ± 100.6 s; 95% CI 43.3-178 s; g = 1.0) and work performed in the severe-intensity domain (+ 5.8 ± 6.6 kJ; 95% CI 1.3-9.9 kJ; g = 0.8) were enhanced with NaHCO 3 supplementation. Furthermore, a larger post-exercise blood lactate concentration was reported in the experimental group (+ 4 ± 2.4 mmol l -1 ; 95% CI 2.2-5.9; g = 1.8), while blood [HCO 3 - ] and pH remained elevated in the NaHCO 3 condition throughout experimentation. In conclusion, this study reported a positive effect of NaHCO 3 under acute moderate hypoxic conditions during intermittent exercise and therefore, may offer an ergogenic strategy to mitigate hypoxic induced declines in exercise performance.

Brain hypothermia therapy for childhood acute encephalopathy based on clinical evidence

OpenAIRE

IMATAKA, GEORGE; ARISAKA, OSAMU

2015-01-01

Although previous studies have reported on the effectiveness of brain hypothermia therapy in childhood acute encephalopathy, additional studies in this field are necessary. In this review, we discussed brain hypothermia therapy methods for two clinical conditions for which sufficient evidences are currently available in the literature. The first condition is known as hypoxic-ischemic encephalopathy and occurs in newborns and the second condition is acute encephalopathy which occurs in adults ...

Post-partum posterior reversible encephalopathy syndrome

DEFF Research Database (Denmark)

Aaen, Anne Albers; Jeppesen, Jørgen; Obaid, Hayder

2015-01-01

Posterior reversible encephalopathy syndrome (PRES) is a complex clinical condition with vasogenic subcortical oedema caused by hypertension. Oedema is often seen on magnetic resonance imaging. The wide clinical spectrum ranges from headaches to vision loss and even death. Early diagnosis...... and treatment is important for the reversibility of the condition. In this case report we emphasize the importance of blood pressure control in a post-partum woman, who had a rather complicated pregnancy. The symptoms of PRES were not recognized immediately because of failure to use and acknowledge a blood...

Post-partum posterior reversible encephalopathy syndrome

DEFF Research Database (Denmark)

Aaen, Anne Albers; Jeppesen, Jørgen; Obaid, Hayder

2015-01-01

and treatment is important for the reversibility of the condition. In this case report we emphasize the importance of blood pressure control in a post-partum woman, who had a rather complicated pregnancy. The symptoms of PRES were not recognized immediately because of failure to use and acknowledge a blood......Posterior reversible encephalopathy syndrome (PRES) is a complex clinical condition with vasogenic subcortical oedema caused by hypertension. Oedema is often seen on magnetic resonance imaging. The wide clinical spectrum ranges from headaches to vision loss and even death. Early diagnosis...

[Post-partum posterior reversible encephalopathy syndrome].

Science.gov (United States)

Aaen, Anne Albers; Jeppesen, Jørgen; Obaid, Hayder; Bülow, Hans Henrik

2015-11-23

Posterior reversible encephalopathy syndrome (PRES) is a complex clinical condition with vasogenic subcortical oedema caused by hypertension. Oedema is often seen on magnetic resonance imaging. The wide clinical spectrum ranges from headaches to vision loss and even death. Early diagnosis and treatment is important for the reversibility of the condition. In this case report we emphasize the importance of blood pressure control in a post-partum woman, who had a rather complicated pregnancy. The symptoms of PRES were not recognized immediately because of failure to use and acknowledge a blood pressure test.

Influence of one-year neurologic outcome of treatment on newborns with moderate and severe hypoxic-ischemic encephalopathy by rhuEP0 combined with ganglioside (GM1).

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Zhu, X-Y; Ye, M-Y; Zhang, A-M; Wang, W-D; Zeng, F; Li, J-L; Fang, F

2015-10-01

To observe the one-year neurologic prognostic outcome of newborns with moderate and severe hypoxic-ischemic encephalopathy (HIE) who received recombinant human erythropoietin (rhuEPO) combined with exogenous monosialotetrahexosylganglioside (GM1) treatment to provide new guidelines for clinical treatment. Seventy-six newborns with moderate and severe HIE were selected from February 2011 to February 2014 in our hospital. This study received the informed consent of our hospital's Ethics Committee and the newborns' guardians. The newborns were divided to an observation group (n = 34 cases) and a control group (n = 42 cases). All newborns underwent hypothermia and conventional treatment for their conditions. The control group received GMl treatment and observation group received rhuEPO combined with GMl treatment. The curative differences and neural behavior from these two groups were compared. The excellent, efficient proportion and total effective rate of the newborns from the observation group were higher than the control group. The death rate, cerebral palsy and the invalid ratio of the newborns from the observation group were lower than that of the control group. Awareness, muscle tension, primitive reflex and increased intracranial pressure recovery time of the newborns in the observation group were less than those of the control group. The Neonatal Behavior Neurological Assessment (NBNA) score of both groups after the treatment of 7, 14 and 28 days were significantly higher and increased with time (p newborns from the two groups all increased after treatment of 3, 6 and 12 months than those of before, which increased with time (p newborns with HIE improves short-term clinical effects and long-term neurological symptoms.

Neuroprotective effects of electro acupuncture on hypoxic-ischemic encephalopathy in newborn rats Ass.

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Xu, Tao; Li, Wenjie; Liang, Yiqun; Yang, Zhonghua; Liu, Jingdong; Wang, Yejun; Su, Nailun

2014-11-01

Hypoxic-ischemic encephalopathy (HIE) is a common and potentially devastating condition in the neonate, associated with high mortality and morbidity. Effective treatment options are limited and therefore alternative therapies such as acupuncture are increasingly used. Previous studies have shown that electro acupuncture promoted proliferation of neural progenitor cell and increased expression of neurotrophic factor in HIE. However, effects of electro acupuncture on downstream signaling pathways have been rarely researched. So, in the present study, we aimed to evaluate the neuroprotective effects of electro acupuncture on HIE and to further investigate the role of GDNF family receptor member RET and its key downstream PI3-K/Akt pathway in the process. A rat HIE model was constructed by the left common carotid artery (LCCA) ligation method in combination with hypoxic treatment. Considering that Baihui (GV20), Dazhui (GV14), Quchi (LI11) and Yongquan (KI1) are commonly used in clinics for stroke treatment and are easy to locate, we chose the above four acupoints as the combination for electro acupuncture treatment which was performed once a day for different time periods. Hematoxylin-eosin (HE) staining and transmission electron microscopy results showed that electro acupuncture could ameliorate neurologic damage and alleviate the degenerative changes of ultra structure of cortical neurons in rats subjected to HIE. And the longer acupuncture treatment lasted, the better its therapeutic effect would be. This was accompanied by gradually increased expression of GDNF family receptor RET at the mRNA level and its downstream signaling Akt at the protein level in the ischemic cortex. These findings suggest that electro acupuncture shows neuroprotective effects in HIE, which at least in part is attributed to activation of PI3-K/Akt signaling pathway.

Neuroprotective body hypothermia among newborns with hypoxic ischemic encephalopathy: three-year experience in a tertiary university hospital. A retrospective observational study

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Mauricio Magalhães

Full Text Available CONTEXT AND OBJECTIVE:Neonatal hypoxic-ischemic encephalopathy is associated with high morbidity and mortality. Studies have shown that therapeutic hypothermia decreases neurological sequelae and death. Our aim was therefore to report on a three-year experience of therapeutic hypothermia among asphyxiated newborns.DESIGN AND SETTING:Retrospective study, conducted in a university hospital.METHODS:Thirty-five patients with perinatal asphyxia undergoing body cooling between May 2009 and November 2012 were evaluated.RESULTS:Thirty-nine infants fulfilled the hypothermia protocol criteria. Four newborns were removed from study due to refractory septic shock, non-maintenance of temperature and severe coagulopathy. The median Apgar scores at 1 and 5 minutes were 2 and 5. The main complication was infection, diagnosed in seven mothers (20% and 14 newborns (40%. Convulsions occurred in 15 infants (43%. Thirty-one patients (88.6% required mechanical ventilation and 14 of them (45% were extubated within 24 hours. The duration of mechanical ventilation among the others was 7.7 days. The cooling protocol was started 1.8 hours after birth. All patients showed elevated levels of creatine phosphokinase, creatine phosphokinase- MB and lactate dehydrogenase. There was no severe arrhythmia; one newborn (2.9% presented controlled coagulopathy. Four patients (11.4% presented controlled hypotension. Twenty-nine patients (82.9% underwent cerebral ultrasonography and 10 of them (34.5% presented white matter hyper-echogenicity. Brain magnetic resonance imaging was performed on 33 infants (94.3% and 11 of them (33.3% presented hypoxic-ischemic changes. The hospital stay was 23 days. All newborns were discharged. Two patients (5.8% needed gastrostomy.CONCLUSION:Hypothermia as therapy for asphyxiated newborns was shown to be safe.

Inflammatory cytokine response and reduced heart rate variability in newborns with hypoxic-ischemic encephalopathy.

Science.gov (United States)

Al-Shargabi, T; Govindan, R B; Dave, R; Metzler, M; Wang, Y; du Plessis, A; Massaro, A N

2017-06-01

To determine whether systemic inflammation-modulating cytokine expression is related to heart rate variability (HRV) in newborns with hypoxic-ischemic encephalopathy (HIE). The data from 30 newborns with HIE were analyzed. Cytokine levels (IL-2, IL-4, IL-6, IL-8, IL-10, IL-13, IL-1β, TNF-α, IFN-λ) were measured either at 24 h of cooling (n=5), 72 h of cooling (n=4) or at both timepoints (n=21). The following HRV metrics were quantified in the time domain: alpha_S, alpha_L, root mean square (RMS) at short time scales (RMS_S), RMS at long time scales (RMS_L), while low-frequency power (LF) and high-frequency power (HF) were quantified in the frequency domain. The relationships between HRV metrics and cytokines were evaluated using mixed-models. IL-6, IL-8, IL-10, and IL-13 levels were inversely related to selected HRV metrics. Inflammation-modulating cytokines may be important mediators in the autonomic dysfunction observed in newborns with HIE.

Cardiovascular dysfunction in infants with neonatal encephalopathy.

LENUS (Irish Health Repository)

Armstrong, Katey

2012-04-01

Severe perinatal asphyxia with hypoxic ischaemic encephalopathy occurs in approximately 1-2\\/1000 live births and is an important cause of cerebral palsy and associated neurological disabilities in children. Multiorgan dysfunction commonly occurs as part of the asphyxial episode, with cardiovascular dysfunction occurring in up to a third of infants. This narrative paper attempts to review the literature on the importance of early recognition of cardiac dysfunction using echocardiography and biomarkers such as troponin and brain type natriuretic peptide. These tools may allow accurate assessment of cardiac dysfunction and guide therapy to improve outcome.

Hypoxic pretreatment protects against neuronal damage of the rat hippocampus induced by severe hypoxia.

Science.gov (United States)

Gorgias, N; Maidatsi, P; Tsolaki, M; Alvanou, A; Kiriazis, G; Kaidoglou, K; Giala, M

1996-04-01

The present study investigates whether under conditions of successive hypoxic exposures pretreatment with mild (15% O(2)) or moderate (10% O(2)) hypoxia, protects hippocampal neurones against damage induced by severe (3% O(2)) hypoxia. The ultrastructural findings were also correlated with regional superoxide dismutase (SOD) activity changes. In unpretreated rats severe hypoxia induced ultrastructural changes consistent with the aspects of delayed neuronal death (DND). However, in preexposed animals hippocampal damage was attenuated in an inversely proportional way with the severity of the hypoxic pretreatment. The ultrastructural hypoxic tolerance findings were also closely related to increased regional SOD activity levels. Thus the activation of the endogenous antioxidant defense by hypoxic preconditioning, protects against hippocampal damage induced by severe hypoxia. The eventual contribution of increased endogenous adenosine and/or reduced excitotoxicity to induce hypoxic tolerance is discussed.

Prognostic Value of the Apparent Diffusion Coefficient in Newborns with Hypoxic-Ischaemic Encephalopathy Treated with Therapeutic Hypothermia.

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Heursen, Eva-Marie; Zuazo Ojeda, Amaya; Benavente Fernández, Isabel; Jimenez Gómez, Gema; Campuzano Fernández-Colima, Rosalía; Paz-Expósito, José; Lubián López, Simón Pedro

2017-01-01

Apparent diffusion coefficient (ADC) quantification has been proven to be of prognostic value in term newborns with hypoxic-ischaemic encephalopathy (HIE) who were treated under normothermia. To evaluate the prognostic value of ADC in standardized brain regions in neonates with HIE who were treated with therapeutic hypothermia (TH). This prospective cohort study included 54 term newborns who were admitted with HIE and treated with TH. All magnetic resonance imaging examinations were performed between days 4 and 6 of life, and ADC values were measured in 13 standardized regions of the brain. At 2 years of age we explored whether ADC values were related to composite outcomes (death or survival with abnormal neurodevelopment). The severity of HIE is inversely related to ADC values in different brain regions. We found that lower ADC values in the posterior limb of the internal capsule (PLIC), the thalami, the semioval centre, and frontal and parietal white matter were related to adverse outcomes. ADC values in the PLIC and thalami are good predictors of adverse outcomes (AUC 0.86 and 0.76). Low ADC values in the PLIC, thalamus, semioval centre, and frontal and parietal white matter in full-term infants with HIE treated with TH were associated with a poor outcome. © 2017 S. Karger AG, Basel.

Can We Predict Functional Outcome in Neonates with Hypoxic Ischemic Encephalopathy by the Combination of Neuroimaging and Electroencephalography?

Science.gov (United States)

Nanavati, Tania; Seemaladinne, Nirupama; Regier, Michael; Yossuck, Panitan; Pergami, Paola

2015-01-01

Background Neonatal hypoxic ischemic encephalopathy (HIE) is a major cause of mortality, morbidity, and long-term neurological deficits. Despite the availability of neuroimaging and neurophysiological testing, tools for accurate early diagnosis and prediction of developmental outcome are still lacking. The goal of this study was to determine if combined use of magnetic resonance imaging (MRI) and electroencephalography (EEG) findings could support outcome prediction. Methods We retrospectively reviewed records of 17 HIE neonates, classified brain MRI and EEG findings based on severity, and assessed clinical outcome up to 48 months. We determined the relation between MRI/EEG findings and clinical outcome. Results We demonstrated a significant relationship between MRI findings and clinical outcome (Fisher’s exact test, p = 0.017). EEG provided no additional information about the outcome beyond that contained in the MRI score. The statistical model for outcome prediction based on random forests suggested that EEG readings at 24 hours and 72 hours could be important variables for outcome prediction, but this needs to be investigated further. Conclusion Caution should be used when discussing prognosis for neonates with mild-to-moderate HIE based on early MR imaging and EEG findings. A robust, quantitative marker of HIE severity that allows for accurate prediction of long-term outcome, particularly for mild-to-moderate cases, is still needed. PMID:25862075

Correlation of hyponatremia with hepatic encephalopathy and severity of liver disease.

Science.gov (United States)

Qureshi, Muhammad Omar; Khokhar, Nasir; Saleem, Atif; Niazi, Tariq Khan

2014-02-01

To assess the frequency of low serum sodium levels and to correlate it with the severity of liver disease and hepatic encephalopathy (HE) in patients coming to the tertiary care hospital. Observational study. Shifa International Hospital, Islamabad, from January 2011 to January 2012. A total of 202 patients with hepatic encephalopathy and chronic liver disease had serum sodium measured. The HE was graded according to the West Haven classification (4 grades). Relationship of hyponatremia was correlated with severity grade of encephalopathy using Spearman rank correlation test. Out of 202 patients, 62 (30.7%) patients had serum sodium less than 130 meq/l. Out of 202, HE was present in 69 (34.15%) patients and out of these, 38 had grade III-IV HE and 31 had grade I - II HE. Out of 69 patients with HE 57 had sodium less than 135 (p liver disease. The existence of serum sodium concentration encephalopathy compared with patients with serum sodium concentration > 135 mmol/L.

Region-specific reduction in brain volume in young adults with perinatal hypoxic-ischaemic encephalopathy.

Science.gov (United States)

Bregant, Tina; Rados, Milan; Vasung, Lana; Derganc, Metka; Evans, Alan C; Neubauer, David; Kostovic, Ivica

2013-11-01

A severe form of perinatal hypoxic-ischaemic encephalopathy (HIE) carries a high risk of perinatal death and severe neurological sequelae while in mild HIE only discrete cognitive disorders may occur. To compare total brain volumes and region-specific cortical measurements between young adults with mild-moderate perinatal HIE and a healthy control group of the same age. MR imaging was performed in a cohort of 14 young adults (9 males, 5 females) with a history of mild or moderate perinatal HIE. The control group consisted of healthy participants, matched with HIE group by age and gender. Volumetric analysis was done after the processing of MR images using a fully automated CIVET pipeline. We measured gyrification indexes, total brain volume, volume of grey and white matter, and of cerebrospinal fluid. We also measured volume, thickness and area of the cerebral cortex in the parietal, occipital, frontal, and temporal lobe, and of the isthmus cinguli, parahippocampal and cingulated gyrus, and insula. The HIE patient group showed smaller absolute volumetric data. Statistically significant (p right hemisphere, of cortical areas in the right temporal lobe and parahippocampal gyrus, of cortical volumes in the right temporal lobe and of cortical thickness in the right isthmus of the cingulate gyrus were found. Comparison between the healthy group and the HIE group of the same gender showed statistically significant changes in the male HIE patients, where a significant reduction was found in whole brain volume; left parietal, bilateral temporal, and right parahippocampal gyrus cortical areas; and bilateral temporal lobe cortical volume. Our analysis of total brain volumes and region-specific corticometric parameters suggests that mild-moderate forms of perinatal HIE lead to reductions in whole brain volumes. In the study reductions were most pronounced in temporal lobe and parahippocampal gyrus. Copyright © 2013 European Paediatric Neurology Society. All rights reserved.

Association of brain injury and neonatal cytokine response during therapeutic hypothermia in newborns with hypoxic-ischemic encephalopathy.

Science.gov (United States)

Orrock, Janet E; Panchapakesan, Karuna; Vezina, Gilbert; Chang, Taeun; Harris, Kari; Wang, Yunfei; Knoblach, Susan; Massaro, An N

2016-05-01

Cytokines have been proposed as mediators of neonatal brain injury via neuroinflammatory pathways triggered by hypoxia-ischemia. Limited data are available on cytokine profiles in larger cohorts of newborns with hypoxic-ischemic encephalopathy (HIE) undergoing therapeutic hypothermia (TH). Serum cytokines interleukin (IL)-1β, IL-2, IL-4, IL-6, IL-8, IL-10, IL-13, tumor necrosis factor-α, and interferon-γ were measured in newborns with HIE at 24 and 72 h of TH. Differences between infants with favorable (survivors with mild/no magnetic resonance imaging (MRI) injury) vs. adverse outcome (death or moderate/severe MRI injury) were compared using mixed models to adjust for covariates. Data from 36 term newborns with HIE (favorable outcome: n = 20, adverse outcome: n = 16) were evaluated. Cytokines IL-1β, IL-2, IL-6, IL-8, IL-10, and IL-13 were elevated in the adverse relative to favorable outcome group at 24 h. IL-6 remained significantly elevated in the adverse outcome group at 72 h. IL-6 and IL-10 remained significantly associated with outcome group after controlling for covariates. Inflammatory cytokines are elevated in HIE newborns with brain injury by MRI. In particular, IL-6 and IL-10 were associated with adverse outcomes after controlling for baseline characteristics and severity of presentation. These data suggest that cytokine response may identify infants in need of additional neuroprotective interventions.

Hypoxic-ischemic encefalopathy: Clinical course and prognosis

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Ćosić-Cerovac Nataša

2003-01-01

Full Text Available Background. Establishing the value of neurological examination, and additional diagnostic methods (ultrasonography and magnetic resonance imaging of the brain in the diagnosis and prognosis of hypoxic-ischemic encephalopathy and its treatment, tracking the clinical course, and making the prognosis of neurological development in newborn infants with hypoxic-ischemic encefalopathy. Methods. The group of 40 term newborn infants with suspected intrauterine asphyxia was examined. All the infants were prospectivelly followed untill the 3rd year of age at the Clinic for Neurology and Psychiatry for Children and Youth in order to estimate their neurological development and to diagnose the occurence of persistent neurological disorders. All the infants were analyzed by their gestational age and Apgar score in the 1st and the 5th minute of life. They were all examined neurologically and by ultrasonography in the first week of life and, repeatedly, at the age of 1, 3, 6, 9, 12, 18, as well as in the 24th month of life. They were treated by the standard methods for this disease. Finally, all the infants were examined neurologically and by magnetic resonance imaging of the brain in their 3rd year of age. On the basis of neurological finding infants were devided into 3 groups: infants with normal neurological finding, infants with mild neurological symptomatology, and infants with severe neurological disorders. Results. It was shown that neurological finding, ultrasonography and magnetic resonance imaging of the brain positively correlated with the later neurological development of the infants with hypoxic-ischemic encephalopathy. Conclusion. Only the combined use of these techniques had full diagnostic and prognostic significance emphasizing that the integrative approach was very important in the diagnosis of brain lesions in infants.

Transient hypoxic respiratory failure in a patient with severe hypophosphatemia.

Science.gov (United States)

Oud, Lavi

2009-03-01

Respiratory failure in severely hypophosphatemic patients has been attributed to respiratory muscle weakness, leading to ventilatory failure. While frequently documenting hypercarbic respiratory failure, previous reports of hypophosphatemia-related respiratory failure in patients otherwise free of pulmonary or airway disease often did not provide sufficient information on gas exchange and pulmonary function, precluding inference on alternative or additional sources of respiratory dysfunction in this population. We report a case of acute hypoxic respiratory failure in a 26 year-old bulimic woman with severe hypophosphatemia. The patient presented with acute onset of dyspnea, paresthesias, limb shaking, and severe hyperventilation. SpO2 was 74%, requiring administration of 100% O2, with normal chest radiograph. Serum phosphate was <0.3 mmol/liter (1.0 mg/dL). Further evaluation did not support pulmonary, vascular, neurogenic or external exposure-related causes of hypoxic respiratory failure, which rapidly resolved with parenteral correction of hypophosphatemia. To date, hypoxic respiratory failure has not been reported in association with hypophosphatemia. Increased awareness and further investigations can help elucidate the mechanisms of hypophosphatemia-associated hypoxemia.

Improvement of post-hypoxic action myoclonus with levetiracetam add-on therapy: A case report

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Božić Ksenija

2014-01-01

Full Text Available Introduction. Chronic post-anoxic myoclonus, also known as Lance-Adams syndrome, may develop following hypoxic brain injury, and is resistant to pharmacological therapy. Case report. The patient we presented developed post-anoxic action myoclonus with severe, completely incapacitating myoclonic jerks. Myoclonus did not respond to the treatment with commonly used agents, i.e. valproate and clonazepam alone or in combination. Improvement of the action myoclonus was observed only after adding levetiracetam. Conclusion. Although Lance-Adams syndrome may not be fully curable at this point, levetiracetam appears to be a promising agent that can significantly improve functional level and overall quality of life of patients with this disorder.

Transcriptome analysis of severe hypoxic stress during development in zebrafish

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I.G. Woods

2015-12-01

Full Text Available Hypoxia causes critical cellular injury both in early human development and in adulthood, leading to cerebral palsy, stroke, and myocardial infarction. Interestingly, a remarkable phenomenon known as hypoxic preconditioning arises when a brief hypoxia exposure protects target organs against subsequent, severe hypoxia. Although hypoxic preconditioning has been demonstrated in several model organisms and tissues including the heart and brain, its molecular mechanisms remain poorly understood. Accordingly, we used embryonic and larval zebrafish to develop a novel vertebrate model for hypoxic preconditioning, and used this model to identify conserved hypoxia-regulated transcripts for further functional study as published in Manchenkov et al. (2015 in G3: Genes|Genomes|Genetics. In this Brief article, we provide extensive annotation for the most strongly hypoxia-regulated genes in zebrafish, including their human orthologs, and describe in detail the methods used to identify, filter, and annotate hypoxia-regulated transcripts for downstream functional and bioinformatic assays using the source data provided in Gene Expression Omnibus Accession GSE68473.

Cerebral CT appearances of toxic encephalopathy of tetramine

International Nuclear Information System (INIS)

Zheng Wenlong; Wu Aiqin; Xu Chongyong; Ying Binyu; Hong Ruizhen

2003-01-01

Objective: To investigate the cerebral CT appearances of toxic encephalopathy of tetramine and improve the recognition on this disease. Methods: Four cases of toxic encephalopathy of tetramine were collected and their cerebral CT appearances were retrospectively analyzed. Results: Cerebral CT appearances in acute phase (within 8 days): (1) cerebral edema in different degree. CT abnormalities consisted of cortical hypodensities and complete loss of gray-white matter differentiation. The CT value were in 11-13 HU, and to be watery density in serious case, (2) subarachnoid hemorrhage. It demonstrated the signs of poisoning hypoxic ischemic encephalopathy in chronic phase. Conclusion: The cerebral CT appearances of toxic encephalopathy of tetramine had some character in acute phase and it can predict the serious degree of intoxication, but there was no characteristic findings in chronic phase

Planned home birth and the association with neonatal hypoxic ischemic encephalopathy.

Science.gov (United States)

Wasden, Shane W; Chasen, Stephen T; Perlman, Jeffrey M; Illuzzi, Jessica L; Chervenak, Frank A; Grunebaum, Amos; Lipkind, Heather S

2017-12-20

To evaluate the association between planned home birth and neonatal hypoxic ischemic encephalopathy (HIE). This is a case-control study in which a database of neonates who underwent head cooling for HIE at our institution from 2007 to 2011 was linked to New York City (NYC) vital records. Four normal controls per case were then randomly selected from the birth certificate data after matching for year of birth, geographic location, and gestational age. Demographic and obstetric information was obtained from the vital records for both the cases and controls. Location of birth was analyzed as hospital or out of hospital birth. Details from the out of hospital deliveries were reviewed to determine if the delivery was a planned home birth. Maternal and pregnancy characteristics were examined as covariates and potential confounders. Logistic regression was used to determine the odds of HIE by intended location of delivery. Sixty-nine neonates who underwent head cooling for HIE had available vital record data on their births. The 69 cases were matched to 276 normal controls. After adjusting for pregnancy characteristics and mode of delivery, neonates with HIE had a 44.0-fold [95% confidence interval (CI) 1.7-256.4] odds of having delivered out of hospital, whether unplanned or planned. Infants with HIE had a 21.0-fold (95% CI 1.7-256.4) increase in adjusted odds of having had a planned home birth compared to infants without HIE. Out of hospital birth, whether planned home birth or unplanned out of hospital birth, is associated with an increase in the odds of neonatal HIE.

EEG source localization in full-term newborns with hypoxic-ischemia

NARCIS (Netherlands)

Jennekens, W.; Dankers, F.; Blijham, P.; Cluitmans, P.; van Pul, C.; Andriessen, P.

2013-01-01

The aim of this study was to evaluate EEG source localization by standardized weighted low-resolution brain electromagnetic tomography (swLORETA) for monitoring of fullterm newborns with hypoxic-ischemic encephalopathy, using a standard anatomic head model. Three representative examples of neonatal

Amplitude Integrated Electroencephalogram as a Prognostic Tool in Neonates with Hypoxic-Ischemic Encephalopathy: A Systematic Review.

Directory of Open Access Journals (Sweden)

Ruth Del Río

Full Text Available Perinatal management and prognostic value of clinical evaluation and diagnostic tools have changed with the generalization of therapeutic hypothermia (TH in infants with hypoxic-ischemic encephalopathy (HIE.to ascertain the prognostic value of amplitude integrated electroencephalogram (aEEG in neonates with HIE considering hours of life and treatment with TH.A systematic review was performed. Inclusion criteria were studies including data of neonates with HIE, treated or not with TH, monitored with aEEG and with neurodevelopmental follow-up of at least 12 months. The period of bibliographic search was until February 2016. No language restrictions were initially applied. Consulted databases were MEDLINE, Scopus, CINHAL and the Spanish language databases GuiaSalud and Bravo. Article selection was performed by two independent reviewers. Quality for each individual paper selected was evaluated using QUADAS-2. Review Manager (RevMan version 5.3 software was used. Forest plots were constructed to graphically show sensitivity and specificity for all included studies, separating patients treated or not with hypothermia. Summary statistics were estimated using bivariate models and random effects approaches with the R package MADA from summary ROC curves. Meta-regression was used to estimate heterogeneity and trends.from the 403 articles initially identified, 17 were finally included and critically reviewed. In infants not treated with hypothermia the maximum reliability of an abnormal aEEG background to predict death or moderate/severe disability was at 36 hours of life, when a positive post-test probability of 97.90% was achieved (95%CI 88.40 to 99.40%. Positive likelihood ratio (+LR at these hours of life was 26.60 (95%CI 4.40 to 94.90 and negative likelihood ratio (-LR was 0.23 (95%CI 0.10 to 0.44. A high predictive value was already present at 6 hours of life in this group of patients, with a positive post-test probability of 88.20% (95%CI 79.80 to

Acute hyperammonemic encephalopathy with features on diffusion-weighted images: Report of two cases

International Nuclear Information System (INIS)

Kim, Ja Young; Yu, In Kyu

2015-01-01

Acute hyperammonemic encephalopathy is a rare toxic encephalopathy caused by accumulated plasma ammonia. A few literatures are reported about MRI findings of acute hyperammonemic encephalopathy. It is different from the well-known chronic hepatic encephalopathy. The clinical symptom and MRI findings of acute hyperammonemic encephalopathy can be reversible with proper treatment. Acute hepatic encephalopathy involves the cingulate cortex, diffuse cerebral cortices, insula, bilateral thalami on diffusion-weighted imaging (DWI), and fluid-attenuated inversion-recovery. Acute hepatic encephalopathy might mimic hypoxic-ischemic encephalopathy because of their similar predominant involving sites. We experienced 2 cases of acute hyperammonemic encephalopathy consecutively. They showed restricted diffusion at the cingulate cortex, cerebral cortices, insula, and bilateral dorsomedial thalami on DWI. One patient underwent acute fulminant hepatitis A, the other patient with underlying chronic liver disease had acute liver failure due to hepatotoxicity of tuberculosis medication. In this report, we presented the characteristic features of DWI in acute hyperammonemic encephalopathy. In addition, we reviewed articles on MRI findings of acute hyperammonemic encephalopathy.

Acute hyperammonemic encephalopathy with features on diffusion-weighted images: Report of two cases

Energy Technology Data Exchange (ETDEWEB)

Kim, Ja Young; Yu, In Kyu [Dept. of Radiology, Eulji University Hospital, Daejeon (Korea, Republic of)

2015-02-15

Acute hyperammonemic encephalopathy is a rare toxic encephalopathy caused by accumulated plasma ammonia. A few literatures are reported about MRI findings of acute hyperammonemic encephalopathy. It is different from the well-known chronic hepatic encephalopathy. The clinical symptom and MRI findings of acute hyperammonemic encephalopathy can be reversible with proper treatment. Acute hepatic encephalopathy involves the cingulate cortex, diffuse cerebral cortices, insula, bilateral thalami on diffusion-weighted imaging (DWI), and fluid-attenuated inversion-recovery. Acute hepatic encephalopathy might mimic hypoxic-ischemic encephalopathy because of their similar predominant involving sites. We experienced 2 cases of acute hyperammonemic encephalopathy consecutively. They showed restricted diffusion at the cingulate cortex, cerebral cortices, insula, and bilateral dorsomedial thalami on DWI. One patient underwent acute fulminant hepatitis A, the other patient with underlying chronic liver disease had acute liver failure due to hepatotoxicity of tuberculosis medication. In this report, we presented the characteristic features of DWI in acute hyperammonemic encephalopathy. In addition, we reviewed articles on MRI findings of acute hyperammonemic encephalopathy.

Correlation of Hyponatremia with Hepatic Encephalopathy and Severity of Liver Disease

International Nuclear Information System (INIS)

Qureshi, M. O.; Khokhar, N.; Saleem, A.; Niazi, T. K.

2014-01-01

Objective: To assess the frequency of low serum sodium levels and to correlate it with the severity of liver disease and hepatic encephalopathy (HE) in patients coming to the tertiary care hospital. Study Design: Observational study. Place and Duration of Study: Shifa International Hospital, Islamabad, from January 2011 to January 2012. Methodology: A total of 202 patients with hepatic encephalopathy and chronic liver disease had serum sodium measured. The HE was graded according to the West Haven classification (4 grades). Relationship of hyponatremia was correlated with severity grade of encephalopathy using Spearman rank correlation test. Results: Out of 202 patients, 62 (30.7%) patients had serum sodium less than 130 meq/l. Out of 202, HE was present in 69 (34.15%) patients and out of these, 38 had grade III-IV HE and 31 had grade I - II HE. Out of 69 patients with HE 57 had sodium less than 135 (p 135 mmol/L. (author)

Arterial spin-labelling perfusion MRI and outcome in neonates with hypoxic-ischemic encephalopathy

Energy Technology Data Exchange (ETDEWEB)

Vis, Jill B. de; Hendrikse, Jeroen [University Medical Center Utrecht, Department of Radiology, HP E 01.132, P.O. Box 85500, Utrecht (Netherlands); Petersen, Esben T. [University Medical Center Utrecht, Department of Radiology, HP E 01.132, P.O. Box 85500, Utrecht (Netherlands); University Medical Center Utrecht, Department of Radiotherapy, Utrecht (Netherlands); Vries, Linda S. de; Bel, Frank van; Alderliesten, Thomas; Negro, Simona; Groenendaal, Floris; Benders, Manon J.N.L. [Wilhelmina Children' s Hospital/University Medical Center Utrecht, Department of Neonatology, Utrecht (Netherlands)

2015-01-15

Hyperperfusion may be related to outcome in neonates with hypoxic-ischemic encephalopathy (HIE). The purpose of this study was to evaluate whether arterial spin labelling (ASL) perfusion is associated with outcome in neonates with HIE and to compare the predictive value of ASL MRI to known MRI predictive markers. Twenty-eight neonates diagnosed with HIE and assessed with MR imaging (conventional MRI, diffusion-weighted MRI, MR spectroscopy [MRS], and ASL MRI) were included. Perfusion in the basal ganglia and thalami was measured. Outcome at 9 or 18 months of age was scored as either adverse (death or cerebral palsy) or favourable. The median (range) perfusion in the basal ganglia and thalami (BGT) was 63 (28-108) ml/100 g/min in the neonates with adverse outcome and 28 (12-51) ml/100 g/min in the infants with favourable outcome (p < 0.01). The area-under-the-curve was 0.92 for ASL MRI, 0.97 for MRI score, 0.96 for Lac/NAA and 0.92 for ADC in the BGT. The combination of Lac/NAA and ASL MRI results was the best predictor of outcome (r {sup 2} = 0.86, p < 0.001). Higher ASL perfusion values in neonates with HIE are associated with a worse neurodevelopmental outcome. A combination of the MRS and ASL MRI information is the best predictor of outcome. (orig.)

Immediate Outcome of Hypoxic Ischaemic Encephalopathy in Hypoxiate Newborns in Nepal Medical College.

Science.gov (United States)

Shrestha, S; Shrestha, G S; Sharma, A

2016-05-01

Birth asphyxia is the fifth major cause of under-five child deaths after pneumonia, diarrhoea, neonatal infections and complications of preterm birth. It is one of the important causes of neonatal mortality and morbidity accounting up to 30% of neonatal death in Nepal. It is also an important cause of long-term neurological disability and impairment. The mortality rate due to birth asphyxia is considered a good guide to the quality of perinatal care. This study was conducted to assess the rate of birth asphyxia, risk factors and outcome of the babies who were asphyxiated at birth. A prospective study was conducted during the period of one year from April 2013 to March 2014 in Nepal Medical College. All the term babies born during the period with APGAR score at 5 minutes of newborn babies were assessed for clinical features of hypoxic ischemic encephalopathy (HIE) and its immediate outcome. Out of 2226 live births, 47 (15.9%) newborns had birth asphyxia with the rate of 21.1/1000 live births. The mortality rate due to birth asphyxia was 4.25%. Meconium stained liquor was present in 31(65.96%) cases during delivery and prolonged rupture of membrane in 7(14.89%). Early identification and close monitoring of high-risk mothers with maintaining partograph during labor help to reduce birth asphyxia.

Bumetanide enhances phenobarbital efficacy in a rat model of hypoxic neonatal seizures.

Science.gov (United States)

Cleary, Ryan T; Sun, Hongyu; Huynh, Thanhthao; Manning, Simon M; Li, Yijun; Rotenberg, Alexander; Talos, Delia M; Kahle, Kristopher T; Jackson, Michele; Rakhade, Sanjay N; Berry, Gerard T; Berry, Gerard; Jensen, Frances E

2013-01-01

Neonatal seizures can be refractory to conventional anticonvulsants, and this may in part be due to a developmental increase in expression of the neuronal Na(+)-K(+)-2 Cl(-) cotransporter, NKCC1, and consequent paradoxical excitatory actions of GABAA receptors in the perinatal period. The most common cause of neonatal seizures is hypoxic encephalopathy, and here we show in an established model of neonatal hypoxia-induced seizures that the NKCC1 inhibitor, bumetanide, in combination with phenobarbital is significantly more effective than phenobarbital alone. A sensitive mass spectrometry assay revealed that bumetanide concentrations in serum and brain were dose-dependent, and the expression of NKCC1 protein transiently increased in cortex and hippocampus after hypoxic seizures. Importantly, the low doses of phenobarbital and bumetanide used in the study did not increase constitutive apoptosis, alone or in combination. Perforated patch clamp recordings from ex vivo hippocampal slices removed following seizures revealed that phenobarbital and bumetanide largely reversed seizure-induced changes in EGABA. Taken together, these data provide preclinical support for clinical trials of bumetanide in human neonates at risk for hypoxic encephalopathy and seizures.

Posterior reversible encephalopathy syndrome and acute post-streptococcal glomerulonephritis mimicking breakthrough seizures

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Kamille Abdool

2015-05-01

Full Text Available We report the case of a 14-year-old boy with a past history of primary generalized seizures, who had been seizure-free for 2 years on sodium valproate and presented with generalized tonic clonic seizures suggestive of breakthrough seizures. Examination revealed hypertension, impetiginous lesions of the lower limbs, microscopic hematuria, elevated antistreptolysin O titre and low complement levels consistent with acute post-streptococcal glomerulonephritis. Cranial magnetic resonance imaging (MRI demonstrated changes consistent with posterior reversible encephalopathy syndrome. Hypertension was controlled with intravenous nitroglycerin followed by oral captopril and amlodipine. Brain MRI changes returned normal within 2 weeks. The nephritis went in to remission within 2 months and after 8 months the patient has been seizure free again. Posterior reversible encephalopathy syndrome appeared to have neither short nor intermediate effect on seizure control in this patient. The relationship between posterior reversible encephalopathy syndrome and seizures is reviewed.

Effect of hyperbaric oxygen therapy on SAS and SDS in children with ischemic encephalopathy

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Pei-Yun Li

2017-08-01

Full Text Available Objective: To study and analyze the effect of early psychological intervention on the scores of SAS and SDS in children with hypoxic-ischemic encephalopathy undergoing hyperbaric oxygen therapy. Methods: A total of 64 children with hypoxic - ischemic encephalopathy enrolled in our hospital from July 2015 to July 2016 and their parents were selected as study subjects. The patients were treated with hyperbaric oxygen therapy, while their parents were given early psychological intervention. By the way of increasing parents’ awareness of the disease, helping parents build confidence in their children’s treatment and encouraging them to participate in daily training for their children to relieve their anxiety and depression. The parents' knowledge of the disease before and during treatment, the treatment of hyperbaric oxygen therapy and the change of SAS and SDS were observed. Results: After effective intervention, the scores of SAS and SDS of 64 patients’ parents were significantly lower than those before treatment. After 1 courses of intervention, the score of SAS was (43.36 ± 1.27 points, and the score of SDS was (45.22 ± 8.13 points. After 2 courses of intervention, the score of SAS was (41.07 ± 1.21 and the score of SDS was (42.35 ± 7.44 points, and parents' awareness of hypoxic-ischemic encephalopathy was significantly increased, and the differences between the two groups were statistically significant. Conclusion: Early psychological intervention on parents of children with hypoxic-ischemic encephalopathy can effectively improve the awareness of parents on the disease, so as to improve their acceptance of hyperbaric oxygen therapy; significantly reduce the parents’ SAS, SDS score. It is beneficial to build a good doctor-patient and nurse-patient relationship, improve the treatment effect and shorten the treatment time.

Performance of the hepatic encephalopathy scoring algorithm in a clinical trial of patients with cirrhosis and severe hepatic encephalopathy

DEFF Research Database (Denmark)

Hassanein, T.; Blei, A.T.; Perry, W.

2009-01-01

OBJECTIVES: The grading of hepatic encephalopathy (HE) is based on a combination of indicators that reflect the state of consciousness, intellectual function, changes in behavior, and neuromuscular alterations seen in patients with liver failure. METHODS: We modified the traditional West Haven...... criteria (WHC) to provide an objective assessment of the cognitive parameters to complement the subjective clinical ratings for the performance of extracorporeal albumin dialysis (ECAD) using a molecular adsorption recirculating system in patients with cirrhosis and severe (grade III / IV) encephalopathy...

Newborns Referred for Therapeutic Hypothermia: Association between Initial Degree of Encephalopathy and Severity of Brain Injury (What About the Newborns with Mild Encephalopathy on Admission?).

Science.gov (United States)

Gagne-Loranger, Maude; Sheppard, Megan; Ali, Nabeel; Saint-Martin, Christine; Wintermark, Pia

2016-01-01

The aim of this article was to describe the severity of brain injury and/or mortality in a cohort of newborns referred for therapeutic hypothermia, in relation to the degree of encephalopathy on admission, and to especially look at the ones with initial mild encephalopathy. Term newborns with perinatal depression referred to our neonatal intensive care unit for possible hypothermia treatment from 2008 to 2012 were enrolled prospectively. The modified Sarnat score on admission was correlated with severity of brain injury on brain imaging and/or autopsy. A total of 215 newborns were referred for possible cooling. Sixty percent (128/215) were cooled. Most of the not-cooled newborns with an available brain magnetic resonance imaging (85% = 50/59) had an initial mild encephalopathy, and 40% (20/50) developed brain injury. Some cooled newborns had an initial mild encephalopathy (12% = 13/108); only 31% (4/13) developed brain injury. Our results demonstrated that several newborns with an initial mild encephalopathy developed subsequent brain injury, especially when they were not cooled. Thieme Medical Publishers 333 Seventh Avenue, New York, NY 10001, USA.

[Disturbed respiratory cycle accompanying hypoxic-ischemic encephalopathy].

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Saito, Yoshiaki; Masuko, Kaori; Kaneko, Kaori; Saito, Kazuyo; Chikumaru, Yuri; Iwamoto, Hiroko; Matsui, Akira; Kimura, Seiji

2005-09-01

We report the case of a 2-year-old boy who experienced total asphyxia at 4 months of age, and suffered abnormalities at specific phases of the respiratory cycle. The patient was bedridden due to severe tetraplegia and showed little response to external stimuli. He has been tube-fed since the initial asphyxia and a tracheotomy was performed after recurrent hypoxic episodes as a result of the respiratory dysfunction. Upon examination, his respiratory pattern was characterized by arrest during the inspiratory phase with a possible over-riding secondary inspiration. The respiratory pause at the inspiratory phase was markedly prolonged during an episode of pulmonary infection, resulting in recurrent cyanosis that necessitated artificial ventilation. The "second" inspiration typically occurred during the mid- or late-inspiratory phases, with this pattern often shown to be variable after epileptic seizures. The characteristic breathing of this patient suggested that difficulty in forming a normal respiratory cycle, other than during periods of hypoventilation or apnoea, could be a significant respiratory dysfunction following asphyxiation. Strategies for the management of such patients should be carefully designed after close observation of breathing patterns within the respiratory cycle, and with consideration for the influence of epileptic seizures and other inputs from somatic afferents.

Effect of Cathodal Transcranial Direct Current Stimulation on a Child with Involuntary Movement after Hypoxic Encephalopathy

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Mayumi Nagai

2018-01-01

Full Text Available The aim of the study was to investigate the effect of cathodal transcranial direct current stimulation to the supplementary motor area to inhibit involuntary movements of a child. An 8-year-old boy who developed hypoxic encephalopathy after asphyxia at the age of 2 had difficulty in remaining standing without support because of involuntary movements. He was instructed to remain standing with his plastic ankle-foot orthosis for 10 s at three time points by leaning forward with his forearms on a desk. He received cathodal or sham transcranial direct current stimulation to the supplementary motor area at 1 mA for 10 min. Involuntary movements during standing were measured using an accelerometer attached to his forehead. The low-frequency power of involuntary movements during cathodal transcranial direct current stimulation significantly decreased compared with that during sham stimulation. No adverse effects were observed. Involuntary movement reduction by cathodal stimulation to supplementary motor areas suggests that stimulations modulated the corticobasal ganglia motor circuit. Cathodal stimulation to supplementary motor areas may be effective for reducing involuntary movements and may be safely applied to children with movement disorders.

A new approach to define acute kidney injury in term newborns with hypoxic ischemic encephalopathy.

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Gupta, Charu; Massaro, An N; Ray, Patricio E

2016-07-01

Current definitions of acute kidney injury (AKI) are not sufficiently sensitive to identify all newborns with AKI during the first week of life. To determine whether the rate of decline of serum creatinine (SCr) during the first week of life can be used to identify newborns with AKI, we reviewed the medical records of 106 term neonates at risk of AKI who were treated with hypothermia for hypoxic ischemic encephalopathy (HIE). Of the newborns enrolled in the study, 69 % showed a normal rate of decline of SCr to ≥50 % and/or reached SCr levels of ≤0.6 mg/dl before the 7th day of life, and therefore had an excellent clinical outcome (control group). Thirteen newborns with HIE (12 %) developed AKI according to an established neonatal definition (AKI-KIDGO group), and an additional 20 newborns (19 %) showed a rate of decline of SCr of newborns in the other two groups required more days of mechanical ventilation and vasopressor drugs and had higher gentamicin levels, more fluid overload, lower urinary epidermal growth factor levels, and a prolonged length of stay. The rate of decline of SCr provides a sensitive approach to identify term newborns with AKI during the first week of life.

Bumetanide enhances phenobarbital efficacy in a rat model of hypoxic neonatal seizures.

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Ryan T Cleary

Full Text Available Neonatal seizures can be refractory to conventional anticonvulsants, and this may in part be due to a developmental increase in expression of the neuronal Na(+-K(+-2 Cl(- cotransporter, NKCC1, and consequent paradoxical excitatory actions of GABAA receptors in the perinatal period. The most common cause of neonatal seizures is hypoxic encephalopathy, and here we show in an established model of neonatal hypoxia-induced seizures that the NKCC1 inhibitor, bumetanide, in combination with phenobarbital is significantly more effective than phenobarbital alone. A sensitive mass spectrometry assay revealed that bumetanide concentrations in serum and brain were dose-dependent, and the expression of NKCC1 protein transiently increased in cortex and hippocampus after hypoxic seizures. Importantly, the low doses of phenobarbital and bumetanide used in the study did not increase constitutive apoptosis, alone or in combination. Perforated patch clamp recordings from ex vivo hippocampal slices removed following seizures revealed that phenobarbital and bumetanide largely reversed seizure-induced changes in EGABA. Taken together, these data provide preclinical support for clinical trials of bumetanide in human neonates at risk for hypoxic encephalopathy and seizures.

Passive hypothermia (≥35 - <36°C during transport of newborns with hypoxic-ischaemic encephalopathy.

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Aurélie Sellam

Full Text Available Hypothermia initiated in the first six hours of life in term infants with hypoxic ischemic encephalopathy reduces the risk of death and severe neurological sequelae. Our study's principal objective was to evaluate transport predictors potentially influencing arrival in NICU (Neonatal Intensive Care Unit at a temperature ≥35-<36°C.A multi-centric, prospective cohort study was conducted during 18 months by the three Neonatal Transport Teams and 13 NICUs. Newborns were selected for inclusion according to biological and clinical criteria before transport using passive hypothermia using a target temperature of ≥35-<36°C. Data on 120 of 126 inclusions were available for analysis. Thirty-three percent of the children arrived in NICU with the target temperature of ≥35-<36°C. The mean temperature for the whole group of infants on arrival in NICU was 35.4°C (34.3-36.5. The median age of all infants on arrival in NICU was 3h03min [2h25min-3h56min]. Three infants arrived in NICU with a temperature of <33°C and eleven with a temperature ≥37°C. Adrenaline during resuscitation was associated with a lower mean temperature on arrival in NICU.Our strategy using ≥35-<36°C passive hypothermia combined with short transport times had little effect on temperature after the arrival of Neonatal Transport Team although did reduce numbers of infants arriving in NICU in deep hypothermia. For those infants where hypothermia was discontinued in NICU our strategy facilitated re-warming. Re-adjustment to a lower target temperature to ≥34.5-<35.5°C may reduce the proportion of infants with high/normothermic temperatures.

Sestrin2 induced by hypoxia inducible factor1 alpha protects the blood-brain barrier via inhibiting VEGF after severe hypoxic-ischemic injury in neonatal rats.

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Shi, Xudan; Doycheva, Desislava Met; Xu, Liang; Tang, Jiping; Yan, Min; Zhang, John H

2016-11-01

Hypoxic ischemic (HI) encephalopathy remains the leading cause of perinatal brain injury resulting in long term disabilities. Stabilization of blood brain barrier (BBB) after HI is an important target, therefore, in this study we aim to determine the role of sestrin2, a stress inducible protein which is elevated after various insults, on BBB stabilization after moderate and severe HI injuries. Rat pups underwent common carotid artery ligation followed by either 150min (severe model) or 100min (moderate model) of hypoxia. 1h post HI, rats were intranasally administered with recombinant human sestrin2 (rh-sestrin2) and sacrificed for infarct area, brain water content, righting reflex and geotaxis reflex. Sestrin2 was silenced using siRNA and an activator/inhibitor of hypoxia inducible factor1α (HIF1α) was used to examine their roles on BBB permeability. Rats subjected to severe HI exhibited larger infarct area and higher sestrin2 expression compared to rats in the moderate HI group. rh-sestrin2 attenuated brain infarct and edema, while silencing sestrin2 reversed these protective effects after severe HI. HIF1α induced sestrin2 activation in severe HI but not in moderate HI groups. A HIF1a agonist was shown to increase permeability of the BBB via vascular endothelial growth factor (VEGF) after moderate HI. However, after severe HI, HIF1α activated both VEGF and sestrin2. But HIF1α dependent sestrin2 activation was the predominant pathway after severe HI which inhibited VEGF and attenuated BBB permeability. rh-sestrin2 attenuated BBB permeability via upregulation of endogenous sestrin2 which was induced by HIF1α after severe HI. However, HIF1α's effects as a prodeath or prosurvival signal were influenced by the severity of HI injury. Copyright © 2016 Elsevier Inc. All rights reserved.

Insulin-Like Growth Factor-1 Levels in Term Newborns with Hypoxic-Ischemic Encephalopathy.

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Umran, Raid M R; Al-Tahir, Mahir; Jagdish, Desai; Chouthai, Nitin

2016-06-01

Objective This study aims to evaluate the correlation of changes in serum insulin-like growth factor-1 (IGF-1) levels with the clinical staging of hypoxic-ischemic encephalopathy (HIE) in term newborns. Study Design A prospective study of 29 newborns with HIE (stage I = 15, stage II + III = 14) and 28 healthy term newborns as the control group was performed in the neonatal intensive care unit. IGF-1 levels were obtained within 6 hours after birth from HIE and control groups and again on day 3 from HIE group. HIE was classified using the Sarnat staging I to III. Results IGF-1 levels were significantly lower in the HIE group than in the control group (p = 0.024). It was lower in the HIE stage II to III group compared with HIE stage I group at birth (p < 0.0001) and on day 3 (p = 0.009). The mean IGF-1 levels were significantly higher on day 3 than on day 1 among stage II to III HIE (p = 0.006) and it was inversely correlated with staging (R =  - 0.475, p = 0.009). There was a significant correlation between IGF-1 levels and Apgar score at 5 (R = 0.39, p = 0.042) and 10 minutes (R = 0.38, p = 0.035). Conclusions IGF-1 was lower in HIE and inversely correlated with clinical staging. It was increased with clinical improvement in the subsequent days. Thieme Medical Publishers 333 Seventh Avenue, New York, NY 10001, USA.

Pattern of brain injury and depressed heart rate variability in newborns with hypoxic ischemic encephalopathy.

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Metzler, Marina; Govindan, Rathinaswamy; Al-Shargabi, Tareq; Vezina, Gilbert; Andescavage, Nickie; Wang, Yunfei; du Plessis, Adre; Massaro, An N

2017-09-01

BackgroundDecreased heart rate variability (HRV) is a measure of autonomic dysfunction and brain injury in newborns with hypoxic ischemic encephalopathy (HIE). This study aimed to characterize the relationship between HRV and brain injury pattern using magnetic resonance imaging (MRI) in newborns with HIE undergoing therapeutic hypothermia.MethodsHRV metrics were quantified in the time domain (α S , α L , and root mean square at short (RMS S ) and long (RMS L ) timescales) and frequency domain (relative low-(LF) and high-frequency (HF) power) over 24-27 h of life. The brain injury pattern shown by MRI was classified as no injury, pure cortical/white matter injury, mixed watershed/mild basal ganglia injury, predominant basal ganglia or global injury, and death. HRV metrics were compared across brain injury pattern groups using a random-effects mixed model.ResultsData from 74 infants were analyzed. Brain injury pattern was significantly associated with the degree of HRV suppression. Specifically, negative associations were observed between the pattern of brain injury and RMS S (estimate -0.224, SE 0.082, P=0.006), RMS L (estimate -0.189, SE 0.082, P=0.021), and LF power (estimate -0.044, SE 0.016, P=0.006).ConclusionDegree of HRV depression is related to the pattern of brain injury. HRV monitoring may provide insights into the pattern of brain injury at the bedside.

Current pathogenetic aspects of hepatic encephalopathy and noncirrhotic hyperammonemic encephalopathy.

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Cichoż-Lach, Halina; Michalak, Agata

2013-01-07

Hepatic encephalopathy is a medical phenomenon that is described as a neuropsychiatric manifestation of chronic or acute liver disease that is characterized by psychomotor, intellectual and cognitive abnormalities with emotional/affective and behavioral disturbances. This article focuses on the underlying mechanisms of the condition and the differences between hepatic encephalopathy and noncirrhotic hyperammonemic encephalopathy. Hepatic encephalopathy is a serious condition that can cause neurological death with brain edema and intracranial hypertension. It is assumed that approximately 60%-80% of patients with liver cirrhosis develop hepatic encephalopathy. This review explores the complex mechanisms that lead to hepatic encephalopathy. However, noncirrhotic hyperammonemic encephalopathy is not associated with hepatic diseases and has a completely different etiology. Noncirrhotic hyperammonemic encephalopathy is a severe occurrence that is connected with multiple pathogeneses.

Perinatal Hypoxic-Ischemic brain injury; MR findings

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Park, Dong Woo; Seo, Chang Hye

1994-01-01

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

Severe valproate induced hyperammonemic encephalopathy successfully managed with peritoneal dialysis.

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Kumar, Amandeep; Suri, Ashish; Sharma, Bhawani S

2014-07-01

Valproic acid (VPA) is a commonly used drug for epilepsy, psychiatric disorders and migraine and is frequently used in neurosurgical intensive care units. Though most of its side-effects are mild and transient, certain idiosyncratic side-effects have been attributed to VPA. Valproate induced hyperammonemia (VIH) is one such side-effect. VIH can produce symptoms of encephalopathy known as valproate induced hyperammonemic encephalopathy (VHE). VIH and VHE usually respond to withdrawal of VPA. However, in some cases VHE can be unresponsive to supportive measures and severe enough to be life-threatening. In such cases, dialysis can be used to rapidly reverse hyperammonemia and VHE and can prove to be a lifesaving measure. We report such a case of VIH and life-threatening VHE in a postoperative neurosurgical patient that was managed successfully with peritoneal dialysis.

Near-infrared spectroscopy versus magnetic resonance imaging to study brain perfusion in newborns with hypoxic-ischemic encephalopathy treated with hypothermia.

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Wintermark, P; Hansen, A; Warfield, S K; Dukhovny, D; Soul, J S

2014-01-15

The measurement of brain perfusion may provide valuable information for assessment and treatment of newborns with hypoxic-ischemic encephalopathy (HIE). While arterial spin labeled perfusion (ASL) magnetic resonance imaging (MRI) provides noninvasive and direct measurements of regional cerebral blood flow (CBF) values, it is logistically challenging to obtain. Near-infrared spectroscopy (NIRS) might be an alternative, as it permits noninvasive and continuous monitoring of cerebral hemodynamics and oxygenation at the bedside. The purpose of this study is to determine the correlation between measurements of brain perfusion by NIRS and by MRI in term newborns with HIE treated with hypothermia. In this prospective cohort study, ASL-MRI and NIRS performed during hypothermia were used to assess brain perfusion in these newborns. Regional cerebral blood flow (CBF) values, measured from 1-2 MRI scans for each patient, were compared to mixed venous saturation values (SctO2) recorded by NIRS just before and after each MRI. Analysis included groupings into moderate versus severe HIE based on their initial background pattern of amplitude-integrated electroencephalogram. Twelve concomitant recordings were obtained of seven neonates. Strong correlation was found between SctO2 and CBF in asphyxiated newborns with severe HIE (r=0.88; p value=0.0085). Moreover, newborns with severe HIE had lower CBF (likely lower oxygen supply) and extracted less oxygen (likely lower oxygen demand or utilization) when comparing SctO2 and CBF to those with moderate HIE. NIRS is an effective bedside tool to monitor and understand brain perfusion changes in term asphyxiated newborns, which in conjunction with precise measurements of CBF obtained by MRI at particular times, may help tailor neuroprotective strategies in term newborns with HIE. Copyright © 2013 Elsevier Inc. All rights reserved.

Prognostic value of brain proton MR spectroscopy and diffusion tensor imaging in newborns with hypoxic-ischemic encephalopathy treated by brain cooling

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Ancora, G.; Testa, C.; Tonon, C.; Manners, D.N.; Gramegna, L.L.; Lodi, R.; Grandi, S.; Sbravati, F.; Savini, S.; Corvaglia, L.T.; Faldella, G.; Tani, G.; Malucelli, E.

2013-01-01

MRI, proton magnetic resonance spectroscopy ( 1 H-MRS), and diffusion tensor imaging (DTI) have been shown to be of great prognostic value in term newborns with moderate-severe hypoxic-ischemic encephalopathy (HIE). Currently, no data are available on 1 H-MRS and DTI performed in the subacute phase after hypothermic treatment. The aim of the present study was to assess their prognostic value in newborns affected by moderate-severe HIE and treated with selective brain cooling (BC). Twenty infants treated with BC underwent conventional MRI and 1 H-MRS at a mean (SD) age of 8.3 (2.8) days; 15 also underwent DTI. Peak area ratios of metabolites and DTI variables, namely mean diffusivity (MD), axial and radial diffusivity, and fractional anisotropy (FA), were calculated. Clinical outcome was monitored until 2 years of age. Adverse outcome was observed in 6/20 newborns. Both 1 H-MRS and DTI variables showed higher prognostic accuracy than conventional MRI. N-acetylaspartate/creatine at a basal ganglia localisation showed 100 % PPV and 93 % NPV for outcome. MD showed significantly decreased values in many regions of white and gray matter, axial diffusivity showed the best predictive value (PPV and NPV) in the genu of corpus callosum (100 and 91 %, respectively), and radial diffusivity was significantly decreased in fronto white matter (FWM) and fronto parietal (FP) WM. The decrement of FA showed the best AUC (0.94) in the FPWM. Selective BC in HIE neonates does not affect the early and accurate prognostic value of 1 H-MRS and DTI, which outperform conventional MRI. (orig.)

Dietary interventions designed to protect the perinatal brain from hypoxic-ischemic encephalopathy--Creatine prophylaxis and the need for multi-organ protection.

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Ellery, Stacey J; Dickinson, Hayley; McKenzie, Matthew; Walker, David W

2016-05-01

Birth asphyxia or hypoxia arises from impaired placental gas exchange during labor and remains one of the leading causes of neonatal morbidity and mortality worldwide. It is a condition that can strike in pregnancies that have been uneventful until these final moments, and leads to fundamental loss of cellular energy reserves in the newborn. The cascade of metabolic changes that occurs in the brain at birth as a result of hypoxia can lead to significant damage that evolves over several hours and days, the severity of which can be ameliorated with therapeutic cerebral hypothermia. However, this treatment is only applied to a subset of newborns that meet strict inclusion criteria and is usually administered only in facilities with a high level of medical surveillance. Hence, a number of neuropharmacological interventions have been suggested as adjunct therapies to improve the efficacy of hypothermia, which alone improves survival of the post-hypoxic infant but does not altogether prevent adverse neurological outcomes. In this review we discuss the prospect of using creatine as a dietary supplement during pregnancy and nutritional intervention that can significantly decrease the risk of brain damage in the event of severe oxygen deprivation at birth. Because brain damage can also arise secondarily to compromise of other fetal organs (e.g., heart, diaphragm, kidney), and that compromise of mitochondrial function under hypoxic conditions may be a common mechanism leading to damage of these tissues, we present data suggesting that dietary creatine supplementation during pregnancy may be an effective prophylaxis that can protect the fetus from the multi-organ consequences of severe hypoxia at birth. Copyright © 2015 Elsevier Ltd. All rights reserved.

Color vision abnormality as the sole manifestation of posterior reversible encephalopathy due to post-partum HELLP syndrome.

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Takahashi, Hironori; Matsubara, Teppei; Makino, Shinji; Horie, Kenji; Matsubara, Shigeki

2017-03-01

Posterior reversible encephalopathy syndrome (PRES) is associated with several symptoms; of those, visual acuity loss, light oversensitivity (photophobia), and light flashes (photopsia) are known as PRES-related eye symptoms. We report a post-partum woman with PRES associated with hemolysis, elevated liver enzymes, and low platelets syndrome (HELLP), in whom color vision abnormality (achromatopsia) was the sole manifestation. Cesarean section was performed at 28 weeks due to headache, epigastralgia, and severe hypertension. HELLP became evident after delivery. On post-partum day 1, she complained of achromatopsia, stating: "all things look brownish-gray". Ophthalmologic examination was normal, but brain magnetic resonance imaging showed occipital lobe lesions, indicative of PRES, and, interestingly, also color vision center (area V4) lesions, suggesting that the achromatopsia had been caused by brain damage. It may be prudent to question HELLP patients concerning achromatopsia. © 2017 Japan Society of Obstetrics and Gynecology.

Bilirubin encephalopathy

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Bilirubin encephalopathy is a rare neurological condition that occurs in some newborns with severe jaundice . ... Bilirubin encephalopathy (BE) is caused by very high levels of bilirubin. Bilirubin is a yellow pigment that is created ...

Newborn Bilirubin Screening for Preventing Severe Hyperbilirubinemia and Bilirubin Encephalopathy: A Rapid Review.

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Bhardwaj, Kalpana; Locke, Tiffany; Biringer, Anne; Booth, Allyson; Darling, Elizabeth K; Dougan, Shelley; Harrison, Jane; Hill, Stephen; Johnson, Ana; Makin, Susan; Potter, Beth; Lacaze-Masmonteil, Thierry; Little, Julian

2017-01-01

According to the 2004 American Academy of Pediatrics guideline on the management of hyperbilirubinemia, every newborn should be assessed for the risk of developing severe hyperbilirubinemia with the help of predischarge total serum bilirubin or transcutaneous bilirubin measurements and/or assessments of clinical risk factors. The aim of this rapid review is 1) to review the evidence for 1) predicting and preventing severe hyperbilirubinemia and bilirubin encephalopathy, 2) determining the efficacy of home/community treatments (home phototherapy) in the prevention of severe hyperbilirubinemia, and 3) non-invasive/transcutaneous methods for estimating serum bilirubin level. In this rapid review, studies were identified through the Medline database. The main outcomes of interest were severe hyperbilirubinemia and encephalopathy. A subset of articles was double screened and all articles were critically appraised using the SIGN and AMSTAR checklists. This review investigated if systems approach is likely to reduce the occurrence of severe hyperbilirubinemia. Fifty-two studies met the inclusion criteria. Included studies assessed the association between bilirubin measurement early in neonatal life and the subsequent development of severe hyperbilirubinemia and chronic bilirubin encephalopathy/kernicterus. It was observed that, highest priority should be given to (i) universal bilirubin screening programs; (ii) implementation of community and midwife practice; (iii) outreach to communities for education of prospective parents; and (iv) development of clinical pathways to monitor, evaluate and track infants with severe hyperbilirubinemia. We found substantial observational evidence that severe hyperbilirubinemia can be accurately predicted and prevented through universal bilirubin screening. So far, there is no evidence of any harm. Copyright© Bentham Science Publishers; For any queries, please email at epub@benthamscience.org.

The application and shielding value of low-dose CT scanning in hypoxic ischemic encephalopathy of neonate

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Wu Aiqin; Zheng Wenlong; Xu Chongyong; Cheng Jianmin; Chen Yu; Chen Tinggang

2006-01-01

Objective: To investigate the application and shielding value of multi-slice spiral CT scanning with low-dose in hypoxic ischemic encephalopathy (HIE) of neonate. Methods: 60 neonates with HIE diagnosed by clinic were prospectively selected and randomly divided into two groups averagely. The technical parameters were tube tension 120 kV, slice thickness and gap 6 mm, conventional tube current 250 mAs and low dose 50 mAs. Weighted CT dose index (CTDI w ) and dose length product (DLP) were compared to each other. The image noise were analyzed with water phantom of children's skull. The mean and standard deviation of CT value were statistically analyzed. The image quality was blindly evaluated in two different dose groups. Results: (1) The mAs, CTDI w and DLP in low dose group were 20 % of conventional dose group; (2) The noise of water phantom in low dose group was larger than in conventional dose group with the significant difference (t=34.533, P < 0.01 ); (3) The imaging quality in low dose group was mostly better, but inferior to conventional dose group, while there is no poor images to influence the diagnosis of HIE. Conclusions: The low dose scanning will be practical in diagnosis of HIE, and beneficial to protect the newborn which corresponds to the optimizing principle of ICRP in medical radiation protection. (authors)

MRI and CT appearances in metabolic encephalopathies due to systemic diseases in adults

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Bathla, G.; Hegde, A.N.

2013-01-01

The term encephalopathy refers to a clinical scenario of diffuse brain dysfunction, commonly due to a systemic, metabolic, or toxic derangement. Often the clinical evaluation is unsatisfactory in this scenario and imaging plays an important role in the diagnosis, assessment of treatment response, and prognostication of the disorder. Hence, it is important for radiologists to be familiar with the imaging features of some relatively frequently acquired metabolic encephalopathies encountered in the hospital setting. This study reviews the computed tomography (CT) and magnetic resonance imaging (MRI) features of a number of metabolic encephalopathies that occur as part of systemic diseases in adults. The following conditions are covered in this review: hypoglycaemic encephalopathy, hypoxic ischaemic encephalopathy, non-ketotic hyperglycaemia, hepatic encephalopathy, uraemic encephalopathy, hyperammonaemic encephalopathy, and posterior reversible encephalopathy syndrome. MRI is the imaging method of choice in evaluating these conditions. Due to their high metabolic activity, bilateral basal ganglia changes are evident in the majority of cases. Concurrent imaging abnormalities in other parts of the central nervous system often provide useful diagnostic information about the likely underlying cause of the encephalopathy. Besides this, abnormal signal intensity and diffusion restriction patterns on MRI and MR spectroscopy features may provide important clues as to the diagnosis and guide further management. Frequently, the diagnosis is not straightforward and typical imaging features require correlation with clinical and laboratory data for accurate assessment

Proinflammatory Cytokines, Enolase and S-100 as Early Biochemical Indicators of Hypoxic-Ischemic Encephalopathy Following Perinatal Asphyxia in Newborns.

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Chaparro-Huerta, Verónica; Flores-Soto, Mario Eduardo; Merin Sigala, Mario Ernesto; Barrera de León, Juan Carlos; Lemus-Varela, María de Lourdes; Torres-Mendoza, Blanca Miriam de Guadalupe; Beas-Zárate, Carlos

2017-02-01

Estimation of the neurological prognosis of infants suffering from perinatal asphyxia and signs of hypoxic-ischemic encephalopathy is of great clinical importance; however, it remains difficult to satisfactorily assess these signs with current standard medical practices. Prognoses are typically based on data obtained from clinical examinations and neurological tests, such as electroencephalography (EEG) and neuroimaging, but their sensitivities and specificities are far from optimal, and they do not always reliably predict future neurological sequelae. In an attempt to improve prognostic estimates, neurological research envisaged various biochemical markers detectable in the umbilical cord blood of newborns (NB). Few studies examining these biochemical factors in the whole blood of newborns exist. Thus, the aim of this study was to determine the expression and concentrations of proinflammatory cytokines (TNF-α, IL-1β and IL-6) and specific CNS enzymes (S-100 and enolase) in infants with perinatal asphyxia. These data were compared between the affected infants and controls and were related to the degree of HIE to determine their utilities as biochemical markers for early diagnosis and prognosis. The levels of the proinflammatory cytokines and enzymes were measured by enzyme-linked immunosorbent assay (ELISA) and Reverse Transcription polymerase chain reaction (RT-PCR). The expression and serum levels of the proinflammatory cytokines, enolase and S-100 were significantly increased in the children with asphyxia compared with the controls. The role of cytokines after hypoxic-ischemic insult has been determined in studies of transgenic mice that support the use of these molecules as candidate biomarkers. Similarly, S-100 and enolase are considered promising candidates because these markers have been correlated with tissue damage in different experimental models. Copyright © 2016. Published by Elsevier B.V.

Prognostic value of brain proton MR spectroscopy and diffusion tensor imaging in newborns with hypoxic-ischemic encephalopathy treated by brain cooling

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Ancora, G. [Neonatal Intensive Care Unit, Department of Mother and Infant Infermi Hospital of Rimini, Rimini (Italy); Testa, C.; Tonon, C.; Manners, D.N.; Gramegna, L.L.; Lodi, R. [Department of Biomedical and Neuromotor Sciences University of Bologna, MR Functional Unit, Bologna (Italy); Grandi, S.; Sbravati, F.; Savini, S.; Corvaglia, L.T.; Faldella, G. [University of Bologna, Neonatology Unit, Department of Woman, Child and Adolescent Health, Bologna (Italy); Tani, G. [University of Bologna, Radiology Unit, Department of Woman, Child and Adolescent Health, Bologna (Italy); Malucelli, E. [University of Bologna, Department of Pharmacy and Biotechnologies, Bologna (Italy)

2013-08-15

MRI, proton magnetic resonance spectroscopy ({sup 1}H-MRS), and diffusion tensor imaging (DTI) have been shown to be of great prognostic value in term newborns with moderate-severe hypoxic-ischemic encephalopathy (HIE). Currently, no data are available on {sup 1}H-MRS and DTI performed in the subacute phase after hypothermic treatment. The aim of the present study was to assess their prognostic value in newborns affected by moderate-severe HIE and treated with selective brain cooling (BC). Twenty infants treated with BC underwent conventional MRI and {sup 1}H-MRS at a mean (SD) age of 8.3 (2.8) days; 15 also underwent DTI. Peak area ratios of metabolites and DTI variables, namely mean diffusivity (MD), axial and radial diffusivity, and fractional anisotropy (FA), were calculated. Clinical outcome was monitored until 2 years of age. Adverse outcome was observed in 6/20 newborns. Both {sup 1}H-MRS and DTI variables showed higher prognostic accuracy than conventional MRI. N-acetylaspartate/creatine at a basal ganglia localisation showed 100 % PPV and 93 % NPV for outcome. MD showed significantly decreased values in many regions of white and gray matter, axial diffusivity showed the best predictive value (PPV and NPV) in the genu of corpus callosum (100 and 91 %, respectively), and radial diffusivity was significantly decreased in fronto white matter (FWM) and fronto parietal (FP) WM. The decrement of FA showed the best AUC (0.94) in the FPWM. Selective BC in HIE neonates does not affect the early and accurate prognostic value of {sup 1}H-MRS and DTI, which outperform conventional MRI. (orig.)

Fetal stress and programming of hypoxic/ischemic-sensitive phenotype in the neonatal brain: mechanisms and possible interventions.

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Li, Yong; Gonzalez, Pablo; Zhang, Lubo

2012-08-01

Growing evidence of epidemiological, clinical and experimental studies has clearly shown a close link between adverse in utero environment and the increased risk of neurological, psychological and psychiatric disorders in later life. Fetal stresses, such as hypoxia, malnutrition, and fetal exposure to nicotine, alcohol, cocaine and glucocorticoids may directly or indirectly act at cellular and molecular levels to alter the brain development and result in programming of heightened brain vulnerability to hypoxic-ischemic encephalopathy and the development of neurological diseases in the postnatal life. The underlying mechanisms are not well understood. However, glucocorticoids may play a crucial role in epigenetic programming of neurological disorders of fetal origins. This review summarizes the recent studies about the effects of fetal stress on the abnormal brain development, focusing on the cellular, molecular and epigenetic mechanisms and highlighting the central effects of glucocorticoids on programming of hypoxic-ischemic-sensitive phenotype in the neonatal brain, which may enhance the understanding of brain pathophysiology resulting from fetal stress and help explore potential targets of timely diagnosis, prevention and intervention in neonatal hypoxic-ischemic encephalopathy and other brain disorders. Copyright © 2012 Elsevier Ltd. All rights reserved.

Doppler imaging of hypoxic-ischemic encephalopathy in term neonates on the first day of life

International Nuclear Information System (INIS)

Wilczynska, M.; Stefanczyk, L.; Zieba, K.; Bieganski, T.; Gulczynska, E.

2004-01-01

Hypoxic-ischaemic encephalopathy (HIE) is the most important neurological cause of mortality and poor neurodevelopmental outcome in neonates and infants. The aim of the study was to perform routine transfontanellar US brain scanning together with doppler evaluation of blood flow in anterior cerebral artery in the group of neonates with perinatal asphyxia studied at the first day of their life. The study group consisted of asphyxiated neonates (n=11), birth weight 3576,0 ± 426,0 g, gestational age 39,4 ± 1,1 weeks, pH of cord arterial blood 6,89 ± 0,45, 1 st minute Apgar score 2 points. The control group were healthy neonates (n=20), , birth weight 3354,0 ± 378,0 g, gestational age 38,9 ± 1,8 weeks, pH of cord arterial blood 7,28 ± 0,41, 1 st minute Apgar score 8 points. As compared to healthy children asphyxiated neonates had significantly decreased RI value (right cerebral artery 0,53 ± 0,02 vs. 0,72 ± 0,02; left cerebral artery 0,55 ± 0,02 vs. 0,73 ± 0,02), despite not all of them had obvious HIE features in routine US examination. None of these neonates lived longer than 10 days. Doppler examination of cerebral blood flow in term neonates born with perinatal asphyxia could be valuable complementary method of US imaging, especially in those patients with very discreet or absent HIE features in routine US scan. Results of doppler imaging could serve as prognostic factor for clinical outcome. (author)

Detection of hypoxic-ischemic brain injury with 3D-enhanced T2* weighted angiography (ESWAN) imaging

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Gang, QiangQiang, E-mail: rousikang@163.com; Zhang, Jianing, E-mail: 1325916060@qq.com; Hao, Peng, E-mail: 1043600590@qq.com; Xu, Yikai, E-mail: yikaivip@163.com

2013-11-01

Objective: To demonstrate the use of 3D-enhanced T2* weighted angiography (ESWAN) imaging for the observation and quantification of the evolution of brain injury induced by a recently developed model of hypoxic-ischemic brain injury (HI/R) in neonatal piglets. Methods: For these experiments, newborn piglets were subjected to HI/R injury, during which ESWAN scanning was performed, followed by H and E staining and immunohistochemistry of AQP-4 expression. Results: In the striatum, values from T2* weighted magnetic resonance imaging (MRI) increased and reached their highest level at 3 days post injury, whereas T2* values increased and peaked at 24 h in the subcortical region. The change in T2* values was concordant with brain edema. Phase values in the subcortical border region were not dependent on time post-injury. Magnitude values were significantly different from the control group, and increased gradually over time in the subcortical border region. Susceptibility-weighted images (SWI) indicated small petechial hemorrhages in the striatum and thalamus, as well as dilated intramedullary veins. Conclusion: SWI images can be used to detect white and gray matter microhemorrhages and dilated intramedullary veins. The T2*, phase, and magnitude map can also reflect the development of brain injury. Our data illustrate that ESWAN imaging can increase the diagnostic sensitivity and specificity of MRI in neonatal hypoxic-ischemic encephalopathy.

Detection of hypoxic-ischemic brain injury with 3D-enhanced T2* weighted angiography (ESWAN) imaging

International Nuclear Information System (INIS)

Gang, QiangQiang; Zhang, Jianing; Hao, Peng; Xu, Yikai

2013-01-01

Objective: To demonstrate the use of 3D-enhanced T2* weighted angiography (ESWAN) imaging for the observation and quantification of the evolution of brain injury induced by a recently developed model of hypoxic-ischemic brain injury (HI/R) in neonatal piglets. Methods: For these experiments, newborn piglets were subjected to HI/R injury, during which ESWAN scanning was performed, followed by H and E staining and immunohistochemistry of AQP-4 expression. Results: In the striatum, values from T2* weighted magnetic resonance imaging (MRI) increased and reached their highest level at 3 days post injury, whereas T2* values increased and peaked at 24 h in the subcortical region. The change in T2* values was concordant with brain edema. Phase values in the subcortical border region were not dependent on time post-injury. Magnitude values were significantly different from the control group, and increased gradually over time in the subcortical border region. Susceptibility-weighted images (SWI) indicated small petechial hemorrhages in the striatum and thalamus, as well as dilated intramedullary veins. Conclusion: SWI images can be used to detect white and gray matter microhemorrhages and dilated intramedullary veins. The T2*, phase, and magnitude map can also reflect the development of brain injury. Our data illustrate that ESWAN imaging can increase the diagnostic sensitivity and specificity of MRI in neonatal hypoxic-ischemic encephalopathy

The value of brainstem evoked potential in clinical decision of a patient with hypoxic-ischemic encephalopathy O valor do potencial evocado auditivo em decisão clínica em paciente com síndrome hipóxico-isquêmica

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Anna Lecticia R. Pinto

2007-09-01

Full Text Available Establishing a prognosis for hypoxic-ischemic encephalopathy during the neonatal period is extremely difficult, as the neuroplasticity of the developing brain makes it almost impossible to measure the affected area. This case report describes a newborn with severe perinatal asphyxia and neonatal neurological syndrome including absent suck reflex. Normal brainstem auditory evoked potential led the diagnosis towards a transitory dysfunction of deglutition, and the subject received daily stimulation in the hospital environment. Suck developed satisfactorily by day of life 30 and the patient was released without having to be tube fed. Neurophysiologic tests can be of value in the clinical decisions and analysis of functional prognosis of patients with hypoxic-ischemic encephalopathy.Estabelecer o prognóstico da encefalopatia hipóxico-isquêmica durante o período neonatal é extremamente difícil, devido à neuroplasticidade do cérebro em desenvolvimento que impede a medida exata das áreas afetadas. Este relato descreve um recém-nascido a termo com grave asfixia perinatal e síndrome neurológica pós-natal, incluindo ausência do reflexo de sucção. O potencial evocado auditivo do tronco cerebral foi normal, sugerindo o diagnóstico de disfunção transitória da deglutição. Após estimulação diária no hospital a sucção foi obtida satisfatoriamente, e o paciente recebeu alta sem necessidade de alimentação enteral. Os testes neurofisiológicos podem ser de grande valor em decisões clínicas e análise funcional prognóstica de pacientes com encefalopatia hipóxico-isquêmica.

Electroencephalogram abnormalities in full term infants with history of severe asphyxia

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Susanti Halim

2016-11-01

Full Text Available Background An electroencephalogram (EEG is an electroimaging tool used to determine developmental and electrical problems in the brain. A history of severe asphyxia is a risk factor for these brain problems in infants. Objective To evaluate the prevalence of abnormal EEGs in full term neonates and to assess for an association with severe asphyxia, hypoxic ischemic encephalopathy (HIE, and spontaneous delivery. Methods This cross-sectional study was conducted at the Pediatric Outpatient Department of Sanglah Hospital, Denpasar, from November 2013 to January 2014. Subjects were fullterm infants aged 1 month who were delivered and/or hospitalized at Sanglah Hospital. All subjects underwent EEG. The EEGs were interpreted by a pediatric neurology consultant, twice, with a week interval between readings. Clinical data were obtained from medical records. Association between abnormal ECG and severe asphyxia were analyzed by Chi-square and multivariable logistic analyses. Results Of 55 subjects, 27 had a history of severe asphyxia and 28 were vigorous babies. Forty percent (22/55 of subjects had abnormal EEG findings, 19/22 of these subjects having history of severe asphyxia, 15/22 had history of hypoxic-ischemic encephalopathy (HIE, and 20/22 were delievered vaginally. There were strong correlations between the prevalence of abnormal EEG and history of severe asphyxia, HIE, and spontaneous delivery. Conclusion Prevalence of abnormal EEG among full-term neonates referred to neurology/growth development clinic is around 40%, with most of them having a history of severe asphyxia. Abnormal EEG is significantly associated to severe asphyxia, HIE, and spontaneous delivery.

Early-Onset Severe Encephalopathy with Epilepsy: The BRAT1 Gene Should Be Added to the List of Causes.

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van de Pol, Laura A; Wolf, Nicole I; van Weissenbruch, Mirjam M; Stam, Cornelie J; Weiss, Janneke M; Waisfisz, Quinten; Kevelam, Sietske H; Bugiani, Mariana; van de Kamp, Jiddeke M; van der Knaap, Marjo S

2015-12-01

A variety of pathologies can underlie early-onset severe encephalopathy with epilepsy. To aid the diagnostic process in such patients we present an overview of causes, including the rapidly expanding list of genes involved. When no explanation is found, whole-exome sequencing (WES) can be used in an attempt to identify gene defects in patients suspected to suffer from a genetic form. We describe three siblings, born to consanguineous parents, with a lethal severe epileptic encephalopathy with early-infantile onset, including their magnetic resonance imaging, electroencephalography and, in one case, neuropathological findings. Using WES a homozygous frameshift mutation in the BRAT1 gene, c.638dup p.(Val214Glyfs*189), was identified. We present our cases in the context of all published cases with mutations in the BRAT1 gene and conclude that BRAT1 should be added to the growing list of genes related to early-onset severe encephalopathy with epilepsy. Georg Thieme Verlag KG Stuttgart · New York.

Treatment of Hyponatremic Encephalopathy in the Critically Ill.

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Achinger, Steven G; Ayus, Juan Carlos

2017-10-01

) and intervene with IV 3% sodium chloride as this is the time to intervene rather than waiting until more severe symptoms develop. Cerebral demyelination is a rare complication of overly rapid correction of hyponatremia. The principal risk factors for cerebral demyelination are correction of the serum sodium more than 25 mEq/L in the first 48 hours of therapy, correction past the point of 140 mEq/L, chronic liver disease, and hypoxic/anoxic episode.

Cerebral Lactate Concentration in Neonatal Hypoxic-Ischemic Encephalopathy: In Relation to Time, Characteristic of Injury, and Serum Lactate Concentration

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Tai-Wei Wu

2018-05-01

Full Text Available BackgroundCerebral lactate concentration can remain detectable in neonatal hypoxic-ischemic encephalopathy (HIE after hemodynamic stability. The temporal resolution of regional cerebral lactate concentration in relation to the severity or area of injury is unclear. Furthermore, the interplay between serum and cerebral lactate in neonatal HIE has not been well defined. The study aims to describe cerebral lactate concentration in neonatal HIE in relation to time, injury, and serum lactate.Design/methodsFifty-two newborns with HIE undergoing therapeutic hypothermia (TH were enrolled. Magnetic resonance imaging and spectroscopy (MRI + MR spectroscopy were performed during and after TH at 54.6 ± 15.0 and 156 ± 57.6 h of life, respectively. Severity and predominant pattern of injury was scored radiographically. Single-voxel 1H MR spectra were acquired using short-echo (35 ms PRESS sequence localized to the basal ganglia (BG, thalamus (Thal, gray matter (GM, and white matter. Cerebral lactate concentration was quantified by LCModel software. Serum and cerebral lactate concentrations were plotted based on age at time of measurement. Multiple comparisons of regional cerebral lactate concentration based on severity and predominant pattern of injury were performed. Spearman’s Rho was computed to determine correlation between serum lactate and cerebral lactate concentration at the respective regions of interest.ResultsOverall, serum lactate concentration decreased over time. Cerebral lactate concentration remained low for less severe injury and decreased over time for more severe injury. Cerebral lactate remained detectable even after TH. During TH, there was a significant higher concentration of cerebral lactate at the areas of injury and also when injury was more severe. However, these differences were no longer observed after TH. There was a weak correlation between serum lactate and cerebral lactate concentration at the BG (rs�

Diagnostic and prognostic values of CT in neonate hypoxic and ischemic encephalopathy

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Yu Hongsheng; Ji Luzhou; Sun Guoyun

2009-01-01

Objective: To explore the relationship between the clinical grades, severity of asphyxia and CT grades, and to investigate the CT value in predicting the outcomes in neonates with hypoxia and ischemia encephalopathy (HIE). Methods: A total of 83 neonates that had obvious history of asphyxia and were diagnosed as HIE were studied. Their clinic and CT data were carefully analyzed. Results: Seventy-nine of 83 HIE neonates CT showed significant abnormalities in various extents. Main manifestations included cerebral edema, infarction, and intracranial hemorrhage. Pure subarachnoid hemorrhage (SAH) was detected most often (28 out of 42) among the intracranial hemorrhage, and followed by complex hemorrhage (14 out of 42). HIE clinic grades were consistent with CT grades (r=0.7989, t r =11.95. P<0.01); while severity of asphyxia and CT grades were significantly correlated (r=0.692, t r =8.63, P<0.01), i.e. more serious asphyxia resulted in higher CT grade indicating more severe brain damage. Follow-up CT showed that the brain parenchyma with mild or mediate abnormalities on initial CT, the hypodense lesions shrank or even disappeared, and SAH was absorbed completely. However, the severe complex intracranial hemorrhage and cerebral infarction resulted in local encephalomalacia, atrophy, hydrocephalus, parenchymal calcification, and porencephalia. Three patients died during the follow-up period (χ = 30.95, P< 0.01). Conclusion: Cerebral edema. infarction, and intracranial hemorrhage are key CT signs in diagnosis of HIE. SAH is the most frequent complication of HIE. CT can provide objective evidences in the diagnosis and prognosis assessment of HIE. (authors)

Severe posterior reversible encephalopathy in pheochromocytoma: Importance of susceptibility-weighted MRI

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Serter, Asil; Alkan, Alpay; Aralasmak, Ayse; Kocakoc, Ercan [Dept. of Radiology, Bezmialem Vakif University School of Medicine, Istanbul (Turkmenistan)

2013-10-15

Pheochromocytoma is a rare cause of hypertension in children. Hypertension is one of the common reasons of posterior reversible encephalopathy. Intracerebral hemorrhage is a serious and unexpected complication of hypertensive encephalopathy due to pheochromocytoma, and very rarely seen in the childhood. Intracerebral hemorrhages should be searched if there are hypertensive reversible signal changes on the brain. Susceptibility weighted imaging (SWI) is a more sensitive method than conventional MRI when demonstrating cerebral microhemorrhagic foci. This is the first report of SWI findings on intracerebral hemorrhages in basal ganglia, brain stem and periventricular white matter due to hypertensive encephalopathy in a child with pheochromocytoma.

The Association between NOS3 Gene Polymorphisms and Hypoxic-Ischemic Encephalopathy Susceptibility and Symptoms in Chinese Han Population

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Yongqin Wu

2016-01-01

Full Text Available Endothelial NOS (NOS3 has a potential role in the prevention of neuronal injury in hypoxic-ischemic encephalopathy (HIE. Thus, we aimed to explore the association between NOS3 gene polymorphisms and HIE susceptibility and symptoms in a Chinese Han population. Three single nucleotide polymorphisms (SNPs in the NOS3 gene, rs1800783, rs1800779, and rs2070744, were detected in 226 children with HIE and 212 healthy children in a Chinese Han population. Apgar scores and magnetic resonance image scans were used to estimate the symptoms and brain damage. The association analyses were conducted by using SNPStats and SPSS 18.0 software. The genotype and allele distributions of rs1800779 and rs1799983 displayed no significant differences between the patients and the controls, while the rs2070744 allele distribution was significantly different (corrected P=0.009. For clinical characteristics, the rs2070744 genotype distribution was significantly different in patients with different Apgar scores (≤5, TT/TC/CC = 6/7/5; 6~7, TT/TC/CC = 17/0/0; 8~9, TT/TC/CC = 6/2/0; 10, TT/TC/CC = 7/1/0; corrected P=0.006 in the 1001 to 1449 g birth weight subgroup. The haplotype test did not show any associations with the risk and clinical characteristics of HIE. The results suggest that NOS3 gene SNP rs2070744 was significantly associated with HIE susceptibility and symptom expression in Chinese Han population.

Conservative management of severe serotonin syndrome with coma, myoclonus, and crossed-extensor reflex complicated by hepatic encephalopathy.

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Ramachandran, Vignesh; Ding, Belicia; George, Rollin; Novakovic, Matthew

2018-01-01

Serotonin syndrome (SS) is an underrecognized and potentially fatal disorder that occurs secondary to combinational use or overdose of a single serotonergic medication. The presentation may be complicated by hepatic encephalopathy in cirrhotic patients, which may also affect metabolism of these serotonergic agents. The authors report a rare case of severe SS complicated by hepatic encephalopathy secondary to cirrhosis in a 52-year-old woman after an increase in her home dosage of fluoxetine and addition of other psychiatric medications.

Sex-related differences in effects of progesterone following neonatal hypoxic brain injury.

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Peterson, Bethany L; Won, Soonmi; Geddes, Rastafa I; Sayeed, Iqbal; Stein, Donald G

2015-06-01

There is no satisfactory therapeutic intervention for neonatal hypoxic-ischemic (HI) encephalopathy. Progesterone is known to be effective in treating traumatic brain injury in adult animals but its effects in neonatal brains have not been reported. Brain injuries were induced by a unilateral common carotid artery ligation plus hypoxia exposure. Progesterone was administered immediately after hypoxia and daily for 5 days at 8 mg/kg, followed by a tapered dose for two days. At six weeks post-injury, lesion size and inflammatory factors were evaluated. Progesterone-treated, HI-injured male animals, but not females, showed significant long-term tissue protection compared to vehicle, suggesting an important sex difference in neuroprotection. Progesterone-treated, HI-injured male rats had fewer activated microglia in the cortex and hippocampus compared to controls. The rats were tested for neurological reflexes, motor asymmetry, and cognitive performance at multiple time points. The injured animals exhibited few detectable motor deficits, suggesting a high level of age- and injury-related neuroplasticity. There were substantial sex differences on several behavioral tests, indicating that immature males and females should be analyzed separately. Progesterone-treated animals showed modest beneficial effects in both sexes compared to vehicle-treated injured animals. Sham animals given progesterone did not behave differently from vehicle-treated sham animals on any measures. Copyright © 2015 Elsevier B.V. All rights reserved.

The evaluation value of the quantitative electroencephalogram for the prognosis of neonatal hypoxic ischemic encephalopathy and its relationship with serological indicators

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Ting-Mei Dou

2017-06-01

Full Text Available Objective: To study the evaluation value of the quantitative electroencephalogram (qEEG for the prognosis of neonatal hypoxic ischemic encephalopathy (HIE and its relationship with serological indicators. Methods: 76 children with HIE who were born and treated in our hospital between April 2013 and February 2017 were collected as observation group, and 50 healthy newborns who were born in our hospital during the same period were collected as normal control group. qEEG parameter values of two groups of children were determined, serum levels of nerve injury indexes, nerve apoptosis indexes and oxidative stress indexes were compared between the two groups, and Pearson test was used to evaluate the inner link between qEEG parameter values and disease severity in children with HIE. Results: qEEG Fp1, Fp2, C3, C4, T3, T4, O1 and O2 loci power spectrum values of observation group were significantly lower than those of normal control group. Serum NSE, NPY, S-100B and MBP contents in observation group were higher than those in normal control group; nerve apoptosis indexes sFas, sFasL and Caspase-3 contents were higher than those in normal control group while Bcl-2 content was lower than that in normal control group; serum oxidative stress indexes AOPP and MDA contents were higher than those in normal control group while SOD content was lower than that in normal control group. Pearson test showed that qEEG Fp1, Fp2, C3, C4, T3, T4, O1 and O2 loci power spectrum values in children with HIE were directly correlated with the contents of nerve injury indexes, nerve apoptosis indexes and oxidative stress indexes. Conclusion: The qEEG parameter values in children with HIE are lower than those in normal children, and the specific values are closely related to the severity of the disease.

The Spectrum of Disease in Chronic Traumatic Encephalopathy

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McKee, Ann C.; Stein, Thor D.; Nowinski, Christopher J.; Stern, Robert A.; Daneshvar, Daniel H.; Alvarez, Victor E.; Lee, Hyo-Soon; Hall, Garth; Wojtowicz, Sydney M.; Baugh, Christine M.; Riley, David O.; Kubilus, Caroline A.; Cormier, Kerry A.; Jacobs, Matthew A.; Martin, Brett R.; Abraham, Carmela R.; Ikezu, Tsuneya; Reichard, Robert Ross; Wolozin, Benjamin L.; Budson, Andrew E.; Goldstein, Lee E.; Kowall, Neil W.; Cantu, Robert C.

2013-01-01

Chronic traumatic encephalopathy is a progressive tauopathy that occurs as a consequence of repetitive mild traumatic brain injury. We analysed post-mortem brains obtained from a cohort of 85 subjects with histories of repetitive mild traumatic brain injury and found evidence of chronic traumatic encephalopathy in 68 subjects: all males, ranging…

[Unusual leukoencephalopathy of post-partum].

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Hsaini, Y; Karouache, A; Bourazza, A

2011-08-01

Neurologic complications of post-partum are serious and usually secondary to eclampsia or stroke. We here report a 26-year-old female who presented with severe headaches, blurred vision, and repeated generalized seizures secondary to posterior reversible encephalopathy that occurred after a caesarean section for fetal death in utero. Outcome was favourable. Although uncommon, this neurologic complication of the post-partum should be discussed in the presence of any sign of encephalopathy occurring in the context of acute hypertension. Copyright © 2010 Société nationale française de médecine interne (SNFMI). Published by Elsevier SAS. All rights reserved.

Goreisan Inhibits Upregulation of Aquaporin 4 and Formation of Cerebral Edema in the Rat Model of Juvenile Hypoxic-Ischemic Encephalopathy

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Yano, Hajime; Takahashi, Hisaaki; Yoshimoto, Kouhei; Tsuda, Shinji; Fujiyama, Kenta; Izumo-Shimizu, Yusuke; Motoie, Ryota; Ito, Masanori; Tanaka, Junya; Ishii, Eiichi

2017-01-01

Secondary cerebral edema regulation is of prognostic significance in hypoxic-ischemic encephalopathy (HIE), and aquaporin 4 (AQP4) plays an important role in the pathogenesis of cerebral edema. The traditional Japanese herbal medicine Goreisan relieves brain edema in adults; however, its effect and pharmacological mechanism in children are unknown. We investigated the effects of Goreisan on HIE-associated brain edema and AQP4 expression in a juvenile rat model, established by combined occlusion of middle cerebral and common carotid arteries. Magnetic resonance imaging showed that the lesion areas were significantly smaller in the Goreisan- (2 g/kg) treated group than in the nontreated (saline) group at 24 and 48 h postoperatively. AQP4 mRNA levels in the lesion and nonlesion sides were significantly suppressed in the Goreisan group compared with the nontreated group 36 h postoperatively. Western blotting revealed that levels of AQP4 protein were significantly decreased in the Goreisan group compared with the nontreated group in the lesion side 72 h postoperatively, but not at 12 or 36 h. After 14 days, the Goreisan group had a significantly better survival rate. These findings suggest that Goreisan suppresses brain edema in HIE and improves survival in juvenile rats, possibly via regulation of AQP4 expression and function. PMID:29234383

Goreisan Inhibits Upregulation of Aquaporin 4 and Formation of Cerebral Edema in the Rat Model of Juvenile Hypoxic-Ischemic Encephalopathy

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Yoshiaki Yano

2017-01-01

Full Text Available Secondary cerebral edema regulation is of prognostic significance in hypoxic-ischemic encephalopathy (HIE, and aquaporin 4 (AQP4 plays an important role in the pathogenesis of cerebral edema. The traditional Japanese herbal medicine Goreisan relieves brain edema in adults; however, its effect and pharmacological mechanism in children are unknown. We investigated the effects of Goreisan on HIE-associated brain edema and AQP4 expression in a juvenile rat model, established by combined occlusion of middle cerebral and common carotid arteries. Magnetic resonance imaging showed that the lesion areas were significantly smaller in the Goreisan- (2 g/kg treated group than in the nontreated (saline group at 24 and 48 h postoperatively. AQP4 mRNA levels in the lesion and nonlesion sides were significantly suppressed in the Goreisan group compared with the nontreated group 36 h postoperatively. Western blotting revealed that levels of AQP4 protein were significantly decreased in the Goreisan group compared with the nontreated group in the lesion side 72 h postoperatively, but not at 12 or 36 h. After 14 days, the Goreisan group had a significantly better survival rate. These findings suggest that Goreisan suppresses brain edema in HIE and improves survival in juvenile rats, possibly via regulation of AQP4 expression and function.

MR imaging for diagnostic evaluation of encephalopathy in the newborn.

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Shroff, Manohar M; Soares-Fernandes, João P; Whyte, Hilary; Raybaud, Charles

2010-05-01

Magnetic resonance (MR) imaging is used with increasing frequency to evaluate the neonatal brain because it can provide important diagnostic and prognostic information that is needed for optimal treatment and appropriate counseling. Special care must be taken in preparing encephalopathic neonates for an MR study, transporting them from the intensive care unit, monitoring their vital signs, and optimizing MR sequences and protocols. Moreover, to accurately interpret the findings, specific knowledge is needed about the normal MR imaging appearances of the physiologic processes of myelination, cell migration, and sulcation, as well as patterns of injury, in the neonatal brain at various stages of gestational development. Hypoxic-ischemic injury, the most common cause of neonatal encephalopathy, has characteristic appearances that depend on the severity and duration of the insult as well as the stage of brain development. Diffusion-weighted MR imaging and MR spectroscopy depict abnormalities earlier than do conventional MR imaging sequences. However, diffusion-weighted imaging, if performed in the first 24 hours after the insult, might lead to underestimation of the extent of injury. When the MR findings are atypical, the differential diagnosis of neonatal encephalopathy also should include congenital and metabolic disorders and infectious diseases. Despite recent advances in the MR imaging-based characterization of these conditions, the clinical history must be borne in mind to achieve an accurate diagnosis.

Genetics Home Reference: MECP2-related severe neonatal encephalopathy

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... and Stroke: Encephalopathy Information Page National Institute of Neurological Disorders and Stroke: Microcephaly Information Page Educational Resources (8 links) Boston Children's Hospital: Seizures Centers for Disease Control and Prevention: ...

The mechanisms and treatment of asphyxial encephalopathy

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Guido eWassink

2014-02-01

Full Text Available Acute post-asphyxial encephalopathy occurring around the time of birth remains a major cause of death and disability. The recent seminal insight that allows active neuroprotective treatment is that even after profound asphyxia (the primary phase, many brain cells show initial recovery from the insult during a short latent phase, typically lasting approximately 6 h, only to die hours to days later after a secondary deterioration characterized by seizures, cytotoxic edema, and progressive failure of cerebral oxidative metabolism. Although many of these secondary processes are potentially injurious, they appear to be primarily epiphenomena of the ‘execution’ phase of cell death. Animal and human studies designed around this conceptual framework have shown that moderate cerebral hypothermia initiated as early as possible but before the onset of secondary deterioration, and continued for a sufficient duration to allow the secondary deterioration to resolve, has been associated with potent, long-lasting neuroprotection. Recent clinical trials show that while therapeutic hypothermia significantly reduces morbidity and mortality, many babies still die or survive with disabilities. The challenge for the future is to find ways of improving the effectiveness of treatment. In this review, we will dissect the known mechanisms of hypoxic-ischemic brain injury in relation to the known effects of hypothermic neuroprotection.

Hepatic encephalopathy: cause and possible management with botanicals.

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Tripathi, Suyash; Tripathi, Yamini B

2014-01-01

Hepatic encephalopathy is a brain functional disorder, characterized by neuropsychiatric abnormalities with liver failure. High blood ammonia, causing glutamate neurotoxicity is the basic cause, finally leading to low-grade cerebral edema. Its manifestation is more likely in patients of sepsis, oxidative stress, generalized inflammation, gut mal-functioning, amoebiaesis, viral hepatitis, nervous imbalance, etc. Thus, the therapeutic goals primarily include the maintenance of proper blood supply and prevention of hypoxic condition in liver, along with management of factors responsible for high blood ammonia, oxidative stress, inflammation, and high GI- serotonin. The drugs in clinical practice include lactulose, sodium benzoate, flumazenil and rifaximin, supplementation of zinc, branched chain amino acids (BCAA), l-ornithine-l aspartate, antioxidants and iNOS inhibitors. However, herbal formulations would be of great importance as it shows multi-targeted action because it possesses a natural cocktail of secondary metabolites. It can collectively act as an antioxidant, anti-inflammatory, prebiotic, hepatoprotective and neuron-protective agents. We have briefly outlined some of these plants and also recent patents useful in the management of hepatic encephalopathy.

Fetal Stress and Programming of Hypoxic/Ischemic-Sensitive Phenotype in the Neonatal Brain: Mechanisms and Possible Interventions

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Li, Yong; Gonzalez, Pablo; Zhang, Lubo

2012-01-01

Growing evidence of epidemiological, clinical and experimental studies has clearly shown a close link between adverse in utero environment and the increased risk of neurological, psychological and psychiatric disorders in later life. Fetal stresses, such as hypoxia, malnutrition, and fetal exposure to nicotine, alcohol, cocaine and glucocorticoids may directly or indirectly act at cellular and molecular levels to alter the brain development and result in programming of heightened brain vulnerability to hypoxic-ischemic encephalopathy and the development of neurological diseases in the postnatal life. The underlying mechanisms are not well understood. However, glucocorticoids may play a crucial role in epigenetic programming of neurological disorders of fetal origins. This review summarizes the recent studies about the effects of fetal stress on the abnormal brain development, focusing on the cellular, molecular and epigenetic mechanisms and highlighting the central effects of glucocorticoids on programming of hypoxicischemic-sensitive phenotype in the neonatal brain, which may enhance the understanding of brain pathophysiology resulting from fetal stress and help explore potential targets of timely diagnosis, prevention and intervention in neonatal hypoxic-ischemic encephalopathy and other for brain disorders. PMID:22627492

Exploratory Use of Decision Tree Analysis in Classification of Outcome in Hypoxic-Ischemic Brain Injury.

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Phan, Thanh G; Chen, Jian; Singhal, Shaloo; Ma, Henry; Clissold, Benjamin B; Ly, John; Beare, Richard

2018-01-01

Prognostication following hypoxic ischemic encephalopathy (brain injury) is important for clinical management. The aim of this exploratory study is to use a decision tree model to find clinical and MRI associates of severe disability and death in this condition. We evaluate clinical model and then the added value of MRI data. The inclusion criteria were as follows: age ≥17 years, cardio-respiratory arrest, and coma on admission (2003-2011). Decision tree analysis was used to find clinical [Glasgow Coma Score (GCS), features about cardiac arrest, therapeutic hypothermia, age, and sex] and MRI (infarct volume) associates of severe disability and death. We used the area under the ROC (auROC) to determine accuracy of model. There were 41 (63.7% males) patients having MRI imaging with the average age 51.5 ± 18.9 years old. The decision trees showed that infarct volume and age were important factors for discrimination between mild to moderate disability and severe disability and death at day 0 and day 2. The auROC for this model was 0.94 (95% CI 0.82-1.00). At day 7, GCS value was the only predictor; the auROC was 0.96 (95% CI 0.86-1.00). Our findings provide proof of concept for further exploration of the role of MR imaging and decision tree analysis in the early prognostication of hypoxic ischemic brain injury.

[Posterior reversible encephalopathy syndrome and cerebrovascular constriction syndrome in the differential diagnosis of post-partum headaches].

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Ruiz López, N; Cano Hernández, B; Balbás Álvarez, S

2016-02-01

Postpartum headache can be due to many causes. In a patient with previous epidural analgesia, the headache can be attributed to post-dural puncture headache, even if the symptoms are not typical of this clinical entity. We report a case of a post-partum with accidental dural tap during the insertion of an epidural catheter for labour analgesia, and who referred to headaches in the third post-partum day. Initially, a post-dural puncture headache was suspected, but the subsequent onset of seizures and visual impairment meant that the diagnosis had to be reconsidered. In this case report, the clinical and pathophysiological features of posterior reversible encephalopathy syndrome and reversible cerebral vasoconstriction syndrome, as well as the differential diagnosis of post-partum headaches are described. Copyright © 2014 Sociedad Española de Anestesiología, Reanimación y Terapéutica del Dolor. Publicado por Elsevier España, S.L.U. All rights reserved.

Memantine, a noncompetitive NMDA receptor antagonist improves hyperammonemia-induced encephalopathy and acute hepatic encephalopathy in rats

NARCIS (Netherlands)

Vogels, B. A.; Maas, M. A.; Daalhuisen, J.; Quack, G.; Chamuleau, R. A.

1997-01-01

The aim of this study was to investigate the possible role of N-methyl-D-aspartate (NMDA)-receptor overactivity in two different experimental rat models of encephalopathy: subacute encephalopathy caused by severe hyperammonemia in portacaval-shunted rats (AI-PCS rats) and acute hepatic

Treatment of Epileptic Encephalopathies.

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Balestrini, Simona; Sisodiya, Sanjay M

2017-01-01

Epileptic encephalopathies represent the most severe epilepsies, with onset in infancy and childhood and seizures continuing in adulthood in most cases. New genetic causes are being identified at a rapid rate. Treatment is challenging and the overall outcome remains poor. Available targeted treatments, based on the precision medicine approach, are currently few. To provide an overview of the treatment of epileptic encephalopathies with known genetic determinants, including established treatment, anecdotal reports of specific treatment, and potential tailored precision medicine strategies. Genes known to be associated to epileptic encephalopathy were selected. Genes where the association was uncertain or with no reports of details on treatment, were not included. Although some of the genes included are associated with multiple epilepsy phenotypes or other organ involvement, we have mainly focused on the epileptic encephalopathies and their antiepileptic treatments. Most epileptic encephalopathies show genotypic and phenotypic heterogeneity. The treatment of seizures is difficult in most cases. The available evidence may provide some guidance for treatment: for example, ACTH seems to be effective in controlling infantile spams in a number of genetic epileptic encephalopathies. There are potentially effective tailored precision medicine strategies available for some of the encephalopathies, and therapies with currently unexplained effectiveness in others. Understanding the effect of the mutation is crucial for targeted treatment. There is a broad range of disease mechanisms underlying epileptic encephalopathies, and this makes the application of targeted treatments challenging. However, there is evidence that tailored treatment could significantly improve epilepsy treatment and prognosis. Copyright© Bentham Science Publishers; For any queries, please email at epub@benthamscience.org.

Adjuvant treatment with monosialoganglioside may improve neurological outcomes in neonatal hypoxic-ischemic encephalopathy: A meta-analysis of randomized controlled trials.

Directory of Open Access Journals (Sweden)

Lei Sheng

Full Text Available Ganglioside has a neuroprotective role in neonatal hypoxic-ischemic encephalopathy (HIE. This study aimed to evaluate the neurological outcomes of monosialoganglioside as adjuvant treatment for neonatal HIE by conducting a meta-analysis.A comprehensive literature search was made in the Pubmed, EMBASE, Cochrane Library, Wanfang, CNKI, VIP databases through October 2016. Randomized controlled trials comparing monosialoganglioside with the usual treatment for newborns having HIE deemed eligible. Weighted mean difference (WMD and risk ratio (RR with 95% confidence interval (CI were calculated for continuous and dichotomous data, respectively.Ten trials consisting of 787 neonates were included. Adjuvant treatment with monosialoganglioside significantly reduced major neurodevelopmental disabilities (RR = 0.35; 95% CI = 0.21-0.57, cerebral palsy (RR = 0.32; 95% CI = 0.12-0.87, mental retardation (RR = 0.31; 95% CI = 0.11-0.88 as well as improved the mental (WMD = 14.95; 95% CI = 7.44-22.46 and psychomotive (WMD = 13.40; 95% CI = 6.69-20.11 development index during the follow-up. Also, monosialoganglioside significantly improved Neonatal Behavioral Neurological Assessment scores (WMD = 2.91; 95% CI = 2.05-3.78 compared with the usual treatment. However, adverse effects associated with monosialoganglioside were poorly reported in the included trials.Adjuvant treatment with monosialoganglioside had beneficial effects in improving neurological outcomes in neonatal HIE. However, these findings should be interpreted with caution because of methodological flaws in the included trials. Furthermore, safety of monosialoganglioside use should also be further evaluated.

Introduction to altitude/hypoxic training symposium.

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Wilber, Randall L

2007-09-01

Altitude/hypoxic training has traditionally been an intriguing and controversial area of research and sport performance. This controversial aspect was evident recently in the form of scholarly debates in highly regarded professional journals, as well as the World Anti-Doping Agency's (WADA) consideration of placing "artificially-induced hypoxic conditions" on the 2007 Prohibited List of Substances/Methods. In light of the ongoing controversy surrounding altitude/hypoxic training, this symposium was organized with the following objectives in mind: 1) to examine the primary physiological responses and underlying mechanisms associated with altitude/hypoxic training, including the influence of genetic predisposition; 2) to present evidence supporting the effect of altitude/hypoxic acclimatization on both hematological and nonhematological markers, including erythrocyte volume, skeletal muscle-buffering capacity, hypoxic ventilatory response, and physiological efficiency/economy; 3) to evaluate the efficacy of several contemporary simulated altitude modalities and training strategies, including hypoxic tents, nitrogen apartments, and intermittent hypoxic exposure (IHE) or training, and to address the legal and ethical issues associated with the use of simulated altitude; and 4) to describe different altitude/hypoxic training strategies used by elite-level athletes, including Olympians and military special forces. In addressing these objectives, papers will be presented on the topics of: 1) effect of hypoxic "dose" on physiological responses and sea-level performance (Drs. Benjamin Levine and James Stray-Gundersen), 2) nonhematological mechanisms of improved performance after hypoxic exposure (Dr. Christopher Gore), 3) application of altitude/hypoxic training by elite athletes (Dr. Randall Wilber), and 4) military applications of hypoxic training (Dr. Stephen Muza).

Feasibility of adjunct therapeutic hypothermia treatment for hyperammonemia and encephalopathy due to urea cycle disorders and organic acidemias.

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Lichter-Konecki, Uta; Nadkarni, Vinay; Moudgil, Asha; Cook, Noah; Poeschl, Johannes; Meyer, Michael T; Dimmock, David; Baumgart, Stephen

2013-08-01

Children with urea cycle disorders (UCDs) or organic acidemias (OAs) and acute hyperammonemia and encephalopathy are at great risk for neurological injury, developmental delay, intellectual disability, and death. Nutritional support, intravenous alternative pathway therapy, and dialysis are used to treat severe hyperammonemia associated with UCDs and nutritional support and dialysis are used to treat severe hyperammonemia in OAs. Brain protective treatment while therapy is initiated may improve neurological and cognitive function for the lifetime of the child. Animal experiments and small clinical trials in hepatic encephalopathy caused by acute liver failure suggest that therapeutic hypothermia provides neuroprotection in hyperammonemia associated encephalopathy. We report results of an ongoing pilot study that assesses if whole body cooling during rescue treatment of neonates with acute hyperammonemia and encephalopathy is feasible and can be conducted safely. Adjunct whole body therapeutic hypothermia was conducted in addition to standard treatment in acutely encephalopathic, hyperammonemic neonates with UCDs and OAs requiring dialysis. Therapeutic hypothermia was initiated using cooling blankets as preparations for dialysis were underway. Similar to standard therapeutic hypothermia treatment for neonatal hypoxic ischemic encephalopathy, patients were maintained at 33.5°C±1°C for 72h, they were then slowly rewarmed by 0.5°C every 3h over 18h. In addition data of age-matched historic controls were collected for comparison. Seven patients were cooled using the pilot study protocol and data of seven historic controls were reviewed. All seven patients survived the initial rescue and cooling treatment, 6 patients were discharged home 2-4weeks after hospitalization, five of them feeding orally. The main complication observed in a majority of patients was hypotension. Adjunct therapeutic hypothermia for neonates with UCDs and OAs receiving standard treatment was

Has the incidence of hypoxic ischaemic encephalopathy in Queensland been reduced with improved education in fetal surveillance monitoring?

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Byford, Sally; Weaver, Edward; Anstey, Chris

2014-08-01

Hypoxic ischaemic encephalopathy (HIE) is secondary to intrapartum asphyxia and the fifth largest cause of death of children under five. Incorrect use and interpretation of intrapartum cardiotocographs has been identified as a contributing factor to the development of HIE. Therefore, RANZCOG introduced the Fetal Surveillance Education Program (FSEP) to improve education and practice of intrapartum care. To investigate the incidence of HIE throughout Queensland between 2003 and 2011 during the introduction and implementation of RANZCOG FSEP. The incidence of HIE admissions at each hospital in Queensland (2003-2011) was collated from Queensland Health Statistics Centre. RANZCOG FSEP provided data regarding course attendees throughout Queensland (2006-2011). Hospitals were grouped into four regions. Statistical analysis was conducted using Stata(TM) (version 12.0) - data appeared to follow a damped harmonic model. The posteducation (2006-2011) HIE rate was significantly lower (P = 0.02) than the pre-education (2003-2005) rate. The final model predicted a stabilisation of HIE occurrence rate at approximately 160 events/100,000 live births by 2012. This rate was stable if the level of education was maintained but rose back to the initial rate of 250 events/100,000 live births if the education participation was discontinued. This study identified a significant reduction in the incidence of HIE--a potentially life-threatening newborn condition--between 2003 and 2011, during and following FSEP implementation. Notwithstanding the inevitable limitations of state-based data collection, these results are encouraging. For such improvements to be sustained, education must reach all staff engaged in intrapartum care and be regularly repeated. © 2014 The Royal Australian and New Zealand College of Obstetricians and Gynaecologists.

Prognostic value of diffusion-weighted imaging summation scores or apparent diffusion coefficient maps in newborns with hypoxic-ischemic encephalopathy

International Nuclear Information System (INIS)

Cavalleri, Francesca; Todeschini, Alessandra; Lugli, Licia; Pugliese, Marisa; Della Casa, Elisa; Gallo, Claudio; Frassoldati, Rossella; Ferrari, Fabrizio; D'Amico, Roberto

2014-01-01

The diagnostic and prognostic assessment of newborn infants with hypoxic-ischemic encephalopathy (HIE) comprises, among other tools, diffusion-weighted imaging (DWI) and apparent diffusion coefficient (ADC) maps. To compare the ability of DWI and ADC maps in newborns with HIE to predict the neurodevelopmental outcome at 2 years of age. Thirty-four term newborns with HIE admitted to the Neonatal Intensive Care Unit of Modena University Hospital from 2004 to 2008 were consecutively enrolled in the study. All newborns received EEG, conventional MRI and DWI within the first week of life. DWI was analyzed by means of summation (S) score and regional ADC measurements. Neurodevelopmental outcome was assessed with a standard 1-4 scale and the Griffiths Mental Developmental Scales - Revised (GMDS-R). When the outcome was evaluated with a standard 1-4 scale, the DWI S scores showed very high area under the curve (AUC) (0.89) whereas regional ADC measurements in specific subregions had relatively modest predictive value. The lentiform nucleus was the region with the highest AUC (0.78). When GMDS-R were considered, DWI S scores were good to excellent predictors for some GMDS-R subscales. The predictive value of ADC measurements was both region- and subscale-specific. In particular, ADC measurements in some regions (basal ganglia, white matter or rolandic cortex) were excellent predictors for specific GMDS-R with AUCs up to 0.93. DWI S scores showed the highest prognostic value for the neurological outcome at 2 years of age. Regional ADC measurements in specific subregions proved to be highly prognostic for specific neurodevelopmental outcomes. (orig.)

Prognostic value of diffusion-weighted imaging summation scores or apparent diffusion coefficient maps in newborns with hypoxic-ischemic encephalopathy

Energy Technology Data Exchange (ETDEWEB)

Cavalleri, Francesca; Todeschini, Alessandra [Azienda Unita Sanitaria Locale di Modena, Neuroradiology Unit, Department of Neuroscience, Nuovo Ospedale Civile S. Agostino Estense di Modena, Modena (Italy); Lugli, Licia; Pugliese, Marisa; Della Casa, Elisa; Gallo, Claudio; Frassoldati, Rossella; Ferrari, Fabrizio [Modena University Hospital, Institute of Pediatrics and Neonatal Medicine and NICU, Modena (Italy); D' Amico, Roberto [University of Modena and Reggio Emilia, Department of Clinical and Diagnostic Medicine and Public Health, Modena (Italy)

2014-09-15

The diagnostic and prognostic assessment of newborn infants with hypoxic-ischemic encephalopathy (HIE) comprises, among other tools, diffusion-weighted imaging (DWI) and apparent diffusion coefficient (ADC) maps. To compare the ability of DWI and ADC maps in newborns with HIE to predict the neurodevelopmental outcome at 2 years of age. Thirty-four term newborns with HIE admitted to the Neonatal Intensive Care Unit of Modena University Hospital from 2004 to 2008 were consecutively enrolled in the study. All newborns received EEG, conventional MRI and DWI within the first week of life. DWI was analyzed by means of summation (S) score and regional ADC measurements. Neurodevelopmental outcome was assessed with a standard 1-4 scale and the Griffiths Mental Developmental Scales - Revised (GMDS-R). When the outcome was evaluated with a standard 1-4 scale, the DWI S scores showed very high area under the curve (AUC) (0.89) whereas regional ADC measurements in specific subregions had relatively modest predictive value. The lentiform nucleus was the region with the highest AUC (0.78). When GMDS-R were considered, DWI S scores were good to excellent predictors for some GMDS-R subscales. The predictive value of ADC measurements was both region- and subscale-specific. In particular, ADC measurements in some regions (basal ganglia, white matter or rolandic cortex) were excellent predictors for specific GMDS-R with AUCs up to 0.93. DWI S scores showed the highest prognostic value for the neurological outcome at 2 years of age. Regional ADC measurements in specific subregions proved to be highly prognostic for specific neurodevelopmental outcomes. (orig.)

Prognostic value of diffusion-weighted imaging summation scores or apparent diffusion coefficient maps in newborns with hypoxic-ischemic encephalopathy.

Science.gov (United States)

Cavalleri, Francesca; Lugli, Licia; Pugliese, Marisa; D'Amico, Roberto; Todeschini, Alessandra; Della Casa, Elisa; Gallo, Claudio; Frassoldati, Rossella; Ferrari, Fabrizio

2014-09-01

The diagnostic and prognostic assessment of newborn infants with hypoxic-ischemic encephalopathy (HIE) comprises, among other tools, diffusion-weighted imaging (DWI) and apparent diffusion coefficient (ADC) maps. To compare the ability of DWI and ADC maps in newborns with HIE to predict the neurodevelopmental outcome at 2 years of age. Thirty-four term newborns with HIE admitted to the Neonatal Intensive Care Unit of Modena University Hospital from 2004 to 2008 were consecutively enrolled in the study. All newborns received EEG, conventional MRI and DWI within the first week of life. DWI was analyzed by means of summation (S) score and regional ADC measurements. Neurodevelopmental outcome was assessed with a standard 1-4 scale and the Griffiths Mental Developmental Scales - Revised (GMDS-R). When the outcome was evaluated with a standard 1-4 scale, the DWI S scores showed very high area under the curve (AUC) (0.89) whereas regional ADC measurements in specific subregions had relatively modest predictive value. The lentiform nucleus was the region with the highest AUC (0.78). When GMDS-R were considered, DWI S scores were good to excellent predictors for some GMDS-R subscales. The predictive value of ADC measurements was both region- and subscale-specific. In particular, ADC measurements in some regions (basal ganglia, white matter or rolandic cortex) were excellent predictors for specific GMDS-R with AUCs up to 0.93. DWI S scores showed the highest prognostic value for the neurological outcome at 2 years of age. Regional ADC measurements in specific subregions proved to be highly prognostic for specific neurodevelopmental outcomes.

Hepatic Encephalopathy

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... Caregiver Support Caregiver Stories Home › What is Hepatic Encephalopathy? Why Your Liver is Important The Connection Between HE and Liver ... Why it’s Important to Treat HE Symptoms of Liver Failure Glossary of terms ... is Hepatic Encephalopathy? Hepatic Encephalopathy, sometimes referred to as portosystemic encephalopathy ...

Hepatic Encephalopathy

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Full Text Available ... Caregiver Support Caregiver Stories Home › What is Hepatic Encephalopathy? Why Your Liver is Important The Connection Between HE and Liver ... Why it’s Important to Treat HE Symptoms of Liver Failure Glossary of terms ... is Hepatic Encephalopathy? Hepatic Encephalopathy, sometimes referred to as portosystemic encephalopathy ...

Chloroquine inhibits autophagy and deteriorates the mitochondrial dysfunction and apoptosis in hypoxic rat neurons.

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Li, Peng; Hao, Lei; Guo, Yan-Yan; Yang, Guang-Lu; Mei, Hua; Li, Xiao-Hua; Zhai, Qiong-Xiang

2018-06-01

Mitochondrial dysfunction (MD) and apoptosis in the neurons are associated with neonatal hypoxic-ischemic (HI) encephalopathy (HIE). The present study was to explore the influence of autophagy on the induction of MD and apoptosis in the neurons in a neonatal HIE rats and in hypoxia-treated neurons in vitro. Ten-day-old HI rat pups were sacrificed for brain pathological examination and immunohistochemical analysis. The induction of autophagy, apoptosis and MD were also determined in the neurons under hypoxia, with or without autophagy inhibitor, chloroquine (CQ) treatment. HI treatment caused atrophy and apoptosis of neurons, with a significantly increased levels of apoptosis- and autophagy-associated proteins, such as cleaved caspase 3 and the B subunit of autophagy-related microtubule-associated protein 1 light chain 3 (LC3-B). in vitro experiments demonstrated that the hypoxia induced autophagy in neurons, as was inhibited by CQ. The hypoxia-induced cytochrome c release, cleaved caspase 3 and cleaved caspase 9 were aggravated by CQ. Moreover, there were higher levels of reactive oxygen species, more mitochondrial superoxide and less mitochondrial membrane potential in the CQ-treated neurons under hypoxia than in the neurons singularly under hypoxia. Apoptosis and autophagy were induced in HI neonatal rat neurons, autophagy inhibition deteriorates the hypoxia-induced neuron MD and apoptosis. It implies a neuroprotection of autophagy in the hypoxic-ischemic encephalopathy. Administration of autophagy inducer agents might be promising in HIE treatment. Copyright © 2018. Published by Elsevier Inc.

Immature rat brain slices exposed to oxygen-glucose deprivation as an in vitro model of neonatal hypoxic-ischemic encephalopathy.

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Fernández-López, David; Martínez-Orgado, José; Casanova, Ignacio; Bonet, Bartolomé; Leza, Juan Carlos; Lorenzo, Pedro; Moro, Maria Angeles; Lizasoain, Ignacio

2005-06-30

To analyze whether exposure to oxygen-glucose deprivation (OGD) of immature rat brain slices might reproduce the main pathophysiologic events leading to neuronal death in neonatal hypoxic-ischemic encephalopathy (NHIE), 500 microm-thick brain slices were obtained from 7-day-old Wistar rats, and incubated in oxygenated physiological solution. In OGD group, oxygen and glucose were removed from the medium for 10-30 min (n = 25); then, slices were re-incubated in normal medium. In control group the medium composition remained unchanged (CG, n = 30). Medium samples were obtained every 30 min for 3 h. To analyze neuronal damage, slices were stained with Nissl and CA1 area of hippocampus and cortex were observed under microscopy. In addition, neuronal death was quantified as LDH released to the medium determined by spectrophotometry. Additionally, medium glutamate (Glu) levels were determined by HPLC and those of TNFalpha by ELISA, whereas inducible nitric oxide synthase expression was determined by Western blot performed on slices homogenate. Optimal OGD time was established in 20 min. After OGD, a significant decrease in the number of neurones in hippocampus and cortex was observed. LDH release was maximal at 30 min, when it was five-fold greater than in CG. Furthermore, medium Glu concentrations were 200 times greater than CG levels at the end of OGD period. A linear relationship between Glu and LDH release was demonstrated. Finally, 3 h after OGD a significant induction of iNOS as well as an increase in TNFalpha release were observed. In conclusion, OGD appears as a feasible and reproducible in vitro model, leading to a neuronal damage, which is physiopathologically similar to that found in NHIE.

Hepatic Encephalopathy

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Full Text Available ... Donate Today Enroll in 123 What is Hepatic Encephalopathy? Hepatic Encephalopathy, sometimes referred to as portosystemic encephalopathy or PSE, is a condition that causes temporary ...

Birth defects in children with newborn encephalopathy

NARCIS (Netherlands)

Felix, JF; Badawi, N; Kurinczuk, JJ; Bower, C; Keogh, JM; Pemberton, PJ

2000-01-01

This study was designed to investigate birth defects found in association with newborn encephalopathy. All possible birth defects were ascertained in a population-based study of 276 term infants with moderate or severe encephalopathy and 564 unmatched term control infants. A strong association

Acute necrotizing encephalopathy in Korean infants and children: imaging findings and diverse clinical outcome

International Nuclear Information System (INIS)

Kim, Ji Hye; Kim, In One; Lim, Myung Kwan

2004-01-01

The purpose of our study was to describe acute necrotizing encephalopathy in Korean infants and children, and we sought to evaluate the prognostic factors. Acute necrotizing encephalopathy was diagnosed in 14 Korean infants and children. We retrospectively analyzed the neuroimaging findings including the follow-up changes. The clinical course of the disease was graded, and we evaluated prognostic factors including age, serum level of the aminotransferase, hemorrhage, and localized atrophy of the brain. This encephalopathy predominantly affected the bilateral thalami (n = 14), pons (n = 12), and midbrain (n = 10) in a symmetrical pattern. Hemorrhage was observed in eight patients (57%). On the follow-up images (n = 12), the brain lesions were reduced in extent for all patients, and generalized atrophy was seen in six patients. Localized tissue loss was observed in five patients and a complete resolution occurred for one patient. All the patients survived and two recovered completely; mild (n = 6) to severe (n = 6) neurological deficits persisted in the remaining 12 patient. The significant prognostic factors identified in this study were the presence of hemorrhage (ρ 0.009) and localized atrophy (ρ = 0.015). Acute necrotizing encephalopathy in Korean patients showed the characteristic patterns of the post-infectious encephalopathy as described in the literature. The high survival rate and the relatively favorable clinical course observed for the present study suggest a more diverse spectrum of disease severity than was previously described. The presence of hemorrhage and localized tissue loss on MR images may suggest a poor prognosis

Hypertensive encephalopathy in a patient with neonatal thyrotoxicosis

NARCIS (Netherlands)

Pijnenburg, MWH; Zweens, MJ; Bink, MTE; Odink, RJ

1999-01-01

Neonatal hyperthyroidism may give rise to serious cardiovascular complications. A girl with severe thyrotoxicosis in whom hypertensive encephalopathy developed is described. Conclusion Neonatal thyrotoxicosis can give rise to hypertension and may lead to hypertensive encephalopathy.

Peptidylarginine deiminases: novel drug targets for prevention of neuronal damage following hypoxic ischemic insult (HI) in neonates.

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Lange, Sigrun; Rocha-Ferreira, Eridan; Thei, Laura; Mawjee, Priyanka; Bennett, Kate; Thompson, Paul R; Subramanian, Venkataraman; Nicholas, Anthony P; Peebles, Donald; Hristova, Mariya; Raivich, Gennadij

2014-08-01

Neonatal hypoxic ischaemic (HI) injury frequently causes neural impairment in surviving infants. Our knowledge of the underlying molecular mechanisms is still limited. Protein deimination is a post-translational modification caused by Ca(+2) -regulated peptidylarginine deiminases (PADs), a group of five isozymes that display tissue-specific expression and different preference for target proteins. Protein deimination results in altered protein conformation and function of target proteins, and is associated with neurodegenerative diseases, gene regulation and autoimmunity. In this study, we used the neonatal HI and HI/infection [lipopolysaccharide (LPS) stimulation] murine models to investigate changes in protein deimination. Brains showed increases in deiminated proteins, cell death, activated microglia and neuronal loss in affected brain areas at 48 h after hypoxic ischaemic insult. Upon treatment with the pan-PAD inhibitor Cl-amidine, a significant reduction was seen in microglial activation, cell death and infarct size compared with control saline or LPS-treated animals. Deimination of histone 3, a target protein of the PAD4 isozyme, was increased in hippocampus and cortex specifically upon LPS stimulation and markedly reduced following Cl-amidine treatment. Here, we demonstrate a novel role for PAD enzymes in neural impairment in neonatal HI Encephalopathy, highlighting their role as promising new candidates for drug-directed intervention in neurotrauma. Hypoxic Ischaemic Insult (HI) results in activation of peptidylarginine deiminases (PADs) because of calcium dysregulation. Target proteins undergo irreversible changes of protein bound arginine to citrulline, resulting in protein misfolding. Infection in synergy with HI causes up-regulation of TNFα, nuclear translocation of PAD4 and change in gene regulation as a result of histone deimination. Pharmacological PAD inhibition significantly reduced HI brain damage. © 2014 The Authors. Journal of Neurochemistry

Rifaximin in the treatment of hepatic encephalopathy

Directory of Open Access Journals (Sweden)

Iadevaia MD

2011-12-01

Full Text Available Maddalena Diana Iadevaia, Anna Del Prete, Claudia Cesaro, Laura Gaeta, Claudio Zulli, Carmelina LoguercioDepartment of Internistica Clinica e Sperimentale, F Magrassi e A Lanzara, Hepatogastroenterology Unit, Second University of Naples, Naples, ItalyAbstract: Hepatic encephalopathy is a challenging complication in patients with advanced liver disease. It can be defined as a neuropsychiatric syndrome caused by portosystemic venous shunting, ranging from minimal to overt hepatic encephalopathy or coma. Its pathophysiology is still unclear, although increased levels of ammonia play a key role. Diagnosis of hepatic encephalopathy is currently based on specific tests evaluating the neuropsychiatric state of patients and their quality of life; the severity of hepatic encephalopathy is measured by the West Haven criteria. Treatment of hepatic encephalopathy consists of pharmacological and corrective measures, as well as nutritional interventions. Rifaximin received approval for the treatment of hepatic encephalopathy in 2010 because of its few side effects and pharmacological benefits. The aim of this work is to review the use and efficacy of rifaximin both in acute and long-term management of hepatic encephalopathy. Treatment of overt hepatic encephalopathy involves management of the acute episode as well as maintenance of remission in those patients who have previously experienced an episode, in order to improve their quality of life. The positive effect of rifaximin in reducing health care costs is also discussed.Keywords: acute hepatic encephalopathy, recurrent hepatic encephalopathy, rifaximin, lactulose, cost, health-related quality of life

Hypoxic stress up-regulates Kir2.1 expression and facilitates cell proliferation in brain capillary endothelial cells

International Nuclear Information System (INIS)

Yamamura, Hideto; Suzuki, Yoshiaki; Yamamura, Hisao; Asai, Kiyofumi; Imaizumi, Yuji

2016-01-01

The blood-brain barrier (BBB) is mainly composed of brain capillary endothelial cells (BCECs), astrocytes and pericytes. Brain ischemia causes hypoxic encephalopathy and damages BBB. However, it remains still unclear how hypoxia affects BCECs. In the present study, t-BBEC117 cells, an immortalized bovine brain endothelial cell line, were cultured under hypoxic conditions at 4–5% oxygen for 72 h. This hypoxic stress caused hyperpolarization of resting membrane potential. Patch-clamp recordings revealed a marked increase in Ba 2+ -sensitive inward rectifier K + current in t-BBEC117 cells after hypoxic culture. Western blot and real-time PCR analyses showed that Kir2.1 expression was significantly up-regulated at protein level but not at mRNA level after the hypoxic culture. Ca 2+ imaging study revealed that the hypoxic stress enhanced store-operated Ca 2+ (SOC) entry, which was significantly reduced in the presence of 100 μM Ba 2+ . On the other hand, the expression of SOC channels such as Orai1, Orai2, and transient receptor potential channels was not affected by hypoxic stress. MTT assay showed that the hypoxic stress significantly enhanced t-BBEC117 cell proliferation, which was inhibited by approximately 60% in the presence of 100 μM Ba 2+ . We first show here that moderate cellular stress by cultivation under hypoxic conditions hyperpolarizes membrane potential via the up-regulation of functional Kir2.1 expression and presumably enhances Ca 2+ entry, resulting in the facilitation of BCEC proliferation. These findings suggest potential roles of Kir2.1 expression in functional changes of BCECs in BBB following ischemia. -- Highlights: •Hypoxic culture of brain endothelial cells (BEC) caused membrane hyperpolarization. •This hyperpolarization was due to the increased expression of Kir2.1 channels. •Hypoxia enhanced store-operated Ca 2+ (SOC) entry via Kir2.1 up-regulation. •Expression levels of putative SOC channels were not affected by hypoxia. �

Serial cytokine alterations and abnormal neuroimaging in newborn infants with encephalopathy.

Science.gov (United States)

O'Hare, Fiona M; Watson, R William G; O'Neill, Amanda; Segurado, Ricardo; Sweetman, Deirdre; Downey, Paul; Mooney, Eoghan; Murphy, John; Donoghue, Veronica; Molloy, Eleanor J

2017-04-01

Inflammatory cytokines may play a role in the final common pathway in the pathogenesis of hypoxic-ischaemic injury in experimental models. We aimed to profile the systemic pro-and anti-inflammatory response over the first week of life in term infants at risk of neonatal encephalopathy. In a tertiary referral university neonatal intensive care unit, serial blood samples were analysed from 41 term infants (requiring resuscitation at birth) in this prospective observational pilot study. Serum levels of 10 pro-and anti-inflammatory cytokines were evaluated including interleukin(IL)-1α, IL-1β, IL-6, IL-8, IL-10, tumour necrosis factor(TNF)-α, interferon (IFN)-γ, vascular endothelial growth factor (VEGF), granulocyte/colony-stimulating factor (G-CSF) and granulocyte macrophage/colony-stimulating factor (GM-CSF). Infants with neonatal encephalopathy and abnormal neuroimaging (n = 15) had significantly elevated granulocyte macrophage/colony-stimulating factor at 0-24 h and interleukin-8, interleukin-6 and interleukin-10 at 24-48 hour. Tumour necrosis factor-α and vascular endothelial growth factor levels were lower at 72-96 hour (p < 0.05). Significantly elevated levels of interleukin-10 were associated with mortality. Serum cytokine changes and innate immune dysregulation in the first week of life may be indicators of outcome in neonatal encephalopathy but require validation in larger studies. ©2017 Foundation Acta Paediatrica. Published by John Wiley & Sons Ltd.

High-Definition transcranial direct current stimulation in early onset epileptic encephalopathy: a case study.

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Meiron, Oded; Gale, Rena; Namestnic, Julia; Bennet-Back, Odeya; David, Jonathan; Gebodh, Nigel; Adair, Devin; Esmaeilpour, Zeinab; Bikson, Marom

2018-01-01

Early onset epileptic encephalopathy is characterized by high daily seizure-frequency, multifocal epileptic discharges, severe psychomotor retardation, and death at infancy. Currently, there are no effective treatments to alleviate seizure frequency and high-voltage epileptic discharges in these catastrophic epilepsy cases. The current study examined the safety and feasibility of High-Definition transcranial direct current stimulation (HD-tDCS) in reducing epileptiform activity in a 30-month-old child suffering from early onset epileptic encephalopathy. HD-tDCS was administered over 10 intervention days spanning two weeks including pre- and post-intervention video-EEG monitoring. There were no serious adverse events or side effects related to the HD-tDCS intervention. Frequency of clinical seizures was not significantly reduced. However, interictal sharp wave amplitudes were significantly lower during the post-intervention period versus baseline. Vital signs and blood biochemistry remained stable throughout the entire study. These exploratory findings support the safety and feasibility of 4 × 1 HD-tDCS in early onset epileptic encephalopathy and provide the first evidence of HD-tDCS effects on paroxysmal EEG features in electroclinical cases under the age of 36 months. Extending HD-tDCS treatment may enhance electrographic findings and clinical effects.

Biallelic Mutations in LIPT2 Cause a Mitochondrial Lipoylation Defect Associated with Severe Neonatal Encephalopathy.

Science.gov (United States)

Habarou, Florence; Hamel, Yamina; Haack, Tobias B; Feichtinger, René G; Lebigot, Elise; Marquardt, Iris; Busiah, Kanetee; Laroche, Cécile; Madrange, Marine; Grisel, Coraline; Pontoizeau, Clément; Eisermann, Monika; Boutron, Audrey; Chrétien, Dominique; Chadefaux-Vekemans, Bernadette; Barouki, Robert; Bole-Feysot, Christine; Nitschke, Patrick; Goudin, Nicolas; Boddaert, Nathalie; Nemazanyy, Ivan; Delahodde, Agnès; Kölker, Stefan; Rodenburg, Richard J; Korenke, G Christoph; Meitinger, Thomas; Strom, Tim M; Prokisch, Holger; Rotig, Agnes; Ottolenghi, Chris; Mayr, Johannes A; de Lonlay, Pascale

2017-08-03

Lipoate serves as a cofactor for the glycine cleavage system (GCS) and four 2-oxoacid dehydrogenases functioning in energy metabolism (α-oxoglutarate dehydrogenase [α-KGDHc] and pyruvate dehydrogenase [PDHc]), or amino acid metabolism (branched-chain oxoacid dehydrogenase, 2-oxoadipate dehydrogenase). Mitochondrial lipoate synthesis involves three enzymatic steps catalyzed sequentially by lipoyl(octanoyl) transferase 2 (LIPT2), lipoic acid synthetase (LIAS), and lipoyltransferase 1 (LIPT1). Mutations in LIAS have been associated with nonketotic hyperglycinemia-like early-onset convulsions and encephalopathy combined with a defect in mitochondrial energy metabolism. LIPT1 deficiency spares GCS deficiency and has been associated with a biochemical signature of combined 2-oxoacid dehydrogenase deficiency leading to early death or Leigh-like encephalopathy. We report on the identification of biallelic LIPT2 mutations in three affected individuals from two families with severe neonatal encephalopathy. Brain MRI showed major cortical atrophy with white matter abnormalities and cysts. Plasma glycine was mildly increased. Affected individuals' fibroblasts showed reduced oxygen consumption rates, PDHc, α-KGDHc activities, leucine catabolic flux, and decreased protein lipoylation. A normalization of lipoylation was observed after expression of wild-type LIPT2, arguing for LIPT2 requirement in intramitochondrial lipoate synthesis. Lipoic acid supplementation did not improve clinical condition nor activities of PDHc, α-KGDHc, or leucine metabolism in fibroblasts and was ineffective in yeast deleted for the orthologous LIP2. Copyright © 2017 American Society of Human Genetics. Published by Elsevier Inc. All rights reserved.

Early-Onset Severe Encephalopathy with Epilepsy: The BRAT1 Gene Should Be Added to the List of Causes

NARCIS (Netherlands)

van de Pol, L.A.; Wolf, N.I.; van Weissenbruch, M.M.; Stam, C.J.; Weiss, M.M.; Waisfisz, Q.; Kevelam, S.H.; Bugiani, M.; van de Kamp, J.M.; Knaap, M.

2015-01-01

A variety of pathologies can underlie early-onset severe encephalopathy with epilepsy. To aid the diagnostic process in such patients we present an overview of causes, including the rapidly expanding list of genes involved. When no explanation is found, whole-exome sequencing (WES) can be used in an

Hyperammonemia Is Associated with Increasing Severity of Both Liver Cirrhosis and Hepatic Encephalopathy

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Abidullah Khan

2016-01-01

Full Text Available Background. Hyperammonemia resulting from chronic liver disease (CLD can potentially challenge and damage any organ system of the body, particularly the brain. However, there is still some controversy regarding the diagnostic or prognostic values of serum ammonia in patients with over hepatic encephalopathy, especially in the setting of acute-on-chronic or chronic liver failure. Moreover, the association of serum ammonia with worsening Child-Pugh grade of liver cirrhosis has not been studied. Objective. This study was conducted to solve the controversy regarding the association between hyperammonemia and cirrhosis, especially hepatic encephalopathy in chronically failed liver. Material and Methods. In this study, 171 cirrhotic patients had their serum ammonia measured and analyzed by SPSS version 16. Chi-squared test and one-way ANOVA were applied. Results. The study had 110 male and 61 female participants. The mean age of all the participants in years was 42.33±7.60. The mean duration (years of CLD was 10.15±3.53 while the mean Child-Pugh (CP score was 8.84±3.30. Chronic viral hepatitis alone was responsible for 71.3% of the cases. Moreover, 86.5% of participants had hepatic encephalopathy (HE. The frequency of hyperammonemia was 67.3%, more frequent in males (N=81, z-score = 2.4, and P<0.05 than in females (N=34, z-score = 2.4, and P<0.05, and had a statistically significant relationship with increasing CP grade of cirrhosis (χ2(2 = 27.46, P<0.001, Phi = 0.40, and P<0.001. Furthermore, serum ammonia level was higher in patients with hepatic encephalopathy than in those without it; P<0.001. Conclusion. Hyperammonemia is associated with both increasing Child-Pugh grade of liver cirrhosis and hepatic encephalopathy.

Protective Effects of N-Acetyl-L-Cysteine in Human Oligodendrocyte Progenitor Cells and Restoration of Motor Function in Neonatal Rats with Hypoxic-Ischemic Encephalopathy

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Dongsun Park

2015-01-01

Full Text Available Objective. Since oligodendrocyte progenitor cells (OPCs are the target cells of neonatal hypoxic-ischemic encephalopathy (HIE, the present study was aimed at investigating the protective effects of N-acetyl-L-cysteine (NAC, a well-known antioxidant and precursor of glutathione, in OPCs as well as in neonatal rats. Methods. In in vitro study, protective effects of NAC on KCN cytotoxicity in F3.Olig2 OPCs were investigated via MTT assay and apoptotic signal analysis. In in vivo study, NAC was administered to rats with HIE induced by hypoxia-ischemia surgery at postnatal day 7, and their motor functions and white matter demyelination were analyzed. Results. NAC decreased KCN cytotoxicity in F3.Olig2 cells and especially suppressed apoptosis by regulating Bcl2 and p-ERK. Administration of NAC recovered motor functions such as the using ratio of forelimb contralateral to the injured brain, locomotor activity, and rotarod performance of neonatal HIE animals. It was also confirmed that NAC attenuated demyelination in the corpus callosum, a white matter region vulnerable to HIE. Conclusion. The results indicate that NAC exerts neuroprotective effects in vitro and in vivo by preserving OPCs, via regulation of antiapoptotic signaling, and that F3.Olig2 human OPCs could be a good tool for screening of candidates for demyelinating diseases.

COMPUTED TOMOGRAPHIC EVALUATION OF POSTERIOR REVERSIBLE ENCEPHALOPATHY SYNDROME

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Vishwaprem Raj

2016-04-01

Full Text Available BACKGROUND AND PURPOSE Posterior Reversible Encephalopathy Syndrome (PRES is a neurotoxic state that occurs secondary to the inability of posterior circulation to autoregulate. The clinical spectrum and the underlying pathophysiology are still poorly defined. No conclusive evidence has been put forward regarding the relationship between clinical conditions and specific imaging findings of severity or location of oedema. PURPOSE To assess the role of computed tomography in evaluation of Posterior Reversible Encephalopathy Syndrome. MATERIALS AND METHODS 55 patients referred to the Department of Radio-Diagnosis, with a history of neurological abnormalities, including altered mental function, visual loss, stupor with a predisposing history favouring PRES and followed up for a period of 10 – 30 days. RESULTS 21 patients (38.2% were females. 32 patients (58.1% were in the age group between 21 to 30 years. Predisposing condition; 16 (29.1% presented with pre-eclampsia, 12 (21.8% with post-partum status in altered sensorium, 9 (16.4% with seizures, 7 (12.7% with hypertension, 6 (10.9% with visual disturbances, 4 (7.3% with eclampsia and 1 (1.8% with uraemia. 20 cases (36.4% showed findings suggestive of posterior reversible encephalopathy syndrome on initial computed tomography examination. 35 cases showed no initial radiological evidence suggestive of posterior reversible encephalopathy syndrome. Of the 20 cases which showed computed tomographic evidence of posterior reversible encephalopathy syndrome, recovery was noted in 5 cases (9.1%. Persistence of findings detected on first CT was noted in 13 patients (23.6%. Regional predominance of the lesions was as follows. Frontal lobe (39%, Parietal lobe (32%, Temporal lobe (15% and occipital lobe (15%. CONCLUSION Varied clinical manifestations are associated with anatomical findings recognisable by neuro-imaging as PRES. Prompt imaging is necessary for the recognition of the condition and appropriate

CT and MRI findings of cyclosporine-related encephalopathy and hypertensive encephalopathy

International Nuclear Information System (INIS)

Yamamoto, Akira; Hayakawa, Katsumi; Houjyou, Makoto

2002-01-01

We present the MRI and CT findings of one child with cyclosporine-related encephalopathy, and one child with hypertensive encephalopathy following cyclosporine-related encephalopathy. The imaging findings were shown well on T2-weighted and fluid-attenuated inversion recovery (FLAIR) MR images. Cyclosporine-related encephalopathy was distributed predominantly in the posterior white matter. Hypertensive encephalopathy showed similar changes of CT attenuation, but with wider distribution. These two disorders seem to have the same pathogenesis. (orig.)

The ketogenic diet is effective for refractory epilepsy associated with acquired structural epileptic encephalopathy.

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Villaluz, Mel Michel; Lomax, Lysa Boissé; Jadhav, Trupti; Cross, J Helen; Scheffer, Ingrid E

2018-07-01

Ketogenic diet therapies have proven efficacy for refractory epilepsy. There are many reports of their use in the genetic developmental and epileptic encephalopathies; however, little attention has been paid as to whether the diet is also effective in individuals with an acquired structural aetiology. We observed remarkable efficacy of the diet in two patients with hypoxic-ischaemic encephalopathy. We then analysed our cases with refractory structural epilepsies of acquired origin to characterize their response to the ketogenic diet. The classical ketogenic diet was implemented with dietary ratios of 3:1 to 4.4:1. Seizure frequency at 1 month, 3 months, 6 months, 1 year, and 2 years was ascertained. A responder was defined as greater than 50% seizure reduction compared to baseline. Seven of the nine patients were responders at 3 months. Somewhat surprisingly we found that the ketogenic diet was effective in patients with a developmental and epileptic encephalopathy due to an acquired structural aetiology. This cohort may not be routinely considered for the ketogenic diet because of their structural and acquired, rather than genetic, basis. The ketogenic diet should be considered early in the management of patients with acquired structural encephalopathies as it can improve seizure control with the potential to improve developmental outcome. The ketogenic diet was effective in children with epilepsy associated with an acquired structural aetiology. © 2018 Mac Keith Press.

Implications of post-gadolinium MRI results in 13 cases with posterior reversible encephalopathy syndrome

International Nuclear Information System (INIS)

Ugurel, Mehmet Sahin; Hayakawa, Minako

2005-01-01

Background: There is a relative lack of definitive information about the contrast-enhancement characteristics of lesions in posterior reversible encephalopathy syndrome (PRES). Objective: Evaluation of contrast-enhanced MRI findings in PRES with a special emphasis on pathophysiology of post-gadolinium behavior of these lesions. Materials and methods: Contrast-enhanced 1.5 T MRI findings and relevant clinical data of the patients were retrospectively reviewed on 13 cases (six males, seven females; age range: 22-78; mean age 47). Although fluid attenuated inversion recovery (FLAIR) and diffusion-weighted MR images were considered for identification of the entity, primarily post-contrast T1-weighted MR images were searched for traces of enhancement in the lesions. Results: No definitely enhancing lesion was identified in the MR images obtained in 6-48 h after onset of symptoms (mostly headaches, seizures and cortical visual field deficits) in this series. Severity of disease indicated by small hemorrhages, confluence of lesions or progression to cytotoxic edema did not seem to alter this result. Typical lesion characteristics were consistent with vasogenic edema on FLAIR and diffusion MR images. Acute elevation of blood pressure on chronic hypertensive background was responsible in four, eclampsia in three, uremia with blood pressure fluctuations in three, and cyclosporine-toxicity in three cases. Conclusion: Although occasional enhancing brain lesions have been reported in the literature on PRES, contrast-enhancement of lesions may be a factor of scan timing and underlying etiology. Prospective studies with larger series on PRES are required for better evaluation of contrast-enhancement in MRI with respect to scan timing, which in turn may help understand its pathophysiology better

Current pathogenetic aspects of hepatic encephalopathy and noncirrhotic hyperammonemic encephalopathy

OpenAIRE

Cichoż-Lach, Halina; Michalak, Agata

2013-01-01

Hepatic encephalopathy is a medical phenomenon that is described as a neuropsychiatric manifestation of chronic or acute liver disease that is characterized by psychomotor, intellectual and cognitive abnormalities with emotional/affective and behavioral disturbances. This article focuses on the underlying mechanisms of the condition and the differences between hepatic encephalopathy and noncirrhotic hyperammonemic encephalopathy. Hepatic encephalopathy is a serious condition that can cause ne...

Evaluation and Management of Hepatic Encephalopathy: Current Status and Future Directions

OpenAIRE

Suraweera, Duminda; Sundaram, Vinay; Saab, Sammy

2016-01-01

Hepatic encephalopathy is a spectrum of neurocognitive manifestations often seen in patients with liver injury or rarely in patients with portosystemic shunting without liver injury. It can be divided into minimal (covert) hepatic encephalopathy and overt hepatic encephalopathy, depending on the severity. Patients with hepatic encephalopathy have compromised clinical outcomes, decreased quality of life, and increased healthcare utilization, often resulting in a heavy financial and personal bu...

STXBP1 encephalopathy

DEFF Research Database (Denmark)

Stamberger, Hannah; Nikanorova, Marina; Willemsen, Marjolein H

2016-01-01

OBJECTIVE: To give a comprehensive overview of the phenotypic and genetic spectrum of STXBP1 encephalopathy (STXBP1-E) by systematically reviewing newly diagnosed and previously reported patients. METHODS: We recruited newly diagnosed patients with STXBP1 mutations through an international networ......, and the degree of ID. Accordingly, we hypothesize that seizure severity and ID present 2 independent dimensions of the STXBP1-E phenotype. STXBP1-E may be conceptualized as a complex neurodevelopmental disorder rather than a primary epileptic encephalopathy....

Hashimoto's encephalopathy: Report of three cases

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Jan-Shun Chang

2014-11-01

Full Text Available Both severe thyrotoxicosis and hypothyroidism may affect brain function and cause a change in consciousness, as seen with a thyroid storm or myxedema coma. However, encephalopathy may also develop in patients with autoimmune thyroid diseases independent of actual thyroid function level, and this is known as Hashimoto's encephalopathy. Although most patients are found to have Hashimoto's thyroiditis, less frequently they have Graves' disease. Clinical manifestations include epilepsy, disturbance of consciousness, cognitive impairment, memory loss, myoclonus, hallucinations, stroke-like episodes, tremor, involuntary movements, language impairment, and gait impairment. Hashimoto's encephalopathy is a relatively rare disease. As a good response can be obtained with corticosteroid therapy, early diagnosis and treatment is very beneficial for patients. Here we report three patients with Hashimoto's encephalopathy with typical manifestations of hallucinations that were associated with hypothyroidism, hyperthyroidism, and euthyroid status, respectively. They all showed a dramatic response to methylprednisolone pulse therapy.

A Rare Case of Reversible Encephalopathy Syndrome Accompanying Late Postpartum Eclampsia or Hypertensive Encephalopathy-A Clinical Dilemma

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Shakuntala PN

2012-04-01

Full Text Available Posterior Reversible Encephalopathy Syndrome (PRES refers to a clinic-radiologic diagnosis. Clinically it is characterized by non specific symptoms such as headache, confusion, visual disturbances and seizures. The radiological findings in PRES are thought to be due to vasogenic oedema, predominantly in the posterior cerebral hemispheres, and are reversible with appropriate management. We report a case of reversible encephalopathy diagnosed by MRI scan occurring in atypical areas like the caudate and lentiform nuclei of the brain following an uneventful lower segment caesarean section in a normotensive patient, who was successfully treated with antihypertensives, anticonvulsants and supportive treatment. The differential diagnosis of convulsions in the post-partum period is discussed.

New Wavelet Neurovascular Bundle for Bedside Evaluation of Cerebral Autoregulation and Neurovascular Coupling in Newborns with Hypoxic-Ischemic Encephalopathy.

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Chalak, Lina F; Zhang, Rong

2017-01-01

Neonatal encephalopathy (NE) resulting from birth asphyxia constitutes a major global public health burden for millions of infants every year, and despite therapeutic hypothermia, half of these neonates have poor neurological outcomes. As new neuroprotective interventions are being studied in clinical trials, there is a critical need to establish physiological surrogate markers of therapeutic efficacy, to guide patient selection and/or to modify the therapeutic intervention. The challenge in the field of neonatal brain injury has been the difficulty of clinically discerning NE severity within the short therapeutic window after birth or of analyzing the dynamic aspects of the cerebral circulation in sick NE newborns. To address this roadblock, we have recently developed a new "wavelet neurovascular bundle" analytical system that can measure cerebral autoregulation (CA) and neurovascular coupling (NVC) at multiple time scales under dynamic, nonstationary clinical conditions. This wavelet analysis may allow noninvasive quantification at the bedside of (1) CA (combining metrics of blood pressure and cerebral near-infrared spectroscopy, NIRS) and (2) NVC (combining metrics obtained from NIRS and EEG) in newborns with encephalopathy without mathematical assumptions of linear and stationary systems. In this concept paper, we present case examples of NE using the proposed physiological wavelet metrics of CA and NVC. The new approach, once validated in large NE studies, has the potential to optimize the selection of candidates for therapeutic decision-making, and the prediction of neurocognitive outcomes. © 2017 S. Karger AG, Basel.

Encephalopathy and liver transplantation.

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Chavarria, Laia; Cordoba, Juan

2013-06-01

Liver transplantation (LT) candidates experience frequently episodic or persistent hepatic encephalopathy. In addition, these patients can exhibit neurological comorbidities that contribute to cognitive impairment in the pre-transplant period. Assessment of the respective contribution of hepatic encephalopathy or comorbidities in the cognitive manifestations is critical to estimate the neurological benefits of restoring liver function. Magnetic resonance imaging and spectroscopy are useful to assess the impact of liver failure or comorbidities. This assessment is critical to decide liver transplant in difficult cases. In the early postoperative period, LT is commonly complicated by a confusional syndrome. The possible role of persisting hepatic encephalopathy in its development has not been clearly established. The origin is usually considered multifactorial and relates to complications following LT, such as infections, rejection, primary liver dysfunction, immunosuppressors, etc.… The diagnosis and treatment is based in the recognition of comorbidities and optimal care of metabolic disturbances. Several studies have demonstrated recovery of cognitive function after LT in patients that have exhibited hepatic encephalopathy. However, some deficits may persist specifically among patients with persistent HE. Other factors present before LT that contribute to a worse neuropsychological outcome after LT are diabetes mellitus and alcohol consumption. Long-term after LT, cognitive function may worsen in relation to vascular risk factors.

Hypoxic stress up-regulates Kir2.1 expression and facilitates cell proliferation in brain capillary endothelial cells

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Yamamura, Hideto; Suzuki, Yoshiaki; Yamamura, Hisao [Department of Molecular & Cellular Pharmacology, Graduate School of Pharmaceutical Sciences, Nagoya City University, Nagoya (Japan); Asai, Kiyofumi [Department of Molecular Neurobiology, Graduate School of Medical Sciences, Nagoya City University, Nagoya (Japan); Imaizumi, Yuji, E-mail: yimaizum@phar.nagoya-cu.ac.jp [Department of Molecular & Cellular Pharmacology, Graduate School of Pharmaceutical Sciences, Nagoya City University, Nagoya (Japan)

2016-08-05

The blood-brain barrier (BBB) is mainly composed of brain capillary endothelial cells (BCECs), astrocytes and pericytes. Brain ischemia causes hypoxic encephalopathy and damages BBB. However, it remains still unclear how hypoxia affects BCECs. In the present study, t-BBEC117 cells, an immortalized bovine brain endothelial cell line, were cultured under hypoxic conditions at 4–5% oxygen for 72 h. This hypoxic stress caused hyperpolarization of resting membrane potential. Patch-clamp recordings revealed a marked increase in Ba{sup 2+}-sensitive inward rectifier K{sup +} current in t-BBEC117 cells after hypoxic culture. Western blot and real-time PCR analyses showed that Kir2.1 expression was significantly up-regulated at protein level but not at mRNA level after the hypoxic culture. Ca{sup 2+} imaging study revealed that the hypoxic stress enhanced store-operated Ca{sup 2+} (SOC) entry, which was significantly reduced in the presence of 100 μM Ba{sup 2+}. On the other hand, the expression of SOC channels such as Orai1, Orai2, and transient receptor potential channels was not affected by hypoxic stress. MTT assay showed that the hypoxic stress significantly enhanced t-BBEC117 cell proliferation, which was inhibited by approximately 60% in the presence of 100 μM Ba{sup 2+}. We first show here that moderate cellular stress by cultivation under hypoxic conditions hyperpolarizes membrane potential via the up-regulation of functional Kir2.1 expression and presumably enhances Ca{sup 2+} entry, resulting in the facilitation of BCEC proliferation. These findings suggest potential roles of Kir2.1 expression in functional changes of BCECs in BBB following ischemia. -- Highlights: •Hypoxic culture of brain endothelial cells (BEC) caused membrane hyperpolarization. •This hyperpolarization was due to the increased expression of Kir2.1 channels. •Hypoxia enhanced store-operated Ca{sup 2+} (SOC) entry via Kir2.1 up-regulation. •Expression levels of putative SOC

Oxygen saturation index and severity of hypoxic respiratory failure.

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Rawat, Munmun; Chandrasekharan, Praveen K; Williams, Ashley; Gugino, Sylvia; Koenigsknecht, Carmon; Swartz, Daniel; Ma, Chang Xing; Mathew, Bobby; Nair, Jayasree; Lakshminrusimha, Satyan

2015-01-01

The oxygenation index (OI = mean airway pressure, MAP × FiO2 × 100 : PaO2) is used to assess the severity of hypoxic respiratory failure (HRF) and persistent pulmonary hypertension of the newborn (PPHN). An indwelling arterial line or arterial punctures are necessary to obtain PaO2 for the calculation of OI. Oxygenation can be continuously and noninvasively assessed using pulse oximetry. The use of the oxygen saturation index (OSI = MAP × FiO2 × 100 : SpO2) can be an alternate method of assessing the severity of HRF. To evaluate the correlation between OSI and OI in the following: (1) neonates with HRF and (2) a lamb model of meconium aspiration syndrome. Human neonates: a retrospective chart review of 74 ventilated late preterm/term neonates with indwelling arterial access and SpO2 values in the first 24 h of life was conducted. OSI and OI were calculated and correlated. Lamb model: arterial blood gases were drawn and preductal SpO2 was documented in 40 term newborn lambs with asphyxia and meconium aspiration. OI and OSI were calculated and correlated with pulmonary vascular resistance (PVR). Mean values of OSI and OI showed a correlation coefficient of 0.952 in neonates (mean value of 308 observations in 74 neonates) and 0.948 in lambs (mean value of 743 observations in 40 lambs). In lambs, with increasing PVR, there was a decrease in OI and OSI. OSI correlates significantly with OI in infants with HRF. This noninvasive measure may be used to assess the severity of HRF and PPHN in neonates without arterial access. © 2015 S. Karger AG, Basel

Neuroprotective effects of Ellagic acid on Neonatal Hypoxic Brain ...

African Journals Online (AJOL)

Purpose: To investigate if ellagic acid exerts neuroprotective effects in hypoxic ischemic (HI) brain injury by inhibiting apoptosis and inflammatory responses. Methods: Separate groups of rat pups from post-natal day 4 (D4) were administered with ellagic acid (10, 20 or 40 mg/kg body weight) orally till post- natal day 10 ...

Basal ganglia perfusion using dynamic color Doppler sonography in infants with hypoxic ischemic encephalopathy receiving therapeutic hypothermia: a pilot study.

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Faingold, Ricardo; Cassia, Guilherme; Morneault, Linda; Saint-Martin, Christine; Sant'Anna, Guilherme

2016-10-01

The objective of this study was to evaluate the cerebral perfusion of the basal ganglia in infants with hypoxic-ischemic encephalopathy (HIE) receiving hypothermia using dynamic color Doppler sonography (CDS) and investigate for any correlation between these measurements and survival. Head ultrasound (HUS) was performed with a 9S4 MHz sector transducer in HIE infants submitted to hypothermia as part of their routine care. Measurements of cerebral perfusion intensity (CPI) with an 11LW4 MHz linear array transducer were performed to obtain static images and DICOM color Doppler videos of the blood flow in the basal ganglia area. Clinical and radiological data were evaluated retrospectively. The video images were analyzed by two radiologists using dedicated software, which allows automatic quantification of color Doppler data from a region of interest (ROI) by dynamically assessing color pixels and flow velocity during the heart cycle. CPI is expressed in cm/sec and is calculated by multiplying the mean velocity of all pixels divided by the area of the ROI. Three videos of 3 seconds each were obtained of the ROI, in the coronal plane, and used to calculate the CPI. Data are presented as mean ± SEM or median (quartiles). A total of 28 infants were included in this study: 16 male, 12 female. HUS was performed within the first 48 hours of therapeutic hypothermia treatment. CPI values were significantly higher in the seven non-survivors when compared to survivors (0.226±0.221 vs . 0.111±0.082 cm/sec; P=0.02). Increased perfusion intensity of the basal ganglia area within the first 48 of therapeutic hypothermia treatment was associated with poor outcome in neonates with HIE.

Impact of Perinatal Systemic Hypoxic–Ischemic Injury on the Brain of Male Offspring Rats: An Improved Model of Neonatal Hypoxic–Ischemic Encephalopathy in Early Preterm Newborns

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Xu, Hongwu; Wu, Weizhao; Lai, Xiulan; Ho, Guyu; Ma, Lian; Chen, Yunbin

2013-01-01

In this study, we attempted to design a model using Sprague-Dawley rats to better reproduce perinatal systemic hypoxic-ischemic encephalopathy (HIE) in early preterm newborns. On day 21 of gestation, the uterus of pregnant rats were exposed and the blood supply to the fetuses of neonatal HIE groups were thoroughly abscised by hemostatic clamp for 5, 10 or 15 min. Thereafter, fetuses were moved from the uterus and manually stimulated to initiate breathing in an incubator at 37 °C for 1 hr in air. We showed that survival rates of offspring rats were decreased with longer hypoxic time. TUNEL staining showed that apoptotic cells were significant increased in the brains of offspring rats from the 10 min and 15 min HIE groups as compared to the offspring rats in the control group at postnatal day (PND) 1, but there was no statistical difference between the offspring rats in the 5 min HIE and control groups. The perinatal hypoxic treatment resulted in decreased neurons and increased cleaved caspase-3 protein levels in the offspring rats from all HIE groups at PND 1. Platform crossing times and the percentage of the time spent in the target quadrant of Morris Water Maze test were significantly reduced in the offspring rats of all HIE groups at PND 30, which were associated with decreased brain-derived neurotrophic factor levels and neuronal cells in the hippocampus of offspring rats at PND 35. These data demonstrated that perinatal ischemic injury led to the death of neuronal cells and long-lasting impairment of memory. This model reproduced hypoxic ischemic encephalopathy in early preterm newborns and may be appropriate for investigating therapeutic interventions. PMID:24324800

Wernicke encephalopathy in a patient with liver failure

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Zhao, Pan; Zhao, Yanling; Wei, Zhenman; Chen, Jing; Yan, Lilong

2016-01-01

Abstract Early recognition and diagnosis of Wernicke encephalopathy is pivotal for the prognosis of this medical emergency, especially in patients with liver failure which predisposes individuals to develop hepatic encephalopathy. For these patients, distinguishing between hepatic encephalopathy and Wernicke encephalopathy is a challenge in real-world clinical practice. A male patient with 21-year medical history of liver cirrhosis presented diarrhea and ascites. One month before this visit, he was noted to have poor appetite and progressive fatigue. After admission, although several major symptoms, including diarrhea, ascites, hyponatremia, and hypoproteinemia, were greatly improved through appropriate treatments, his laboratory indicators were not changed much. His appetite was not reversed at discharge. On the 5th day after discharge, the patient suddenly became reluctant to speak and did not remember the recent happenings. Simultaneously, unsteady gait and strabismus occurred. On the basis of clinical manifestations and brain magnetic resonance imaging scan results, the patient was diagnosed as Wernicke encephalopathy and these relative symptoms were resolved after intravenous vitamin B1. To our knowledge, this is the second case report of Wernicke encephalopathy developing in a critically ill cirrhotic patient without hepatocellular carcinoma or operative intervention. Wernicke encephalopathy may be underdiagnosed in these patients and this case raises physicians’ awareness of its possible onset. PMID:27399058

[The contribution of the clinical examination, electroencephalogram, and brain MRI in assessing the prognosis in term newborns with neonatal encephalopathy. A cohort of 30 newborns before the introduction of treatment with hypothermia].

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Jadas, V; Brasseur-Daudruy, M; Chollat, C; Pellerin, L; Devaux, A M; Marret, S

2014-02-01

Perinatal asphyxia complicated by hypoxic ischemic brain injury remains a source of neurological lesions. A major aim of neonatologists is to evaluate the severity of neonatal encephalopathy (NE) and to evaluate prognosis. The purpose of this study was to determine the contribution of brain MRI compared to electroencephalogram (EEG) and clinical data in assessing patients' prognosis. Thirty newborns from the pediatric resuscitation unit at Rouen university hospital were enrolled in a retrospective study between January 2006 and December 2008, prior to introduction of hypothermia treatment. All 30 newborns had at least two anamnestic criteria of perinatal asphyxia, one brain MRI in the first 5 days of life and another after 7 days of life as well as an early EEG in the first 2 days of life. Then, the infants were seen in consultation to assess neurodevelopment. This study showed a relation between NE stage and prognosis. During stage 1, prognosis was good, whereas stage 3 was associated with poor neurodevelopment outcome. Normal clinical examination before the 8th day of life was a good prognostic factor in this study. There was a relationship between severity of EEG after the 5th day of life and poor outcome. During stage 2, EEG patterns varied in severity, and brain MRI provided a better prognosis. Lesions of the basal ganglia and a decreased or absent signal of the posterior limb of the internal capsule were poor prognostic factors during brain MRI. These lesions were underestimated during standard MRI in the first days of life but were visible with diffusion sequences. Cognitive impairment affected 40% of surviving children, justifying extended pediatric follow-up. This study confirms the usefulness of brain MRI as a diagnostic tool in hypoxic ischemic encephalopathy in association with clinical data and EEG tracings. Copyright © 2013 Elsevier Masson SAS. All rights reserved.

Postnatal morphology of hematoencephalic barrier in hypoxic lesion

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E. V. Kikhtenko

2012-12-01

Full Text Available In infants with perinatal hypoxic lesion of the central nervous system swelling and death of the endothelium, thickening of the capillary basement membranes, karyorrhexis and plasmorrhexis of astrocytes are observed. The severity and degree of pathological changes depends on the time of hypoxic exposure (antenatal or intrapartum period and the term of postnatal life.

Evaluation and Management of Hepatic Encephalopathy: Current Status and Future Directions

Science.gov (United States)

Suraweera, Duminda; Sundaram, Vinay; Saab, Sammy

2016-01-01

Hepatic encephalopathy is a spectrum of neurocognitive manifestations often seen in patients with liver injury or rarely in patients with portosystemic shunting without liver injury. It can be divided into minimal (covert) hepatic encephalopathy and overt hepatic encephalopathy, depending on the severity. Patients with hepatic encephalopathy have compromised clinical outcomes, decreased quality of life, and increased healthcare utilization, often resulting in a heavy financial and personal burden on caregivers. The diagnosis remains largely clinical, with the exclusion of possible other causes for the altered mental status. Current treatment strategies include nonabsorbable disaccharides and antibiotics. This review will focus on the diagnosis, management and clinical impact of hepatic encephalopathy. PMID:27377741

SUMO Signaling by Hypoxic Inactivation of SUMO-Specific Isopeptidases

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Kathrin Kunz

2016-09-01

Full Text Available Post-translational modification of proteins with ubiquitin-like SUMO modifiers is a tightly regulated and highly dynamic process. The SENP family of SUMO-specific isopeptidases comprises six cysteine proteases. They are instrumental in counterbalancing SUMO conjugation, but their regulation is not well understood. We demonstrate that in hypoxic cell extracts, the catalytic activity of SENP family members, in particular SENP1 and SENP3, is inhibited in a rapid and fully reversible process. Comparative mass spectrometry from normoxic and hypoxic cells defines a subset of hypoxia-induced SUMO1 targets, including SUMO ligases RanBP2 and PIAS2, glucose transporter 1, and transcriptional regulators. Among the most strongly induced targets, we identified the transcriptional co-repressor BHLHE40, which controls hypoxic gene expression programs. We provide evidence that SUMOylation of BHLHE40 is reversed by SENP1 and contributes to transcriptional repression of the metabolic master regulator gene PGC-1α. We propose a pathway that connects oxygen-controlled SENP activity to hypoxic reprogramming of metabolism.

A new infectious encephalopathy syndrome, clinically mild encephalopathy associated with excitotoxicity (MEEX).

Science.gov (United States)

Hirai, Nozomi; Yoshimaru, Daisuke; Moriyama, Yoko; Yasukawa, Kumi; Takanashi, Jun-Ichi

2017-09-15

Acute infectious encephalopathy is often observed in children in East Asia including Japan. More than 40% of the patients remain unclassified into specific syndromes. To investigate the underlying pathomechanisms in those with unclassified encephalopathy, we evaluated brain metabolism by MR spectroscopy. Among seven patients with acute encephalopathy admitted to our hospital from June 2016 to May 2017, three were classified into acute encephalopathy with biphasic seizures and late reduced diffusion (AESD). The other four showed consciousness disturbance lasting more than three days with no parenchymal lesion visible on MRI, which led to a diagnosis of unclassified encephalopathy. MR spectroscopy in these four patients, however, revealed an increase of glutamine with a normal N-acetyl aspartate level on days 5 to 8, which had normalized by follow-up studies on days 11 to 16. The four patients clinically recovered completely. Among 27 patients with encephalopathy, including the present seven patients, admitted to our hospital from January 2015 to March 2017, seven (26%) were classified into this type, which we propose is a new encephalopathy syndrome, clinically mild encephalopathy associated with excitotoxicity (MEEX). MEEX is the second most common subtype, following AESD (30%). This study suggests that excitotoxicity may be a common underlying pathomechanism of acute infectious encephalopathy, and prompt astrocytic neuroprotection from excitotoxicity may prevent progression of MEEX into AESD. Copyright © 2017 Elsevier B.V. All rights reserved.

Semi-quantitative Assessment of Brain Maturation by Conventional Magnetic Resonance Imaging in Neonates with Clinically Mild Hypoxic-ischemic Encephalopathy

Science.gov (United States)

Gao, Jie; Sun, Qin-Li; Zhang, Yu-Miao; Li, Yan-Yan; Li, Huan; Hou, Xin; Yu, Bo-Lang; Zhou, Xi-Hui; Yang, Jian

2015-01-01

Background: Mild hypoxic-ischemic encephalopathy (HIE) injury is becoming the major type in neonatal brain diseases. The aim of this study was to assess brain maturation in mild HIE neonatal brains using total maturation score (TMS) based on conventional magnetic resonance imaging (MRI). Methods: Totally, 45 neonates with clinically mild HIE and 45 matched control neonates were enrolled. Gestated age, birth weight, age after birth and postmenstrual age at magnetic resonance (MR) scan were homogenous in the two groups. According to MR findings, mild HIE neonates were divided into three subgroups: Pattern I, neonates with normal MR appearance; Pattern II, preterm neonates with abnormal MR appearance; Pattern III, full-term neonates with abnormal MR appearance. TMS and its parameters, progressive myelination (M), cortical infolding (C), involution of germinal matrix tissue (G), and glial cell migration bands (B), were employed to assess brain maturation and compare difference between HIE and control groups. Results: The mean of TMS was significantly lower in mild HIE group than it in the control group (mean ± standard deviation [SD] 11.62 ± 1.53 vs. 12.36 ± 1.26, P < 0.001). In four parameters of TMS scores, the M and C scores were significantly lower in mild HIE group. Of the three patterns of mild HIE, Pattern I (10 cases) showed no significant difference of TMS compared with control neonates, while Pattern II (22 cases), III (13 cases) all had significantly decreased TMS than control neonates (mean ± SD 10.56 ± 0.93 vs. 11.48 ± 0.55, P < 0.05; 12.59 ± 1.28 vs. 13.25 ± 1.29, P < 0.05). It was M, C, and GM scores that significantly decreased in Pattern II, while for Pattern III, only C score significantly decreased. Conclusions: The TMS system, based on conventional MRI, is an effective method to detect delayed brain maturation in clinically mild HIE. The conventional MRI can reveal the different retardations in subtle structures and development processes

GRIN2B encephalopathy

DEFF Research Database (Denmark)

Platzer, Konrad; Yuan, Hongjie; Schuetz, Hannah

2017-01-01

BACKGROUND: We aimed for a comprehensive delineation of genetic, functional and phenotypic aspects of GRIN2B encephalopathy and explored potential prospects of personalised medicine. METHODS: Data of 48 individuals with de novo GRIN2B variants were collected from several diagnostic and research c...

Application of altitude/hypoxic training by elite athletes.

Science.gov (United States)

Wilber, Randall L

2007-09-01

At the Olympic level, differences in performance are typically less than 0.5%. This helps explain why many contemporary elite endurance athletes in summer and winter sport incorporate some form of altitude/hypoxic training within their year-round training plan, believing that it will provide the "competitive edge" to succeed at the Olympic level. The purpose of this paper is to describe the practical application of altitude/hypoxic training as used by elite athletes. Within the general framework of the paper, both anecdotal and scientific evidence will be presented relative to the efficacy of several contemporary altitude/hypoxic training models and devices currently used by Olympic-level athletes for the purpose of legally enhancing performance. These include the three primary altitude/hypoxic training models: 1) live high+train high (LH+TH), 2) live high+train low (LH+TL), and 3) live low+train high (LL+TH). The LH+TL model will be examined in detail and will include its various modifications: natural/terrestrial altitude, simulated altitude via nitrogen dilution or oxygen filtration, and hypobaric normoxia via supplemental oxygen. A somewhat opposite approach to LH+TL is the altitude/hypoxic training strategy of LL+TH, and data regarding its efficacy will be presented. Recently, several of these altitude/hypoxic training strategies and devices underwent critical review by the World Anti-Doping Agency (WADA) for the purpose of potentially banning them as illegal performance-enhancing substances/methods. This paper will conclude with an update on the most recent statement from WADA regarding the use of simulated altitude devices.

A case of posterior reversible encephalopathy syndrome in the setting of post-partum preeclampsia with suppressed plasma aldosterone levels and plasma renin activity

Directory of Open Access Journals (Sweden)

Aurelio Negro

2013-12-01

Full Text Available Posterior reversible encephalopathy syndrome (PRES is characterized by headache, altered mental status, visual loss, and seizures. PRES is associated with neuroradiological findings: white matter abnormalities, predominantly in the parieto-occipital regions of the brain. PRES has been described in association with hypertensive encephalopathy, eclampsia, renal failure, or following immunosuppressive or anticancer therapy. We report a case of PRES in a severe preeclampsia occurring in the late postpartum period, with suppressed plasma aldosterone levels and plasma renin activity. These laboratory abnormalities may be due to an apparent mineralocorticoid excess syndrome.

Hypoxic enhancement of exosome release by breast cancer cells

International Nuclear Information System (INIS)

King, Hamish W; Michael, Michael Z; Gleadle, Jonathan M

2012-01-01

Exosomes are nanovesicles secreted by tumour cells which have roles in paracrine signalling during tumour progression, including tumour-stromal interactions, activation of proliferative pathways and bestowing immunosuppression. Hypoxia is an important feature of solid tumours which promotes tumour progression, angiogenesis and metastasis, potentially through exosome-mediated signalling. Breast cancer cell lines were cultured under either moderate (1% O 2 ) or severe (0.1% O 2 ) hypoxia. Exosomes were isolated from conditioned media and quantitated by nanoparticle tracking analysis (NTA) and immunoblotting for the exosomal protein CD63 in order to assess the impact of hypoxia on exosome release. Hypoxic exosome fractions were assayed for miR-210 by real-time reverse transcription polymerase chain reaction and normalised to exogenous and endogenous control genes. Statistical significance was determined using the Student T test with a P value of < 0.05 considered significant. Exposure of three different breast cancer cell lines to moderate (1% O 2 ) and severe (0.1% O 2 ) hypoxia resulted in significant increases in the number of exosomes present in the conditioned media as determined by NTA and CD63 immunoblotting. Activation of hypoxic signalling by dimethyloxalylglycine, a hypoxia-inducible factor (HIF) hydroxylase inhibitor, resulted in significant increase in exosome release. Transfection of cells with HIF-1α siRNA prior to hypoxic exposure prevented the enhancement of exosome release by hypoxia. The hypoxically regulated miR-210 was identified to be present at elevated levels in hypoxic exosome fractions. These data provide evidence that hypoxia promotes the release of exosomes by breast cancer cells, and that this hypoxic response may be mediated by HIF-1α. Given an emerging role for tumour cell-derived exosomes in tumour progression, this has significant implications for understanding the hypoxic tumour phenotype, whereby hypoxic cancer cells may release

Posterior encephalopathy with vasospasm: MRI and angiography

International Nuclear Information System (INIS)

Weidauer, S.; Gaa, J.; Lanfermann, H.; Zanella, F.E.; Sitzer, M.; Hefner, R.

2003-01-01

Posterior encephalopathy is characterised by headache, impairment of consciousness, seizures and progressive visual loss. MRI shows bilateral, predominantly posterior, cortical and subcortical lesions with a distribution. Our aim was to analyse the MRI lesion pattern and angiographic findings because the pathophysiology of posterior encephalopathy is incompletely understood. We report three patients with clinical and imaging findings consistent with posterior encephalopathy who underwent serial MRI including diffusion-weighted imaging (DWI) and construction of apparent diffusion coefficient (ADC) maps, and four-vessel digital subtraction angiography (DSA). DWI revealed symmetrical subcortical and cortical parieto-occipital high signal. High and also low ADCs indicated probable vasogenic and cytotoxic oedema. On follow-up there was focal cortical laminar necrosis, while the white-matter lesions resolved almost completely, except in the arterial border zones. DSA revealed diffuse arterial narrowing, slightly more marked in the posterior circulation. These findings suggest that posterior encephalopathy may in some cases be due to diffuse, severe vasospasm affecting especially in the parieto-occipital grey matter, with its higher vulnerability to ischemia. Cerebral vasospasm due to digitoxin intoxication, resulting in posterior encephalopathy, has not yet been described previously. (orig.)

Autism spectrum disorder and epileptic encephalopathy: common causes, many questions.

Science.gov (United States)

Srivastava, Siddharth; Sahin, Mustafa

2017-01-01

Epileptic encephalopathies represent a particularly severe form of epilepsy, associated with cognitive and behavioral deficits, including impaired social-communication and restricted, repetitive behaviors that are the hallmarks of autism spectrum disorder (ASD). With the advent of next-generation sequencing, the genetic landscape of epileptic encephalopathies is growing and demonstrates overlap with genes separately implicated in ASD. However, many questions remain about this connection, including whether epileptiform activity itself contributes to the development of ASD symptomatology. In this review, we compiled a database of genes associated with both epileptic encephalopathy and ASD, limiting our purview to Mendelian disorders not including inborn errors of metabolism, and we focused on the connection between ASD and epileptic encephalopathy rather than epilepsy broadly. Our review has four goals: to (1) discuss the overlapping presentations of ASD and monogenic epileptic encephalopathies; (2) examine the impact of the epilepsy itself on neurocognitive features, including ASD, in monogenic epileptic encephalopathies; (3) outline many of the genetic causes responsible for both ASD and epileptic encephalopathy; (4) provide an illustrative example of a final common pathway that may be implicated in both ASD and epileptic encephalopathy. We demonstrate that autistic features are a common association with monogenic epileptic encephalopathies. Certain epileptic encephalopathy syndromes, like infantile spasms, are especially linked to the development of ASD. The connection between seizures themselves and neurobehavioral deficits in these monogenic encephalopathies remains open to debate. Finally, advances in genetics have revealed many genes that overlap in ties to both ASD and epileptic encephalopathy and that play a role in diverse central nervous system processes. Increased attention to the autistic features of monogenic epileptic encephalopathies is warranted for

Prognostic Value of EEG in Asphyxiated Newborns Treated with Hypothermia

OpenAIRE

J Gordon Millichap

2008-01-01

Researchers at Children’s Hospitals in Milan, Italy, determined the prognostic value of electroencephalographic patterns in 23 newborns with severe perinatal hypoxic-ischemic encephalopathy, treated with hypothermia.

Hashimoto's encephalopathy : epidemiology, pathogenesis and management.

Science.gov (United States)

Mocellin, Ramon; Walterfang, Mark; Velakoulis, Dennis

2007-01-01

of a severe vasculitis are often absent. The links between the clinical pictures, thyroid disease, auto-antibody pattern and brain pathology await further clarification through research. It may be that Hashimoto's encephalopathy will be subsumed into a group of nonvasculitic autoimmune inflammatory meningoencephalopathies. This group may include disorders such as limbic encephalitis associated with voltage-gated potassium channel antibodies. Some authors have suggested abandoning any link to Hashimoto and renaming the condition 'steroid responsive encephalopathy associated with autoimmune thyroiditis' to better reflect current, if limited, understanding of this condition.

Hepatic Encephalopathy

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Full Text Available ... OVERVIEW Donate Now Join an Event Volunteer Your Time The Legacy Society Make Gifts of Stock Donate ... problem from liver disease that gets worse over time. Hepatic Encephalopathy, sometimes referred to as portosystemic encephalopathy ...

Hepatic Encephalopathy

Medline Plus

Full Text Available ... Now Hepatic Encephalopathy Back Hepatic Encephalopathy is a brain disorder that develops in some individuals with liver ... is a condition that causes temporary worsening of brain function in people with advanced liver disease. When ...

Hepatic Encephalopathy

Medline Plus

Full Text Available ... that can be corrected . It may also occur as part of a chronic problem from liver disease ... worse over time. Hepatic Encephalopathy, sometimes referred to as portosystemic encephalopathy or PSE, is a condition that ...

Benzodiazepine receptor antagonists for acute and chronic hepatic encephalopathy

DEFF Research Database (Denmark)

Als-Nielsen, B; Kjaergard, L L; Gluud, C

2001-01-01

The pathogenesis of hepatic encephalopathy is unknown. It has been suggested that liver failure leads to the accumulation of substances that bind to a receptor-complex in the brain resulting in neural inhibition which may progress to coma. Several trials have assessed benzodiazepine receptor...... antagonists for hepatic encephalopathy, but the results are conflicting....

Hepatic Encephalopathy

Medline Plus

Full Text Available ... Disease Type 1 (von Gierke) Hemochromatosis Hepatic Encephalopathy Hepatitis A Hepatitis B Hepatitis C Intrahepatic Cholestasis of Pregnancy ( ... Disease Type 1 (von Gierke) Hemochromatosis Hepatic Encephalopathy Hepatitis A Hepatitis B Hepatitis C Intrahepatic Cholestasis of Pregnancy ( ...

Post-TIPS Hepatic Encephalopathy Treated by Occlusion Balloon-Assisted Retrograde Embolization of a Coexisting Spontaneous Splenorenal Shunt

International Nuclear Information System (INIS)

Shioyama, Yasukazu; Matsueda, Kiyoshi; Horihata, Koushi; Kimura, Masashi; Nishida, Norifumi; Kishi, Kazushi; Terada, Masaki; Sato, Morio; Yamada, Ryusaku

1996-01-01

A 51-year-old man with posthepatitis cirrhosis underwent a transjugular intrahepatic portosystemic shunt (TIPS) for bleeding of recurrent esophageal varices. The patient had a coexisting, spontaneous, splenorenal shunt. He subsequently developed hepatic encephalopathy, presumably due to excessive portosystemic shunting. Since medical management resulted in no significant improvement, the splenorenal shunt was embolized from the jugular vein approach via renal vein access during temporary balloon occlusion. Within a few days, the patient's hepatic encephalopathy resolved. Twelve months later the patient showed no recurrence of encephalopathy and had maintained a patent TIPS

Antepartum risk factors for newborn encephalopathy: the Western Australian case-control study

Science.gov (United States)

Badawi, Nadia; Kurinczuk, Jennifer J; Keogh, John M; Alessandri, Louisa M; O’Sullivan, Fiona; Burton, Paul R; Pemberton, Patrick J; Stanley, Fiona J

1998-01-01

Objective To ascertain antepartum predictors of newborn encephalopathy in term infants. Design Population based, unmatched case-control study. Setting Metropolitan area of Western Australia, June 1993 to September 1995. Subjects All 164 term infants with moderate or severe newborn encephalopathy; 400 randomly selected controls. Main outcome measures Adjusted odds ratio estimates. Results The birth prevalence of moderate or severe newborn encephalopathy was 3.8/1000 term live births. The neonatal fatality was 9.1%. The risk of newborn encephalopathy increased with increasing maternal age and decreased with increasing parity. There was an increased risk associated with having a mother who was unemployed (odds ratio 3.60), an unskilled manual worker (3.84), or a housewife (2.48). Other risk factors from before conception were not having private health insurance (3.46), a family history of seizures (2.55), a family history of neurological disease (2.73), and infertility treatment (4.43). Risk factors during pregnancy were maternal thyroid disease (9.7), severe pre-eclampsia (6.30), moderate or severe bleeding (3.57), a clinically diagnosed viral illness (2.97), not having drunk alcohol (2.91); and placenta described at delivery as abnormal (2.07). Factors related to the baby were birth weight adjusted for gestational age between the third and ninth centile (4.37) or below the third centile (38.23). The risk relation with gestational age was J shaped with 38 and 39 weeks having the lowest risk. Conclusions The causes of newborn encephalopathy are heterogeneous and many of the causal pathways start before birth. Key messagesThe birth prevalence of moderate or severe newborn encephalopathy was 3.8 per 1000 term live births and the neonatal case fatality was 9.1%Independent risk factors before conception and in the antepartum period for newborn encephalopathy include socioeconomic status, family history of seizures or other neurological disease, conception after

Bronchiolitis-associated encephalopathy in critically-ill infants: an underestimated complication?

Science.gov (United States)

Antonucci, Roberto; Chiappe, Stefano; Porcella, Annalisa; Rosatelli, Daniela; Fanos, Vassilios

2010-05-01

To investigate the bronchiolitis-associated encephalopathy in critically ill infants. The records of infants with severe bronchiolitis admitted to our intensive care unit between 1991 and 2003 were reviewed. Subjects with underlying neurological disorders were excluded. Encephalopathy was defined as occurrence of seizures or at least two nonconvulsive neurologic manifestations. A semistructured telephone interview investigated long-term neurodevelopmental outcome. Twenty-one infants (11 newborns) were enrolled. All patients required oxygen supplementation and 14 required mechanical ventilation. Encephalopathy occurred in 10 infants, six of whom developed seizures. Encephalopathic infants frequently (six of nine) showed transient EEG abnormalities, and occasionally (one of nine) cranial ultrasound abnormalities. A positive respiratory syncytial virus test was found in five of nine encephalopathic infants. One encephalopathic patient died, while 20 infants clinically normalised before discharge and showed a good neurodevelopmental outcome. Acute encephalopathy was frequently observed in our patients with severe bronchiolitis. Long-term prognosis of encephalopathic infants was good.

MRI findings in acute hyperammonemic encephalopathy resulting from decompensated chronic liver disease.

Science.gov (United States)

Sureka, Jyoti; Jakkani, Ravi Kanth; Panwar, Sanuj

2012-06-01

Hyperammonemic encephalopathy is a type of metabolic encephalopathy with diversified etiology. Hyperammonemia is the end result of several metabolic disorders such as congenital deficiencies of urea cycle enzymes, hepatic encephalopathy, Reye's syndrome and other toxic encephalopathies. Non-specific clinical presentation poses a great challenge in early diagnosis of this entity. Irrespective of the underlying etiology, hyperammonemia causes a distinctive pattern of brain parenchymal injury. The cingulate gyrus and insular cortex are more vulnerable to this type of toxic insult. Characteristic magnetic resonance imaging findings in combination with laboratory parameters can help to differentiate this entity from other metabolic encephalopathy and thus aiding in early diagnosis and treatment.

Pathogenesis of Hepatic Encephalopathy

Directory of Open Access Journals (Sweden)

Irena Ciećko-Michalska

2012-01-01

Full Text Available Hepatic encephalopathy can be a serious complication of acute liver failure and chronic liver diseases, predominantly liver cirrhosis. Hyperammonemia plays the most important role in the pathogenesis of hepatic encephalopathy. The brain-blood barrier disturbances, changes in neurotransmission, neuroinflammation, oxidative stress, GABA-ergic or benzodiazepine pathway abnormalities, manganese neurotoxicity, brain energetic disturbances, and brain blood flow abnormalities are considered to be involved in the development of hepatic encephalopathy. The influence of small intestine bacterial overgrowth (SIBO on the induction of minimal hepatic encephalopathy is recently emphasized. The aim of this paper is to present the current views on the pathogenesis of hepatic encephalopathy.

Pathogenesis of Hepatic Encephalopathy

Science.gov (United States)

Ciećko-Michalska, Irena; Szczepanek, Małgorzata; Słowik, Agnieszka; Mach, Tomasz

2012-01-01

Hepatic encephalopathy can be a serious complication of acute liver failure and chronic liver diseases, predominantly liver cirrhosis. Hyperammonemia plays the most important role in the pathogenesis of hepatic encephalopathy. The brain-blood barrier disturbances, changes in neurotransmission, neuroinflammation, oxidative stress, GABA-ergic or benzodiazepine pathway abnormalities, manganese neurotoxicity, brain energetic disturbances, and brain blood flow abnormalities are considered to be involved in the development of hepatic encephalopathy. The influence of small intestine bacterial overgrowth (SIBO) on the induction of minimal hepatic encephalopathy is recently emphasized. The aim of this paper is to present the current views on the pathogenesis of hepatic encephalopathy. PMID:23316223

The TOBY Study. Whole body hypothermia for the treatment of perinatal asphyxial encephalopathy: A randomised controlled trial

Directory of Open Access Journals (Sweden)

Thoresen Marianne

2008-04-01

Full Text Available Abstract Background A hypoxic-ischaemic insult occurring around the time of birth may result in an encephalopathic state characterised by the need for resuscitation at birth, neurological depression, seizures and electroencephalographic abnormalities. There is an increasing risk of death or neurodevelopmental abnormalities with more severe encephalopathy. Current management consists of maintaining physiological parameters within the normal range and treating seizures with anticonvulsants. Studies in adult and newborn animals have shown that a reduction of body temperature of 3–4°C after cerebral insults is associated with improved histological and behavioural outcome. Pilot studies in infants with encephalopathy of head cooling combined with mild whole body hypothermia and of moderate whole body cooling to 33.5°C have been reported. No complications were noted but the group sizes were too small to evaluate benefit. Methods/Design TOBY is a multi-centre, prospective, randomised study of term infants after perinatal asphyxia comparing those allocated to "intensive care plus total body cooling for 72 hours" with those allocated to "intensive care without cooling". Full-term infants will be randomised within 6 hours of birth to either a control group with the rectal temperature kept at 37 +/- 0.2°C or to whole body cooling, with rectal temperature kept at 33–34°C for 72 hours. Term infants showing signs of moderate or severe encephalopathy +/- seizures have their eligibility confirmed by cerebral function monitoring. Outcomes will be assessed at 18 months of age using neurological and neurodevelopmental testing methods. Sample size At least 236 infants would be needed to demonstrate a 30% reduction in the relative risk of mortality or serious disability at 18 months. Recruitment was ahead of target by seven months and approvals were obtained allowing recruitment to continue to the end of the planned recruitment phase. 325 infants were

CDKL5 mutations in boys with severe encephalopathy and early-onset intractable epilepsy.

Science.gov (United States)

Elia, M; Falco, M; Ferri, R; Spalletta, A; Bottitta, M; Calabrese, G; Carotenuto, M; Musumeci, S A; Lo Giudice, M; Fichera, M

2008-09-23

To search for CDKL5 gene mutations in boys presenting with severe early-onset encephalopathy and intractable epilepsy, a clinical picture very similar to that already described in girls with CDKL5 mutations. Eight boys (age range 3-16 years, mean age 8.5 years, SD 4.38) with severe or profound mental retardation and early-onset intractable seizures were selected for CDKL5 gene mutation screening by denaturing high-performance liquid chromatography analysis. We found three unrelated boys carrying three different missense mutations of the CDKL5 gene: c.872G>A (p.C291Y), c.863C>T (p.T288I), and c.533G>C (p.R178P). They presented early-onset, polymorphous, and drug-resistant seizures, mostly myoclonic and tonic or spasms. EEG showed epileptiform abnormalities which were multifocal during wakefulness, and pseudoperiodic bisynchronous during sleep. This study describes three boys carrying CDKL5 missense mutations and their detailed clinical and EEG data, and indicates that CDKL5 gene mutations may represent a cause of severe or profound mental retardation and early-onset intractable seizures, also in boys. Screening for CDKL5 mutations is strongly recommended in individuals with these clinical features.

The Thompson Encephalopathy Score and Short-Term Outcomes in Asphyxiated Newborns Treated With Therapeutic Hypothermia

NARCIS (Netherlands)

Thorsen, Patricia; Jansen-van der Weide, Martine C.; Groenendaal, Floris; Onland, Wes; van Straaten, Henrika L. M.; Zonnenberg, Inge; Vermeulen, Jeroen R.; Dijk, Peter H.; Dudink, Jeroen; Rijken, Monique; van Heijst, Arno; Dijkman, Koen P.; Cools, Filip; Zecic, Alexandra; van Kaam, Anton H.; de Haan, Timo R.

2016-01-01

The Thompson encephalopathy score is a clinical score to assess newborns suffering from perinatal asphyxia. Previous studies revealed a high sensitivity and specificity of the Thompson encephalopathy score for adverse outcomes (death or severe disability). Because the Thompson encephalopathy score

Dopaminergic agonists for hepatic encephalopathy

DEFF Research Database (Denmark)

Als-Nielsen, B; Gluud, L L; Gluud, C

2004-01-01

Hepatic encephalopathy may be associated with an impairment of the dopaminergic neurotransmission. Dopaminergic agonists may therefore have a beneficial effect on patients with hepatic encephalopathy.......Hepatic encephalopathy may be associated with an impairment of the dopaminergic neurotransmission. Dopaminergic agonists may therefore have a beneficial effect on patients with hepatic encephalopathy....

Nationwide survey of rotavirus-associated encephalopathy and sudden unexpected death in Japan.

Science.gov (United States)

Kawamura, Yoshiki; Ohashi, Masahiro; Ihira, Masaru; Hashimoto, Shuji; Taniguchi, Koki; Yoshikawa, Tetsushi

2014-08-01

Rotavirus can cause severe complications such as encephalopathy/encephalitis and sudden unexpected death. The incidence of rotavirus-associated encephalopathy/encephalitis or sudden unexpected death remains unknown. To clarify the clinical features of rotavirus-associated encephalitis/encephalopathy and sudden unexpected death, we conducted a nationwide survey in Japan. A two-part questionnaire was designed to determine the number of the cases and the clinical features of severe cases of rotavirus infection, including encephalitis/encephalopathy and sudden unexpected death, between 2009 and 2011. Of the 1365 questionnaires sent to hospitals, 963 (70.5%) were returned and eligible for analysis. We determined 58 cases of rotavirus-associated encephalitis/encephalopathy and 7 cases of sudden unexpected death. These patients were diagnosed with rotavirus infection by immunochromatography. Although 36/58 (62.1%) encephalitis/encephalopathy patients had no sequelae, 15/58 (25.9%) patients had neurological sequelae, and 7/58 (12.1%) patients had fatal outcomes. Pleocytosis was observed in 9/40 (22.5%) patients and cerebrospinal fluid protein levels were elevated in only 4/40 (10%) patients. Elevated lactate dehydrogenase (LDH) (>500 IU/L) or acidemia (pHdeath were 44.0 and 4.9 cases in Japan, respectively. Elevated LDH (>500 IU/L) or acidemia (pH<7.15) were related to a poor prognosis of the encephalitis/encephalopathy. Copyright © 2013 The Japanese Society of Child Neurology. Published by Elsevier B.V. All rights reserved.

Localized Cerebral Energy Failure in DNA Polymerase Gamma-Associated Encephalopathy Syndromes

Science.gov (United States)

Tzoulis, Charalampos; Neckelmann, Gesche; Mork, Sverre J.; Engelsen, Bernt E.; Viscomi, Carlo; Moen, Gunnar; Ersland, Lars; Zeviani, Massimo; Bindoff, Laurence A.

2010-01-01

Mutations in the catalytic subunit of the mitochondrial DNA-polymerase gamma cause a wide spectrum of clinical disease ranging from infantile hepato-encephalopathy to juvenile/adult-onset spinocerebellar ataxia and late onset progressive external ophthalmoplegia. Several of these syndromes are associated with an encephalopathy that…

Understanding Hypoxic Drive and the Release of Hypoxic Vasoconstriction.

Science.gov (United States)

Inkrott, Jon C

2016-01-01

Understanding the hypoxic drive and release of hypoxic vasoconstriction in the chronic obstructive pulmonary disease population can be somewhat confusing and misunderstood. Furthermore, the hypoxic drive theory is one in which there really is no scientific evidence to support and yet continues to prosper in every aspect of care in regard to the chronic lung patient, from prehospital all the way to intensive care unit and home care therapy. This subject review will hopefully enhance some understanding of what exactly goes on with these patients and the importance of providing oxygen when it is desperately needed. Copyright © 2016 Air Medical Journal Associates. Published by Elsevier Inc. All rights reserved.

Lesion Size Is Exacerbated in Hypoxic Rats Whereas Hypoxia-Inducible Factor-1 Alpha and Vascular Endothelial Growth Factor Increase in Injured Normoxic Rats: A Prospective Cohort Study of Secondary Hypoxia in Focal Traumatic Brain Injury.

Science.gov (United States)

Thelin, Eric Peter; Frostell, Arvid; Mulder, Jan; Mitsios, Nicholas; Damberg, Peter; Aski, Sahar Nikkhou; Risling, Mårten; Svensson, Mikael; Morganti-Kossmann, Maria Cristina; Bellander, Bo-Michael

2016-01-01

Hypoxia following traumatic brain injury (TBI) is a severe insult shown to exacerbate the pathophysiology, resulting in worse outcome. The aim of this study was to investigate the effects of a hypoxic insult in a focal TBI model by monitoring brain edema, lesion volume, serum biomarker levels, immune cell infiltration, as well as the expression of hypoxia-inducible factor-1 alpha (HIF-1α) and vascular endothelial growth factor (VEGF). Female Sprague-Dawley rats (n = 73, including sham and naive) were used. The rats were intubated and mechanically ventilated. A controlled cortical impact device created a 3-mm deep lesion in the right parietal hemisphere. Post-injury, rats inhaled either normoxic (22% O2) or hypoxic (11% O2) mixtures for 30 min. The rats were sacrificed at 1, 3, 7, 14, and 28 days post-injury. Serum was collected for S100B measurements using ELISA. Ex vivo magnetic resonance imaging (MRI) was performed to determine lesion size and edema volume. Immunofluorescence was employed to analyze neuronal death, changes in cerebral macrophage- and neutrophil infiltration, microglia proliferation, apoptosis, complement activation (C5b9), IgG extravasation, HIF-1α, and VEGF. The hypoxic group had significantly increased blood levels of lactate and decreased pO2 (p hypoxic animals (p hypoxic group at 1 day after trauma (p = 0.0868). No differences were observed between the groups in cytotoxic and vascular edema, IgG extravasation, neutrophils and macrophage aggregation, microglia proliferation, or C5b-9 expression. Hypoxia following focal TBI exacerbated the lesion size and neuronal loss. Moreover, there was a tendency to higher levels of S100B in the hypoxic group early after injury, indicating a potential validity as a biomarker of injury severity. In the normoxic group, the expression of HIF-1α and VEGF was found elevated, possibly indicative of neuro-protective responses occurring in this less severely injured group. Further studies are

Hypoxic training methods for improving endurance exercise performance

Directory of Open Access Journals (Sweden)

Jacob A. Sinex

2015-12-01

Full Text Available Endurance athletic performance is highly related to a number of factors that can be altered through altitude and hypoxic training including increases in erythrocyte volume, maximal aerobic exercise capacity, capillary density, and economy. Physiological adaptations in response to acute and chronic exposure to hypoxic environments are well documented and range from short-term detrimental effects to longer-term adaptations that can improve performance at altitude and in sea-level competitions. Many altitude and hypoxic training protocols have been developed, employing various combinations of living and training at sea-level, low, moderate, and high altitudes and utilizing natural and artificial altitudes, with varying degrees of effectiveness. Several factors have been identified that are associated with individual responses to hypoxic training, and techniques for identifying those athletes most likely to benefit from hypoxic training continue to be investigated. Exposure to sufficiently high altitude (2000–3000 m for more than 12 h/day, while training at lower altitudes, for a minimum of 21 days is recommended. Timing of altitude training related to competition remains under debate, although general recommendations can be considered.

A global amnesia associated with the specific variant of posterior reversible encephalopathy syndrome (PRES) that developed due to severe preeclampsia and malignant hypertension.

Science.gov (United States)

Borovac, Josip Anđelo; Božić, Joško; Žaja, Nikola; Kolić, Krešimir; Hrboka, Vedran

2016-04-01

A case is reported of a 26-year-old primiparous woman in the 32nd week of gestation who presented to the emergency department with the symptoms of a severe headache, nausea and vomiting. The patient was diagnosed with preeclampsia that later progressed to eclampsia. This state was characterized by a sudden onset of a headache and diplopia that advanced to cortical blindness and precipitated significant alterations in mental status, most notable being global amnesia that resolved within 48 h. A post-partum magnetic resonance imaging of the brain in FLAIR mode revealed multiple cortico-subcortical areas of hyperintense signals suggestive of edematous lesions that chiefly involved occipital and parietal lobes with additional atypical manifestations. Such radiologic findings suggested a posterior reversible encephalopathy syndrome variant with the global amnesia as an extraordinary constituent. This unique feature should be acknowledged when treating a preeclamptic or hypertensive patient that exhibits neurological symptomatology and vision disturbances.

The Thompson Encephalopathy Score and Short-Term Outcomes in Asphyxiated Newborns Treated With Therapeutic Hypothermia.

Science.gov (United States)

Thorsen, Patricia; Jansen-van der Weide, Martine C; Groenendaal, Floris; Onland, Wes; van Straaten, Henrika L M; Zonnenberg, Inge; Vermeulen, Jeroen R; Dijk, Peter H; Dudink, Jeroen; Rijken, Monique; van Heijst, Arno; Dijkman, Koen P; Cools, Filip; Zecic, Alexandra; van Kaam, Anton H; de Haan, Timo R

2016-07-01

The Thompson encephalopathy score is a clinical score to assess newborns suffering from perinatal asphyxia. Previous studies revealed a high sensitivity and specificity of the Thompson encephalopathy score for adverse outcomes (death or severe disability). Because the Thompson encephalopathy score was developed before the use of therapeutic hypothermia, its value was reassessed. The purpose of this study was to assess the association of the Thompson encephalopathy score with adverse short-term outcomes, defined as death before discharge, development of severe epilepsy, or the presence of multiple organ failure in asphyxiated newborns undergoing therapeutic hypothermia. The study period ranged from November 2010 to October 2014. A total of 12 tertiary neonatal intensive care units participated. Demographic and clinical data were collected from the "PharmaCool" multicenter study, an observational cohort study analyzing pharmacokinetics of medication during therapeutic hypothermia. With multiple logistic regression analyses the association of the Thompson encephalopathy scores with outcomes was studied. Data of 142 newborns were analyzed (male: 86; female: 56). Median Thompson score was 9 (interquartile range: 8 to 12). Median gestational age was 40 weeks (interquartile range 38 to 41), mean birth weight was 3362 grams (standard deviation: 605). All newborns manifested perinatal asphyxia and underwent therapeutic hypothermia. Death before discharge occurred in 23.9% and severe epilepsy in 21.1% of the cases. In total, 59.2% of the patients had multiple organ failure. The Thompson encephalopathy score was not associated with multiple organ failure, but a Thompson encephalopathy score ≥12 was associated with death before discharge (odds ratio: 3.9; confidence interval: 1.3 to 11.2) and with development of severe epilepsy (odds ratio: 8.4; confidence interval: 2.5 to 27.8). The Thompson encephalopathy score is a useful clinical tool, even in cooled asphyxiated

Synaptic damage underlies EEG abnormalities in postanoxic encephalopathy: A computational study.

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Ruijter, B J; Hofmeijer, J; Meijer, H G E; van Putten, M J A M

2017-09-01

In postanoxic coma, EEG patterns indicate the severity of encephalopathy and typically evolve in time. We aim to improve the understanding of pathophysiological mechanisms underlying these EEG abnormalities. We used a mean field model comprising excitatory and inhibitory neurons, local synaptic connections, and input from thalamic afferents. Anoxic damage is modeled as aggravated short-term synaptic depression, with gradual recovery over many hours. Additionally, excitatory neurotransmission is potentiated, scaling with the severity of anoxic encephalopathy. Simulations were compared with continuous EEG recordings of 155 comatose patients after cardiac arrest. The simulations agree well with six common categories of EEG rhythms in postanoxic encephalopathy, including typical transitions in time. Plausible results were only obtained if excitatory synapses were more severely affected by short-term synaptic depression than inhibitory synapses. In postanoxic encephalopathy, the evolution of EEG patterns presumably results from gradual improvement of complete synaptic failure, where excitatory synapses are more severely affected than inhibitory synapses. The range of EEG patterns depends on the excitation-inhibition imbalance, probably resulting from long-term potentiation of excitatory neurotransmission. Our study is the first to relate microscopic synaptic dynamics in anoxic brain injury to both typical EEG observations and their evolution in time. Copyright © 2017 International Federation of Clinical Neurophysiology. Published by Elsevier B.V. All rights reserved.

Hypoxic radiosensitization: adored and ignored

DEFF Research Database (Denmark)

Overgaard, Jens

2007-01-01

resistance can be eliminated or modified by normobaric or hyperbaric oxygen or by the use of nitroimidazoles as hypoxic radiation sensitizers. More recently, attention has been given to hypoxic cytotoxins, a group of drugs that selectively or preferably destroys cells in a hypoxic environment. An updated......Since observations from the beginning of the last century, it has become well established that solid tumors may contain oxygen-deficient hypoxic areas and that cells in such areas may cause tumors to become radioresistant. Identifying hypoxic cells in human tumors has improved by the help of new...

Metformin inhibits glutaminase activity and protects against hepatic encephalopathy.

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Javier Ampuero

Full Text Available AIM: To investigate the influence of metformin use on liver dysfunction and hepatic encephalopathy in a retrospective cohort of diabetic cirrhotic patients. To analyze the impact of metformin on glutaminase activity and ammonia production in vitro. METHODS: Eighty-two cirrhotic patients with type 2 diabetes were included. Forty-one patients were classified as insulin sensitizers experienced (metformin and 41 as controls (cirrhotic patients with type 2 diabetes mellitus without metformin treatment. Baseline analysis included: insulin, glucose, glucagon, leptin, adiponectin, TNFr2, AST, ALT. HOMA-IR was calculated. Baseline HE risk was calculated according to minimal hepatic encephalopathy, oral glutamine challenge and mutations in glutaminase gene. We performed an experimental study in vitro including an enzymatic activity assay where glutaminase inhibition was measured according to different metformin concentrations. In Caco2 cells, glutaminase activity inhibition was evaluated by ammonia production at 24, 48 and 72 hours after metformina treatment. RESULTS: Hepatic encephalopathy was diagnosed during follow-up in 23.2% (19/82: 4.9% (2/41 in patients receiving metformin and 41.5% (17/41 in patients without metformin treatment (logRank 9.81; p=0.002. In multivariate analysis, metformin use [H.R.11.4 (95% CI: 1.2-108.8; p=0.034], age at diagnosis [H.R.1.12 (95% CI: 1.04-1.2; p=0.002], female sex [H.R.10.4 (95% CI: 1.5-71.6; p=0.017] and HE risk [H.R.21.3 (95% CI: 2.8-163.4; p=0.003] were found independently associated with hepatic encephalopathy. In the enzymatic assay, glutaminase activity inhibition reached 68% with metformin 100 mM. In Caco2 cells, metformin (20 mM decreased glutaminase activity up to 24% at 72 hours post-treatment (p<0.05. CONCLUSIONS: Metformin was found independently related to overt hepatic encephalopathy in patients with type 2 diabetes mellitus and high risk of hepatic encephalopathy. Metformin inhibits glutaminase

Maternal or neonatal infection: association with neonatal encephalopathy outcomes.

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Jenster, Meike; Bonifacio, Sonia L; Ruel, Theodore; Rogers, Elizabeth E; Tam, Emily W; Partridge, John Colin; Barkovich, Anthony James; Ferriero, Donna M; Glass, Hannah C

2014-07-01

Perinatal infection may potentiate brain injury among children born preterm. The objective of this study was to examine whether maternal and/or neonatal infection are associated with adverse outcomes among term neonates with encephalopathy. This study is a cohort study of 258 term newborns with encephalopathy whose clinical records were examined for signs of maternal infection (chorioamnionitis) and infant infection (sepsis). Multivariate regression was used to assess associations between infection, pattern, and severity of injury on neonatal magnetic resonance imaging, as well as neurodevelopment at 30 mo (neuromotor examination, or Bayley Scales of Infant Development, second edition mental development index encephalopathy, chorioamnionitis was associated with a lower risk of brain injury and adverse outcomes, whereas signs of neonatal sepsis carried an elevated risk. The etiology of encephalopathy and timing of infection and its associated inflammatory response may influence whether infection potentiates or mitigates injury in term newborns.

Need for early diagnosis of mental and mobility changes in Wernicke encephalopathy.

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Wijnia, Jan W; Oudman, Erik; Bresser, Esmay L; Gerridzen, Ineke J; van de Wiel, Albert; Beuman, Carla; Mulder, Cornelis L

2014-12-01

Korsakoff syndrome is a chronic form of amnesia resulting from thiamine deficiency. The syndrome can develop from unrecognized or undertreated Wernicke encephalopathy. The intra-individual course of Wernicke-Korsakoff syndrome has not been studied extensively, nor has the temporal progression of gait disturbances and other symptoms of Wernicke encephalopathy. Here we present the detailed history of a patient whose acute symptoms of Wernicke encephalopathy were far from stable. We follow his mobility changes and the shifts in his mental status from global confusion and impaired consciousness to more selective cognitive deficits. His Wernicke encephalopathy was missed and left untreated, being labeled as "probable" Korsakoff syndrome. Patients with a history of self-neglect and alcohol abuse, at risk of or suffering with Wernicke encephalopathy, should receive immediate and adequate vitamin replacement. Self-neglecting alcoholics who are bedridden may have severe illness and probably active Wernicke encephalopathy. In these patients, mobility changes, delirium, or impaired consciousness can be an expression of Wernicke encephalopathy, and should be treated to prevent further damage from the neurologic complications of thiamine deficiency.

Correlative study of proton magnetic resonance spectroscopy and histopathology in a neonatal piglet model of hypoxic-ischemic encephalopathy

International Nuclear Information System (INIS)

Wang Xiaoming; Guo Qiyong; Lin Nan; Ding Changwei; Wang Shuxuan; Chen Liying; Lv Qingjie; Jiang Weiguo

2005-01-01

Objective: To evaluate proton magnetic resonance spectroscopy ( 1 H-MRS) in the diagnosis of hypoxic ischemic brain damage (HIBD) in hyperacute period using an animal model. Methods: Twenty-five term piglets at the age of 3 to 7 days were subjected and divided into one control group (n=5) and two experimental groups. 1 H spectrum curve was measured continuously in all cases at 0-6, 20-24, 44-48, and 68-72 h after hypoxic ischemia in frontoparietal region, basal ganglia, and hippocampus. Lac/Cr was calculated. Histopathologic examination included hematoxylin and glial fibrillary acidic protein (GFAP) stain, teminal transferase mediated dUTP-biotin nick- end eosin (HE) stain, labeling (TUNEL) stain, and transmission electron microscope. Results: Lac/Cr in hippocampus region was 0.95 ± 0.88 in control group compared with 5.65 ± 1.93 in model group 1 and 8.93 ± 6.95 in model group 2. Model group 1 showed significantly glial cells swelling in hippocampus region on histopathologic examination. Model group 2 showed neurons and glial cells swelling significantly in hippocampus, and prominent apoptosis was seen in the peripheral neurons and glial cells. Further more Lac/Cr remained high within 72 h. Lac /Cr was 0.41 ± 0.03 in basal ganglia in control group compared with no significant elevation in model group 1 and 13.59 ± 10.23 in model group 2. Model group 1 did not show significant neuron and glial cell pathological changes in basal ganglia. Model group 2 showed obvious glial cell swelling, while neurons changed mildly. Lac/Cr was high within 48 h, and then declined. Lac/Cr in frontoparietal region also increased, but the value was lower than the former two regions. Conclusion: Neurons have an acute energy consumption after hypoxic ischemia, and Lac/Cr reflectes the extent of lesions correctly. (authors)

Successful Reversal of Chronic Incapacitating Post-TIPS Encephalopathy by Balloon Occlusion of the Stent

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Daphna Fenyves

1994-01-01

Full Text Available Transjugular intrahepatic portosystemic shunt (TIPS placement is a new technique allowing decompression of the portal system without the need for abdominal surgery or general anesthetic. This promising procedure appears safe, and is being evaluated in the context of life threatening uncontrollable variceal hemorrhage as well as ascites refractory to medical treatment. Following TIPS, portal flow diversion is associated with hepatic encephalopathy in up to 25% of patients. This is most often mild and treatable but may become uncontrollable, incapacitating and even life threatening in up to 3 to 5% of cases. The authors present two patients in whom such life threatening encephalopathy and stupor was reversed by transjugular balloon occlusion of the TIPS.

Current state of knowledge of hepatic encephalopathy (part IV): Management of Hepatic Encephalopathy by liver support systems.

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Hassanein, Tarek

2017-04-01

Hepatic Encephalopathy is a devastating complication of End-Stage Liver Disease. In its severe grades it requires extra intervention beyond the standard medical approaches. In this article were view the role of liver support systems in managing hepatic encephalopthy.

Severe hepatic encephalopathy in a patient with liver cirrhosis after administration of angiotensin-converting enzyme inhibitor/angiotensin II receptor blocker combination therapy: a case report

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Podda Mauro

2010-05-01

Full Text Available Abstract Introduction A combination therapy of angiotensin-converting enzyme inhibitors and angiotensin II receptor blockers has been used to control proteinuria, following initial demonstration of its efficacy. However, recently concerns about the safety of this therapy have emerged, prompting several authors to urge for caution in its use. In the following case report, we describe the occurrence of a serious and unexpected adverse drug reaction after administration of a combination of angiotensin-converting enzyme inhibitors and angiotensin II receptor blockers to a patient with nephrotic syndrome and liver cirrhosis with severe portal hypertension. Case presentation We administered this combination therapy to a 40-year-old Caucasian man with liver cirrhosis in our Hepatology Clinic, given the concomitant presence of glomerulopathy associated with severe proteinuria. While the administration of one single drug appeared to be well-tolerated, our patient developed severe acute encephalopathy after the addition of the second one. Discontinuation of the therapy led to the disappearance of the side-effect. A tentative rechallenge with the same drug combination led to a second episode of acute severe encephalopathy. Conclusion We speculate that this adverse reaction may be directly related to the effect of angiotensin II on the excretion of blood ammonia. Therefore, we suggest that patients with liver cirrhosis and portal hypertension are at risk of developing clinically relevant encephalopathy when angiotensin-converting enzyme inhibitor and angiotensin II receptor blocker combination therapy is administered, thus indicating the need for a careful clinical follow-up. In addition, the incidence of this serious side-effect should be rigorously evaluated in all patients with liver cirrhosis administered with this common treatment combination.

Genetic control of yeast cell radiosensitivity modification by oxygen and hypoxic sensitizers

International Nuclear Information System (INIS)

Zhuranovskaya, G.P.; Petin, V.G.

1984-01-01

Diploid yeast cells Saccharomyces cerevisiae ''of the wild type'', individual mutants, homozygous in rad 2 and rad 54 and double mutants, containing both these loci in homozygous state are considered to prove genetic determination of radiosensitivity modification of hypoxic cells by oxygen and electron acceptor compounds previously demonstrated on yeast cells of other genotypes. It is shown that both ''oxygen effect'' and the effect of hypoxic sensitizers depend on the activity of repair systems. The possible mechanism of participation of post-radiation restoration processes in the modification of cell radiosensitivity, is discussed

Hepatic Encephalopathy: Early Diagnosis in Pediatric Patients With Cirrhosis

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DARA, Naghi; SAYYARI, Ali-Akbar; IMANZADEH, Farid

2014-01-01

Objective As acute liver failure (ALF) and chronic liver disease (cirrhosis) continue to increase in prevalence, we will see more cases of hepatic encephalopathy. Primary care physician are often the first to suspect it, since they are familiar with the patient’s usual physical and mental status. This serious complication typically occurs in patients with severe comorbidities and needs multidisciplinary evaluation and care. Hepatic encephalopathy should be considered in any patient with acute liver failure and cirrhosis who presents with neuropsychiatric manifestations, decrease level of consciousness (coma), change of personality, intellectual and behavioral deterioration, speech and motor dysfunction. Every cirrhotic patient may be at risk; potential precipitating factors should be addressed in regular clinic visits. The encephalopathy of liver disease may be prominent, or can be present in subtle forms, such as decline of school performance, emotional outbursts, or depression. “Subtle form” of hepatic encephalopathy may not be obvious on clinical examination, but can be detected by neurophysiologic and neuropsychiatric testing. PMID:24665321

Wernicke encephalopathy in children and adolescents.

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Lallas, Matt; Desai, Jay

2014-11-01

Wernicke encephalopathy is caused by thiamine (vitamin B1) deficiency. It is generally considered to be a disease of adult alcoholics. However, it is known to occur in the pediatric population and in non-alcoholic conditions. We searched PubMed with the key words Wernicke, thiamine, pediatric, children and adolescents and selected publications that were deemed appropriate. The global prevalence rates of hunger, poverty and resultant nutrient deprivation have decreased in the 21st century. However, several scenarios which may predispose to Wernicke encephalopathy may be increasingly prevalent in children and adolescents such as malignancies, intensive care unit stays and surgical procedures for the treatment of obesity. Other predisposing conditions include magnesium deficiency and defects in the SLC19A3 gene causing thiamine transporter-2 deficiency. The classic triad consists of encephalopathy, oculomotor dysfunction and gait ataxia but is not seen in a majority of patients. Treatment should be instituted immediately when the diagnosis is suspected clinically without waiting for laboratory confirmation. Common magnetic resonance findings include symmetric T2 hyperintensities in dorsal medial thalamus, mammillary bodies, periaqueductal gray matter, and tectal plate. Wernicke encephalopathy is a medical emergency. Delay in its recognition and treatment may lead to significant morbidity, irreversible neurological damage or even death. This article aims to raise the awareness of this condition among pediatricians.

Wernicke’s encephalopathy following hyperemesis gravidarum

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Leila Pourali

2016-06-01

Full Text Available Background: ″Wernicke’s Korsakoff″ syndrome is the most important complication of severe thiamine deficiency. The term refers to two different syndromes, each representing a different stage of the disease. Wernicke’s encephalopathy (WE is an acute syndrome requiring emergent treatment to prevent death and neurologic morbidity. Korsakoff syndrome (KS refers to a chronic neurologic condition that usually occurs as a consequence of WE. It is a rare complication of hyperemesis gravidarum that confusion, ocular signs, and gait ataxia are the most prevalent symptoms, respectively. Typical brain lesions of wernicke’s encephalopathy (WE are observed at autopsy in 0.4 to 2.8 percent of the general population in the western world and the majority of affected patients are alcoholic. The prevalence of wernicke’s encephalopathy lesions seen on autopsy was 12.5% of alcohol abusers in one report. Among those who with alcohol-related death, it has been reported to be even higher, 29 to 59%. The aim of this study was to report a case of wernicke’s encephalopathy following hyperemesis gravidarum. Case Presentation: A 28-year-old-pregnant woman in 19th weeks of gestation referred to the hospital with hyperemesis, gait ataxia, and dysarthria before that she had hyperemesis gravidarum with weight loss and unresponsive to outpatient and inpatient medical therapy. MRI showed hyperdense lesion around thalamus which was characteristic of wernicke’s encephalopathy. Rapid improvement in patient’s condition occurred after high dose thiamine infusion. Conclusion: In hyperemesis gravidarum, presence of either symptoms of ocular or mental disorder or ataxia must be considered to rule out and appropriate treatment of Wernicke’s syndrome which can cause maternal and fetal death.

The effect of whole-body cooling on brain metabolism following perinatal hypoxic-ischemic injury.

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Corbo, Elizabeth T; Bartnik-Olson, Brenda L; Machado, Sandra; Merritt, T Allen; Peverini, Ricardo; Wycliffe, Nathaniel; Ashwal, Stephen

2012-01-01

Magnetic resonance imaging (MRI) and spectroscopy (MRS) have proven valuable in evaluating neonatal hypoxic-ischemic injury (HII). MRI scores in the basal ganglia of HII/HT(+) neonates were significantly lower than HII/HT(-) neonates, indicating less severe injury and were associated with lower discharge encephalopathy severity scores in the HII/HT(+) group (P = 0.01). Lactate (Lac) was detected in the occipital gray matter (OGM) and thalamus (TH) of significantly more HII/HT(-) neonates (31.6 and 35.3%) as compared to the HII/HT(+) group (10.5 and 15.8%). In contrast, the -N-acetylaspartate (NAA)-based ratios in the OGM and TH did not differ between the HII groups. Our data show that the HT was associated with a decrease in the number of HII neonates with detectable cortical and subcortical Lac as well as a decrease in the number of MRI-detectable subcortical lesions. We retrospectively compared the medical and neuroimaging data of 19 HII neonates who received 72 h of whole-body cooling (HII/HT(+)) with those of 19 noncooled HII neonates (HII/HT(-)) to determine whether hypothermia was associated with improved recovery from the injury as measured by MRI and MRS within the first 14 days of life. MRI scores and metabolite ratios of HII/HT(+) and HII/HT(-) neonates were also compared with nine healthy, nonasphyxiated "control" neonates.

Neonatal jaundice and birth asphyxia as major causes of cerebral ...

African Journals Online (AJOL)

Background: Cerebral Palsy is permanent sequela of severe nonprogressive insult to the immature brain of children. In Nigeria, kernicterus from neonatal jaundice and hypoxic ischaemic encephalopathy form severe birth asphyxia have been identified as among the leading causes of this scourge. Poor management of ...

Wernicke encephalopathy in a patient with liver failure: Clinical case report.

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Zhao, Pan; Zhao, Yanling; Wei, Zhenman; Chen, Jing; Yan, Lilong

2016-07-01

Early recognition and diagnosis of Wernicke encephalopathy is pivotal for the prognosis of this medical emergency, especially in patients with liver failure which predisposes individuals to develop hepatic encephalopathy. For these patients, distinguishing between hepatic encephalopathy and Wernicke encephalopathy is a challenge in real-world clinical practice.A male patient with 21-year medical history of liver cirrhosis presented diarrhea and ascites. One month before this visit, he was noted to have poor appetite and progressive fatigue. After admission, although several major symptoms, including diarrhea, ascites, hyponatremia, and hypoproteinemia, were greatly improved through appropriate treatments, his laboratory indicators were not changed much. His appetite was not reversed at discharge. On the 5th day after discharge, the patient suddenly became reluctant to speak and did not remember the recent happenings. Simultaneously, unsteady gait and strabismus occurred. On the basis of clinical manifestations and brain magnetic resonance imaging scan results, the patient was diagnosed as Wernicke encephalopathy and these relative symptoms were resolved after intravenous vitamin B1.To our knowledge, this is the second case report of Wernicke encephalopathy developing in a critically ill cirrhotic patient without hepatocellular carcinoma or operative intervention. Wernicke encephalopathy may be underdiagnosed in these patients and this case raises physicians' awareness of its possible onset.

Interstitial administration of perfluorochemical emulsions for reoxygenation of hypoxic tumor cells

International Nuclear Information System (INIS)

Woo, D.V.; Seegenschmiedt, H.; Schweighardt, F.K.; Emrich, J.; McGarvey, K.; Caridi, M.; Brady, L.W.

1987-01-01

Microparticulate perfluorochemical (PFC) emulsions have the capacity to solubilize significant quantities of oxygen compared to water. Although systemic administration of such emulsions may enhance oxygen delivery to some tissues, hypoxic tumor cells have marginal vascular supplies. The authors report studies which directly attempt to oxygenate hypoxic tumor cells by interstitial administration of oxygenated PFC emulsions followed by radiation therapy. Fortner MMI malignant melanomas (21 day old) grown in Syrian Golden hamsters were injected directly with either oxygenated PFC emulsions or Ringers solution. The volume of test substance administered was equal to 50% of the tumor volume. The tumors were immediately irradiated with 25 Gy of 10 MeV photons (Clinac 18). The tumor dimensions were measured daily post irradiation and the tumor doubling time determined. The results suggest that interstitial administration of oxygenated PFC emulsions directly into tumors followed by radiation therapy may increase the likelihood of killing hypoxic tumor cells

Proinflammatory Cytokines, Enolase and S-100 as Early Biochemical Indicators of Hypoxic-Ischemic Encephalopathy Following Perinatal Asphyxia in Newborns

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Verónica Chaparro-Huerta

2017-02-01

Conclusion: The role of cytokines after hypoxic-ischemic insult has been determined in studies of transgenic mice that support the use of these molecules as candidate biomarkers. Similarly, S-100 and enolase are considered promising candidates because these markers have been correlated with tissue damage in different experimental models.

Prognostic factors for acute encephalopathy with bright tree appearance.

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Azuma, Junji; Nabatame, Shin; Nakano, Sayaka; Iwatani, Yoshiko; Kitai, Yukihiro; Tominaga, Koji; Kagitani-Shimono, Kuriko; Okinaga, Takeshi; Yamamoto, Takehisa; Nagai, Toshisaburo; Ozono, Keiichi

2015-02-01

To determine the prognostic factors for encephalopathy with bright tree appearance (BTA) in the acute phase through retrospective case evaluation. We recruited 10 children with encephalopathy who presented with BTA and classified them into 2 groups. Six patients with evident regression and severe psychomotor developmental delay after encephalopathy were included in the severe group, while the remaining 4 patients with mild mental retardation were included in the mild group. We retrospectively analyzed their clinical symptoms, laboratory data, and magnetic resonance imaging (MRI) and magnetic resonance spectroscopy (MRS) findings. Patients in the severe group developed subsequent complications such as epilepsy and severe motor impairment. Univariate analysis revealed that higher maximum lactate dehydrogenase (LDH) levels (p=0.055) were a weak predictor of poor outcome. Maximum creatinine levels were significantly higher (p<0.05) and minimal platelet counts were significantly lower (p<0.05) in the severe group than in the mild group. Acute renal failure was not observed in any patient throughout the study. MRS of the BTA lesion during the BTA period showed elevated lactate levels in 5 children in the severe group and 1 child in the mild group. MRI performed during the chronic phase revealed severe brain atrophy in all patients in the severe group. Higher creatinine and LDH levels and lower platelet counts in the acute phase correlated with poor prognosis. Increased lactate levels in the BTA lesion during the BTA period on MRS may predict severe physical and mental disability. Copyright © 2014 The Japanese Society of Child Neurology. Published by Elsevier B.V. All rights reserved.

Hypoxic conditioning as a new therapeutic modality

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Samuel eVerges

2015-06-01

Full Text Available Preconditioning refers to a procedure by which a single noxious stimulus below the threshold of damage is applied to the tissue in order to increase resistance to the same or even different noxious stimuli given above the threshold of damage. Hypoxic preconditioning relies on complex and active defenses that organisms have developed to counter the adverse consequences of oxygen deprivation. The protection it confers against ischemic attack for instance as well as the underlying biological mechanisms have been extensively investigated in animal models. Based on these data, hypoxic conditioning (consisting in recurrent exposure to hypoxia has been suggested a potential non-pharmacological therapeutic intervention to enhance some physiological functions in individuals in whom acute or chronic pathological events are anticipated or existing. In addition to healthy subjects, some benefits have been reported in patients with cardiovascular and pulmonary diseases as well as in overweight and obese individuals. Hypoxic conditioning consisting in sessions of intermittent exposure to moderate hypoxia repeated over several weeks may induce hematological, vascular, metabolic and neurological effects. This review addresses the existing evidence regarding the use of hypoxic conditioning as a potential therapeutic modality and emphasizes on many remaining issues to clarify and future researches to be performed in the field.

Neonatal jaundice and birth asphyxia as major causes of cerebral ...

African Journals Online (AJOL)

McRoy

Background: Cerebral Palsy is permanent sequela of severe non- progressive insult to the immature brain of children. In Nigeria, kernicterus from neonatal jaundice and hypoxic ischaemic encephalopathy form severe birth asphyxia have been identified as among the leading causes of this scourge. Poor management of ...

Delayed encephalopathy after acute carbon monoxide poisoning

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Mehmet İbrahim Turan

2014-03-01

Full Text Available Carbon monoxide poisoning is a major cause of death following attempted suicide and accidental exposures. Although clinical presentation depends on the duration and the intensity of exposure, the assessment of the severity of intoxication is difficult. A small percentage of patients who show complete initial recovery may develop delayed neurological deficits. Delayed encephalopathy after acute carbon monoxide poisoning is a rare and poor prognosis neurologic disorders and there is no specific treatment. We present a case with early onset of delayed encephalopathy after acute carbon monoxide poisoning with typical cranial imaging findings in a child with atypical history and clinical presentation.

Anatomy of the late radiation encephalopathy

Energy Technology Data Exchange (ETDEWEB)

De Reuck, J; vander Eecken, H

1975-01-01

The clinico-pathological data and the topography of the lesions were determined in 13 cases of late radiation encephalopathy. In one case the arterial vascularisation was studied by the translucidation technique after filling of the blood vessels with a colloidal barium sulphate solution. The radiation lesions consisted of areas of focal necrosis and of diffuse demyelination and necrosis of the deep cerebral structures and the brain stem. Demyelination was predominantly present in cases of late appearance of the neurological symptoms while necrosis was found in cases with a short latency period. The cerebral cortex and the arcuate fibres were always the most preserved structures. The topography of the focal lesions in the cerebral hemispheres and in the brain stem corresponded well to the vascular supply areas of the deep perforating arteries, while the diffuse lesions always had a predominant distribution in the periventricular arterial end- and border-zones. These observations were also confirmed by a post mortem angiographic study. The present report argues once more for a vascular aetiology as cause of the late radiation encephalopathy.

Dinitrobenzamide mustard prodrugs - hypoxic cytotoxins and dual substrates for E.coli nitroreductase

International Nuclear Information System (INIS)

Patterson, A.V.; Hogg, A.; Pullen, S.; Degenkolbe, A.; Li, D.; Chappell, A.; Ying, S.; Atwell, G.J.; Denny, W.A.; Anderson, R.F.; Wilson, W.R.

2003-01-01

selectivity for E.coli NTR (A549NTR). Four compounds were identified as dual P450R/NTR substrates and were evaluated in vivo for hypoxic cytotoxicity in the Rif-1 murine tumour excision assay. Oxic tumour cells are sterilised through the application of 15Gy and the impact of post-irradiation prodrug administration upon the hypoxic cell subpopulation was quantitated. Two DNBMs (SN 27744 and SN 27762) were found to be highly active and another (SN 27645) had modest activity. A secondary in vivo screening using the human A549 xenograft excision assay ± 20Gy (± P450R overexpression) revealed a similar SAR. Notably, overexpression of P450R was not mandatory for in vivo activity. We have identified several DNBMs with the potential for activation by NTR 'armed' CRAds whilst independently functioning as hypoxic cytotoxins. These prodrugs may have utility in circumstances where vector geometry is constrained and hypoxic tumour cells are distal from viral deposition and spread. We are currently developing an NTR 'armed' variant of the CRAd, ONYX-411, to test these observations. However the NTR-independent activity of these prodrugs provides an opportunity for their early development as single-agents for use in radiotherapy

Synthesis and radiolabelling of novel nitrogen mustards for the imaging of hypoxic tissue

International Nuclear Information System (INIS)

Falzon, C.; Ackermann, U.; Tochon-Danguy, H.J.; O'Keefe, G.J.; White, J.; Spratt, N.; Howells, D.; Scott, A.M.

2005-01-01

Hypoxic tissue is of great significance in stroke and oncology. Among the radiotracers currently used to detect hypoxia, derivatives based on the 2-nitro-imidazole ring such as FMISO or FAZA have received considerable attention in medical imaging. Unfortunately, due to slow clearance of these tracers from normoxic tissue a waiting period of two hours is required between tracer injection and the scanning of the patient. In addition the target to background ratio is low and the quality of the image is therefore poor. Nitrogen mustards are another class of compounds that have great affinity to hypoxic tissue. Derivatives of these compounds labelled with a positron emitting radionuclide, such as [ 18 F], may allow for the imaging of hypoxic regions in the ischemic penumbra. It therefore, may be a useful diagnostic tool in stroke. Radiolabeled N-(2-[ 18 F]-fluoroethyl)-N-(2-chloroethyl)-4-methylsulfinylaniline was successfully synthesised using a potassium fluoride kryptofix complex, giving the desired product in 40% radiochemical yield (10 min at 100 Degrees C). In vitro analysis to determine the stability of the radiotracer in plasma and saline indicated no defluorination. Biological evaluation studies of the radiotracer were undertaken using a rat stroke model (Middle cerebral Arterial Occlusion (MCAO)) to determine whether the ischemic penumbra can be imaged using PET. 150//Ci (5.5MBq) of the radiotracer was injected into the tail vein of the rat immediately after the MCAO. The rat was sacrificed 2 hours post injection and ex-vivo autoradiography was performed. Uptake of the radiotracer was observed in hypoxic regions of the brain (n=6). Dynamic PET images revealed that the ischemic penumbra can be imaged 15 minutes post injection of this tracer. With these promising results, we are now synthesizing other analogues to determine their relationship between selectivity for hypoxic tissue and brain uptake

Chronic traumatic encephalopathy: contributions from the Boston University Center for the Study of Traumatic Encephalopathy.

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Riley, David O; Robbins, Clifford A; Cantu, Robert C; Stern, Robert A

2015-01-01

Chronic Traumatic Encephalopathy (CTE) is a neurodegenerative disease associated with repetitive brain trauma (RBT). Initially described in boxers, CTE has now been found in other contact sport athletes with a history of RBT. In recent years, there has been tremendous media attention regarding CTE, primarily because of the deaths of high profile American football players who were found to have CTE upon neuropathological examination. However, the study of CTE remains in its infancy. This review focuses on research from the Centre for the Study of Traumatic Encephalopathy (CSTE) at Boston University. This study reviews the formation of the CSTE, major CSTE publications and current ongoing research projects at the CSTE. The neuropathology of CTE has been well-described. Current research focuses on: methods of diagnosing the disease during life (including the development of biomarkers), examination of CTE risk factors (including genetic susceptibility and head impact exposure variables); description of the clinical presentation of CTE; development of research diagnostic criteria for Traumatic Encephalopathy Syndrome; and assessment of mechanism and pathogenesis. Current research at the BU CSTE is aimed at increasing understanding of the long-term consequences of repetitive head impacts and attempting to begin to answer several of the unanswered questions regarding CTE.

Bovine Spongiform Encephalopathy: Atypical Pros and Cons

Science.gov (United States)

Transmissible spongiform encephalopathies (TSEs) are fatal neurologic diseases that affect several mammalian species including human beings. Four animal TSE agents have been reported: scrapie of sheep and goats; chronic wasting disease (CWD) of deer, elk, and moose; transmissible mink encephalopath...

Benzodiazepine receptor antagonists for hepatic encephalopathy

DEFF Research Database (Denmark)

Als-Nielsen, B; Gluud, L L; Gluud, C

2004-01-01

Hepatic encephalopathy may be associated with accumulation of substances that bind to a receptor-complex in the brain resulting in neural inhibition. Benzodiazepine receptor antagonists may have a beneficial effect on patients with hepatic encephalopathy.......Hepatic encephalopathy may be associated with accumulation of substances that bind to a receptor-complex in the brain resulting in neural inhibition. Benzodiazepine receptor antagonists may have a beneficial effect on patients with hepatic encephalopathy....

Clinical and pathological aspects of human African trypanosomiasis (T. b. gambiense) with particular reference to reactive arsenical encephalopathy.

Science.gov (United States)

Haller, L; Adams, H; Merouze, F; Dago, A

1986-01-01

Fourteen of 330 patients treated with melarsoprol (Mel B) for human African trypanosomiasis (HAT) developed a severe reactive arsenical encephalopathy (RAE). Six of these cases were fatal and postmortem examination was performed on 5 patients. Symptoms of "sleeping sickness" were compared with symptoms after treatment with arsenicals and the subsequent onset of RAE. There are 3 characteristic syndromes of RAE: convulsive status associated with acute cerebral edema, rapidly progressive coma without convulsions, and acute nonlethal mental disturbances without neurological signs. Three subjects revealed hypoxic brain damage with acute cerebral edema, and multiple hemorrhages of brain stem in those comatose. The pathology of the underlying HAT (chronic perivascular inflammation and plasma cytic infiltration of the brain) and the pathology of the RAE (characterized by acute vasculitis) are distinct. RAE occurs in the first as well as in the second stage (CNS involvement) of trypanosomiasis but the reason for this is unclear; an exclusive toxicity of the drug, or a Herxheimer reaction are possible but seem unlikely. Both clinical and laboratory findings point rather to a drug-related, delayed immune response.

Turnover rate of hypoxic cells in solid tumors

International Nuclear Information System (INIS)

Ljungkvist, A.S.E.; Bussink, J.; Rijken, P.F.J.W.; Van Der Kogel, A.J.

2003-01-01

Most solid tumors contain hypoxic cells, and both the amount and duration of tumor hypoxia has been shown to influence the effect of radiation treatment negatively. It is important to understand the dynamic processes within the hypoxic cell population in non-treated tumors, and the effect of different treatment modalities on the kinetics of hypoxic cells to be able to design optimal combined modality treatments. The turnover rate of hypoxic cells was analyzed in three different solid tumor models with a double bio-reductive hypoxic marker assay with sequential injection of the two hypoxic markers. Previously it was shown that this assay could be used to detect both a decrease and an increase of tumor hypoxia in relation to the tumor vasculature with high spatial resolution. In this study the first hypoxic marker, pimonidazole, was administered at variable times relative to tumor harvest, and the second hypoxic marker, CCI-103F, was injected at a fixed time before harvest. The hypoxic cell turnover rate was calculated as the loss of pimonidazole positive cells relative to CCI-103F. The murine C38 line had the fastest hypoxic turnover rate of 60% /24h and the human xenograft line SCCNij3 had the slowest hypoxic turnover rate of 30% /24 h. The hypoxic turnover rate was most heterogeneous in the SCCNij3 line that even contained viable groups of cells that had been hypoxic for at least 5 days. The human xenograft line MEC82 fell in between with a hypoxic turnover rate of 50% /24 h. The hypoxic cell turnover was related to the potential tumor volume doubling time (Tpot) with a Tpot of 26h in C38 and 103h in SCCNij3. The dynamics of hypoxic cells, quantified with a double hypoxic marker method, showed large differences in hypoxic cell turnover rate and were related to Tpot

Clinical and experimental aspects of hepatic encephalopathy

NARCIS (Netherlands)

M. Groeneweg (Michael)

1998-01-01

textabstractHepatic encephalopathy (HE) is a neuropsychiatnc syndrome associated with severe liver disease. Clinical symptoms range from minimal changes in mental state and neuromuscular defects to unresponsive coma. 1-' The syndrome of HE can be divided into three major groups: HE associated with

Computedtomographic findings in natal encephalopathies and their significance for the prognosis for the near future and long-term development

International Nuclear Information System (INIS)

Kotlarek, F.

1981-01-01

190 premature babies and newborn with a hypoxic or traumatic natal encephalopathy were examined in the newborn period with cranial computed tomography. 10 other neonatals with cyanotic vitia even without neurologic syndromes were included into this study. 73 of these infants were intubated for a while and supplied with air. The CT findings were compared with those of a ''control group'' of neonatals who provided externally visible malformations but no burdening perinatal anamnesis. 82 premature and neonatal babies showed abnormal morphologic basic findings. Due to kind, localisation and size of the lesion, different morphologic patterns - depending on the birth weight - can be delineated. (orig./MG) [de

Subcortical arteriosclerotic encephalopathy (Binswanger disease)

International Nuclear Information System (INIS)

Settanni, F.; Dumont, P.; Casella, C.L.; Pascuzzi, L.; Cecilio, S.; Caldas, J.G.

1992-01-01

Four patients with variable clinical and tomographic features were diagnosed as having subcortical arteriosclerotic encephalopathy (Binswanger disease). This diagnosis was done based on the presence of subacute progression of focal cerebral deficits, presence of hypertension, systemic vascular disease and dementia. The pathogenesis of subcortical arteriosclerotic encephalopathy is unknown; possible mechanism include diffuse ischemia and fluid transudation with subsequent gliosis related to subacute hypertensive encephalopathy. (author)

The Thompson Encephalopathy Score and Short-Term Outcomes in Asphyxiated Newborns Treated With Therapeutic Hypothermia

NARCIS (Netherlands)

Thorsen, Patricia; Jansen-van der Weide, Martine C; Groenendaal, Floris; Onland, Wes; van Straaten, Henrika L M; Zonnenberg, Inge; Vermeulen, Jeroen R.; Dijk, Peter H; Dudink, Jeroen; Rijken, Monique; van Heijst, Arno; Dijkman, Koen P; Cools, Filip; Zecic, Alexandra; van Kaam, Anton H; de Haan, Timo R

BACKGROUND: The Thompson encephalopathy score is a clinical score to assess newborns suffering from perinatal asphyxia. Previous studies revealed a high sensitivity and specificity of the Thompson encephalopathy score for adverse outcomes (death or severe disability). Because the Thompson

Case of hepatic encephalopathy induced by thortrast

Energy Technology Data Exchange (ETDEWEB)

Shirato, H.; Kudo, N.; Takita, K. (Nakatori Hospital, Akita (Japan))

1980-09-01

A case of hepatic encephalopathy induced by thorotrast injected as a contrast 40 years before was reported. The patient was a 64-year-old man with severe liver dysfunction, and had psychic and neurological symptoms, and hyperammonemia. There was a relationship between ammonium concentration in blood and psychic and neurological symptoms. Electroencephalogram showed three phases waves peculiar to hepatic coma intermittently. Thorotrast in the liver was detected by radiological methods and in vivo measurement of the radioactivity. From the above-mentioned result, this disease was diagnosed as hepatic encephalopathy induced by long-term sedimentation of thorotrast without complication of malignant tumors. Because of the concurrent presence of cerebral infarction, the diagnosis was difficult to make.

Recent advances in hepatic encephalopathy

Science.gov (United States)

DeMorrow, Sharon

2017-01-01

Hepatic encephalopathy describes the array of neurological alterations that occur during acute liver failure or chronic liver injury. While key players in the pathogenesis of hepatic encephalopathy, such as increases in brain ammonia, alterations in neurosteroid levels, and neuroinflammation, have been identified, there is still a paucity in our knowledge of the precise pathogenic mechanism. This review gives a brief overview of our understanding of the pathogenesis of hepatic encephalopathy and then summarizes the significant recent advances made in clinical and basic research contributing to our understanding, diagnosis, and possible treatment of hepatic encephalopathy. A literature search using the PubMed database was conducted in May 2017 using “hepatic encephalopathy” as a keyword, and selected manuscripts were limited to those research articles published since May 2014. While the authors acknowledge that many significant advances have been made in the understanding of hepatic encephalopathy prior to May 2014, we have limited the scope of this review to the previous three years only. PMID:29026534

Celiac crisis presenting with status epilepticus and encephalopathy.

Science.gov (United States)

Hijaz, Nadia M; Bracken, Julia M; Chandratre, Sonal R

2014-12-01

Celiac crisis is a life-threatening presentation of celiac disease which is described in the context of classic gastrointestinal (GI) symptoms of diarrhea, leading to dehydration and electrolyte imbalance. Neurologic manifestations are atypical symptoms of celiac crisis. To the best of our knowledge, there is no published report on seizure or encephalopathy as the presenting manifestation of celiac crisis. We describe a 2-year-old boy presenting with acute status epilepticus and lethargy. Prior to presentation, he had mild abdominal distention and intermittent diarrhea. Laboratory analysis revealed hyponatremia, anemia, hypocalcemia, transaminitis, and hyperglycemia. Electroencephalography revealed severe diffuse encephalopathy, and complete infectious work-up was negative. Initial brain magnetic resonance imaging was normal; however, repeat imaging showed osmotic demyelination syndrome. Given the history of GI symptoms and hyperglycemia, celiac serology was obtained revealing elevated tissue transglutaminase, and a diagnosis was confirmed by Marsh 3c lesions in the duodenum. He significantly improved with steroid therapy in addition to adequate nutrition, fluids, and initiation of a gluten-free diet. We report herein on the first case of celiac crisis presenting with status epilepticus and encephalopathy in the absence of profound GI symptoms. Our case suggests that celiac crisis should be considered in the differential of seizures and encephalopathy in children.

New avenues in hypoxic cell sensitization

International Nuclear Information System (INIS)

Huilgol, N.G.; Chatterjee, N.A.; Singh, B.B.

1995-01-01

Hypoxic cells in tumors represent a population of cells that are resistant to radiotherapy. Bio-reductive agents like RSU 1069, RBU 6145 and EOg and vasoactive drugs in conjunction with hypoxic cell sensitizers are being evaluated as hypoxic cell cytotoxins. Chlorpromazine a membrane active drug and AK-2123- a nitrotriazole with a potential to deplete intracellular thiols induced vasoconstriction and sensitize hypoxic cells have stretched the boundaries of innovation. A preliminary experience with these drugs is discussed. 8 refs., 2 tabs., 2 figs

In vitro effects of piracetam on the radiosensitivity of hypoxic cells (adaptation of MTT assay to hypoxic conditions)

International Nuclear Information System (INIS)

Gheuens, E.E.O.; Bruijn, E.A. de; Van der Heyden, S.; Van Oosterom, A.T.; Lagarde, P.; Pooter, C.M.J. de; Chomy, F.

1995-01-01

This paper describes the adaptation of the MTT assay to hypoxic conditions in order to test the in vitro effect of piracetam on hypoxic cells and particularly on the radiosensitivity of hypoxic cells since this drug has shown clinical effect on acute and chronic hypoxia. The V79 cell line was selected by reference to preliminary hypoxic experiments using clonogenic assay and euoxic experiments using clonogenic and MTT assays. Cell growth and survival in our hypoxic conditions were assessed using MTT assay with an enclosure and special 48-well plates both made of glass. Growth curves on glass plates after 1-hour exposure to nitrogen versus air were comparable, so there is no bias effect due to gas composition. Survival curves using MTT versus reference clonogenic assay were comparable after radiation exposure in eu- and hypoxic conditions, and confirm the validity of our original technique for creating hypoxia. The Oxygen Enhancement Ratio was of about 3 for 1-hour hypoxic exposure. Piracetam gave no cytotoxic effect up to 10 mM of piracetam. Growth curves after continuous drug exposure and 1-hour euoxic versus hypoxic exposure gave no cytotoxic effect up to 10 mM of piracetam. Survival curves after continuous drug exposure to 10 mM of piracetam gave no significant effect on the radiosensitivity of hypoxic V79 cells using MTT or clonogenic assay. (author). 32 refs., 6 figs

Seeing more clearly through the fog of encephalopathy.

Science.gov (United States)

Kaplan, Peter W; Sutter, Raoul

2013-10-01

Patients with acute confusional states (often referred to as encephalopathy or delirium) pose diagnostic and management challenges for treating physicians. Encephalopathy is associated with a high morbidity and mortality rate, and the diagnosis rests on clinical grounds but may also be supported by the finding of electroencephalographic (EEG) evidence for diffuse cerebral dysfunction. The myriad cerebral transmitter and metabolic disruptions are generated by systemic organ system failures, principal among which are those of the liver, kidneys, lungs, heart, and endocrine system, along with the effects of exogenous toxins and medications. In most cases, several of these organ failures together contribute to the confusional state, frequently in the context of a diffuse cerebral atrophy that affects the aging brain. This special issue of the Journal of Clinical Neurophysiology is dedicated to exploring the electrophysiology of these conditions. It reviews the pathophysiology, psychiatric manifestations, clinical and imaging correlations of the many causes and types of encephalopathy. A literature review of the EEG abnormalities in the various types of encephalopathy provides an overview that ranges from paraneoplastic causes, through organ system failures, postcardiorespiratory arrest, to postoperative delirium. The issue is supplemented by tables of relevant clinical correlations, graphs, Venn diagrams, and the use of mathematical modeling used to explain how defects in the neuronal interplay might generate the EEG patterns seen in encephalopathy. We hope that this assembly will act as a springboard for further discussion and investigation into the EEG underpinnings, clinical correlations, diagnosis. and prognostication of these common and morbid disturbances of brain function.

Colectomy for porto-systemic encephalopathy: is it still topical?

Directory of Open Access Journals (Sweden)

Rym Ennaifer

2013-06-01

Full Text Available Hepatic encephalopathy (HE is a common long term complication of porto-systemic shunt. We report herein the case of a 59-year-old man with Child-Pugh A cirrhosis treated successfully 9 years earlier with distal splenorenal shunt for uncontrolled variceal bleeding. In the last year, he developed a severe and persistent hepatic encephalopathy secondary to the shunt, which was resistant to medical therapy. As liver transplantation was not available and obliteration of the shunt was hazardous, we performed subtotal colectomy in order to reduce ammonia production. This therapeutic option proved successful, as the grade of encephalopathy decreased and the patient improved. Our experience indicates that colonic exclusion should be considered as an option in the management of HE refractory to medical treatment in highly selected patients when liver transplantation is not available or even as a bridge given the long waiting time on lists.

Branched-chain amino acids for hepatic encephalopathy

DEFF Research Database (Denmark)

Als-Nielsen, B; Koretz, R L; Kjaergard, L L

2003-01-01

Hepatic encephalopathy may be caused by a decreased plasma ratio of branched-chain amino acids (BCAA) to aromatic amino acids. Treatment with BCAA may therefore have a beneficial effect on patients with hepatic encephalopathy.......Hepatic encephalopathy may be caused by a decreased plasma ratio of branched-chain amino acids (BCAA) to aromatic amino acids. Treatment with BCAA may therefore have a beneficial effect on patients with hepatic encephalopathy....

Dopamine agents for hepatic encephalopathy

DEFF Research Database (Denmark)

Junker, Anders Ellekær; Als-Nielsen, Bodil; Gluud, Christian

2014-01-01

BACKGROUND: Patients with hepatic encephalopathy may present with extrapyramidal symptoms and changes in basal ganglia. These changes are similar to those seen in patients with Parkinson's disease. Dopamine agents (such as bromocriptine and levodopa, used for patients with Parkinson's disease) have...... therefore been assessed as a potential treatment for patients with hepatic encephalopathy. OBJECTIVES: To evaluate the beneficial and harmful effects of dopamine agents versus placebo or no intervention for patients with hepatic encephalopathy. SEARCH METHODS: Trials were identified through the Cochrane...... hepatic encephalopathy that were published during 1979 to 1982 were included. Three trials assessed levodopa, and two trials assessed bromocriptine. The mean daily dose was 4 grams for levodopa and 15 grams for bromocriptine. The median duration of treatment was 14 days (range seven to 56 days). None...

Hypoxic tumor environments exhibit disrupted collagen I fibers and low macromolecular transport.

Directory of Open Access Journals (Sweden)

Samata M Kakkad

Full Text Available Hypoxic tumor microenvironments result in an aggressive phenotype and resistance to therapy that lead to tumor progression, recurrence, and metastasis. While poor vascularization and the resultant inadequate drug delivery are known to contribute to drug resistance, the effect of hypoxia on molecular transport through the interstitium, and the role of the extracellular matrix (ECM in mediating this transport are unexplored. The dense mesh of fibers present in the ECM can especially influence the movement of macromolecules. Collagen 1 (Col1 fibers form a key component of the ECM in breast cancers. Here we characterized the influence of hypoxia on macromolecular transport in tumors, and the role of Col1 fibers in mediating this transport using an MDA-MB-231 breast cancer xenograft model engineered to express red fluorescent protein under hypoxia. Magnetic resonance imaging of macromolecular transport was combined with second harmonic generation microscopy of Col1 fibers. Hypoxic tumor regions displayed significantly decreased Col1 fiber density and volume, as well as significantly lower macromolecular draining and pooling rates, than normoxic regions. Regions adjacent to severely hypoxic areas revealed higher deposition of Col1 fibers and increased macromolecular transport. These data suggest that Col1 fibers may facilitate macromolecular transport in tumors, and their reduction in hypoxic regions may reduce this transport. Decreased macromolecular transport in hypoxic regions may also contribute to poor drug delivery and tumor recurrence in hypoxic regions. High Col1 fiber density observed around hypoxic regions may facilitate the escape of aggressive cancer cells from hypoxic regions.

Neuro-overprotection? A functional evaluation of clomethiazole-induced neuroprotection following hypoxic-ischemic injury.

Science.gov (United States)

Gilby, K L; Kelly, M E; McIntyre, D C; Robertson, H A

2005-01-01

Hypoxic-ischemic (H-I) injury produces extensive damage to the hippocampus of young rats. We have recently shown that administration of 125 mg kg-1 clomethiazole (CMZ), a GABA(A)-agonist, provides complete histological protection against H-I injury if administered 3 h post-H-I (Brain Res 1035 (2005) 194). However, whether that histological protection translates into lasting functional preservation is unclear. To determine whether hippocampal-based circuits remain functionally intact in CMZ-protected H-I rats, we administered 125 mg kg-1 (high dose [CMZ-HD]) or 65 mg kg-1 (low dose [CMZ-LD]) CMZ, 3 h post-H-I, and examined numerous kindling parameters in the dorsal hippocampus 60 days following H-I. Kindling parameters included afterdischarge (AD) thresholds (ADTs), AD durations and kindling rates. Additional groups assessed included vehicle-injected H-I (VIH), hypoxic, ligated and naive rats. VIH, CMZ-HD, CMZ-LD and hypoxic rats all exhibited significantly faster kindling rates than naive rats. Thus, a previous traumatic event, even hypoxia alone, facilitated subsequent seizure propagation. Still, a significantly slower kindling rate was evident in CMZ-HD rats than in hypoxic, VIH or CMZ-LD rats. Moreover, while longer pre-kindling AD durations were observed in the damaged hippocampus of VIH compared with naive rats, this was not true for either CMZ-treated groups, hypoxic or ligated rats. Collectively, these findings suggest CMZ can suppress the epileptogenic effects of H-I. Surprisingly, however, both groups of CMZ-treated rats exhibited a four to nine times greater ADT than any other group and this effect was most profound in the CMZ-protected hippocampus. Thus, CMZ administration protected local neurons against terminal insult and left network excitability relatively normal with respect to seizure offset mechanisms but also caused profound elevation of local ADTs, which suggests a local hypoexcitability/increased inhibition. Finally, this study demonstrates

Developmental Expression and Hypoxic Induction of Hypoxia Inducible Transcription Factors in the Zebrafish.

Science.gov (United States)

Köblitz, Louise; Fiechtner, Birgit; Baus, Katharina; Lussnig, Rebecca; Pelster, Bernd

2015-01-01

The hypoxia inducible transcription factor (HIF) has been shown to coordinate the hypoxic response of vertebrates and is expressed in three different isoforms, HIF-1α, HIF-2α and HIF-3α. Knock down of either Hif-1α or Hif-2α in mice results in lethality in embryonic or perinatal stages, suggesting that this transcription factor is not only controlling the hypoxic response, but is also involved in developmental phenomena. In the translucent zebrafish embryo the performance of the cardiovascular system is not essential for early development, therefore this study was designed to analyze the expression of the three Hif-isoforms during zebrafish development and to test the hypoxic inducibility of these transcription factors. To complement the existing zfHif-1α antibody we expressed the whole zfHif-2α protein and used it for immunization and antibody generation. Similarly, fragments of the zfHif-3α protein were used for immunization and generation of a zfHif-3α specific antibody. To demonstrate presence of the Hif-isoforms during development [between 1 day post fertilization (1 dpf) and 9 dpf] affinity-purified antibodies were used. Hif-1α protein was present under normoxic conditions in all developmental stages, but no significant differences between the different developmental stages could be detected. Hif-2α was also present from 1 dpf onwards, but in post hatching stages (between 5 and 9 dpf) the expression level was significantly higher than prior to hatching. Similarly, Hif-3α was expressed from 1 dpf onwards, and the expression level significantly increased until 5 dpf, suggesting that Hif-2α and Hif-3α play a particular role in early development. Hypoxic exposure (oxygen partial pressure = 5 kPa) in turn caused a significant increase in the level of Hif-1α protein even at 1 dpf and in later stages, while neither Hif-2α nor Hif-3α protein level were affected. In these early developmental stages Hif-1α therefore appears to be more important for

Delayed administration of neural stem cells after hypoxia-ischemia reduces sensorimotor deficits, cerebral lesion size, and neuroinflammation in neonatal mice

NARCIS (Netherlands)

Braccioli, Luca; Heijnen, Cobi J.; Coffer, Paul J.; Nijboer, Cora H.A.

2017-01-01

Background Hypoxic-ischemic (HI) encephalopathy causes mortality and severe morbidity in neonates. Treatments with a therapeutic window >6 hours are currently not available. Here we explored whether delayed transplantation of allogenic neural stem cells (NSCs) at 10 days after HI could be a tool to

[Hashimoto's encephalopathy and autoantibodies].

Science.gov (United States)

Yoneda, Makoto

2013-04-01

Encephalopathy occasionally occurs in association with thyroid disorders, but most of these are treatable. These encephalopathies include a neuropsychiatric disorder associated with hypothyroidism, called myxedema encephalopathy. Moreover, Hashimoto's encephalopathy (HE) has been recognized as a new clinical disease based on an autoimmune mechanism associated with Hashimoto's thyroiditis. Steroid treatment was successfully administered to these patients. Recently, we discovered that the serum autoantibodies against the NH2-terminal of α-enolase (NAE) are highly specific diagnostic biomarkers for HE. Further, we analyzed serum anti-NAE autoantibodies and the clinical features in many cases of HE from institutions throughout Japan and other countries. Approximately half of assessed HE patients carry anti-NAE antibodies. The age was widely distributed with 2 peaks (20-30 years and 50-70 years). Most HE patients were in euthyroid states, and all patients had anti-thyroid (TG) antibodies and anti-thyroid peroxidase (TPO) antibodies. Anti-TSH receptor (TSH-R) antibodies were observed in some cases. The common neuropsychiatry features are consciousness disturbance and psychosis, followed by cognitive dysfunction, involuntary movements, seizures, and ataxia. Abnormalities on electroencephalography (EEG) and decreased cerebral blood flow on brain SPECT were common findings, whereas abnormal findings on brain magnetic resonance imaging (MRI) were rare. HE patients have various clinical phenotypes such as the acute encephalopathy form, the chronic psychiatric form, and other particular clinical forms, including limbic encephalitis, progressive cerebellar ataxia, and Creutzfeldt-Jakob disease (CJD)-like form. The cerebellar ataxic form of HE clinically mimics spinocerebellar degeneration (SCD) and is characterized by the absence of nystagmus, absent or mild cerebellar atrophy, and lazy background activities on EEG. Taken together, these data suggest that the possibility of

A case of hepatic encephalopathy induced by trotrast

International Nuclear Information System (INIS)

Shirato, Hideo; Kudo, Norishige; Takita, Kyoji

1980-01-01

A case of hepatic encephalopathy induced by thorotrast injected as a contrast 40 years before was reported. The patient was a 64-year-old man with severe liver dysfunction, and had psychic and neurological symptoms, and hyperammonemia. There was a relationship between ammonium concentration in blood and psychic and neurological symptoms. Electroencephalogram showed three phases waves peculiar to hepatic coma intermittently. Throtrast in the liver was detected by radiological methods and in vivo measurement of the radioactivity. From the above-mentioned result, this disease was diagnosed as hepatic encephalopathy induced by long-term sedimentation of thorotrast without complication of malignant tumors. Because of the concurrent presence of cerebral infarction, the diagnosis was difficult to make. (Tsunoda, M.)

Neuroprotective actions of taurine on hypoxic-ischemic brain damage in neonatal rats.

Science.gov (United States)

Zhu, Xiao-Yun; Ma, Peng-Sheng; Wu, Wei; Zhou, Ru; Hao, Yin-Ju; Niu, Yang; Sun, Tao; Li, Yu-Xiang; Yu, Jian-Qiang

2016-06-01

Taurine is an abundant amino acid in the nervous system, which has been proved to possess antioxidation, osmoregulation and membrane stabilization. Previously it has been demonstrated that taurine exerts ischemic brain injury protective effect. This study was designed to investigate whether the protective effect of taurine has the possibility to be applied to treat neonatal hypoxic-ischemic brain damage. Seven-day-old Sprague-Dawley rats were treated with left carotid artery ligation followed by exposure to 8% oxygen to generate the experimental group. The cerebral damage area was measured after taurine post-treatment with 2,3,5-triphenyltetrazolium chloride (TTC) staining, Hematoxyline-Eosin (HE) staining and Nissl staining. The activities of superoxide dismutase (SOD), malondialdehyde (MDA), glutathione peroxidase (GSH-Px), total antioxidant capacity (T-AOC), myeloperoxtidase (MPO), ATP and Lactic Acid productions were assayed with ipsilateral hemisphere homogenates. Western-blot and immunofluorescence assay were processed to detect the expressions of AIF, Cyt C, Bax, Bcl-2 in brain. We found that taurine significantly reduced brain infarct volume and ameliorated morphological injury obviously reversed the changes of SOD, MDA, GSH-Px, T-AOC, ATP, MPO, and Lactic Acid levels. Compared with hypoxic-ischemic group, it showed marked reduction of AIF, Cyt C and Bax expressions and increase of Bcl-2 after post-treatment. We conclude that taurine possesses an efficacious neuroprotective effect after cerebral hypoxic-ischemic damage in neonatal rats. Copyright © 2016 Elsevier Inc. All rights reserved.

Screening of subclinical hepatic encephalopathy

NARCIS (Netherlands)

Groeneweg, M; Moerland, W; Quero, J C; Hop, W C; Krabbe, P F; Schalm, S W

BACKGROUND/AIMS: Subclinical hepatic encephalopathy adversely affects daily functioning. The aim of this study was to determine which elements of daily life have predictive value for subclinical hepatic encephalopathy. METHODS: The study was performed in 179 outpatients with liver cirrhosis.

The clinical outcome and neuroimaging of acute encephalopathy after status epilepticus in Dravet syndrome.

Science.gov (United States)

Tian, Xiaojuan; Ye, Jintang; Zeng, Qi; Zhang, Jing; Yang, Xiaoling; Liu, Aijie; Yang, Zhixian; Liu, Xiaoyan; Wu, Xiru; Zhang, Yuehua

2018-06-01

To analyze the clinical outcome and neuroimaging over a long duration follow-up in the currently largest series of acute encephalopathy after status epilepticus in patients with Dravet syndrome. Clinical and neuroimaging data of patients with Dravet syndrome with a history of acute encephalopathy (coma >24h) after status epilepticus from February 2005 to December 2016 at Peking University First Hospital were reviewed retrospectively. Thirty-five patients (15 males, 20 females) with a history of acute encephalopathy were enrolled from a total of 624 patients with Dravet syndrome (5.6%). The median onset age of acute encephalopathy was 3 years 1 month. The duration of status epilepticus varied between 40 minutes to 12 hours. Thirty-four patients had a high fever when status epilepticus occurred, and only one had a normal temperature. Coma lasted from 2 to 20 days. Twelve patients died and 23 survived with massive neurological regression. The median follow-up time was 2 years 1 month. Neuroimaging of 20 out of 23 survivors during the recovery phase showed diverse degrees of cortical atrophy with or without subcortical lesions. Acute encephalopathy after status epilepticus is more prone to occur in patients with Dravet syndrome who had a high fever. The mortality rate is high in severe cases. Survivors are left with severe neurological sequelae but often with either no seizure or low seizure frequency. Acute encephalopathy is more prone to occur in patients with Dravet syndrome with a high fever. The mortality rate is high for acute encephalopathy after status epilepticus in patients with Dravet syndrome. Survivors have neurological sequelae. © 2018 The Authors. Developmental Medicine & Child Neurology published by John Wiley & Sons Ltd on behalf of Mac Keith Press.

Mutations of PTPN23 in developmental and epileptic encephalopathy

KAUST Repository

Sowada, Nadine

2017-10-31

Developmental and epileptic encephalopathies (DEE) are a heterogeneous group of neurodevelopmental disorders with poor prognosis. Recent discoveries have greatly expanded the repertoire of genes that are mutated in epileptic encephalopathies and DEE, often in a de novo fashion, but in many patients, the disease remains molecularly uncharacterized. Here, we describe a new form of DEE in patients with likely deleterious biallelic variants in PTPN23. The phenotype is characterized by early onset drug-resistant epilepsy, severe and global developmental delay, microcephaly, and sometimes premature death. PTPN23 encodes a tyrosine phosphatase with strong brain expression, and its knockout in mouse is embryonically lethal. Structural modeling supports a deleterious effect of the identified alleles. Our data suggest that PTPN23 mutations cause a rare severe form of autosomal-recessive DEE in humans, a finding that requires confirmation.

SCN8A encephalopathy: Research progress and prospects.

Science.gov (United States)

Meisler, Miriam H; Helman, Guy; Hammer, Michael F; Fureman, Brandy E; Gaillard, William D; Goldin, Alan L; Hirose, Shinichi; Ishii, Atsushi; Kroner, Barbara L; Lossin, Christoph; Mefford, Heather C; Parent, Jack M; Patel, Manoj; Schreiber, John; Stewart, Randall; Whittemore, Vicky; Wilcox, Karen; Wagnon, Jacy L; Pearl, Phillip L; Vanderver, Adeline; Scheffer, Ingrid E

2016-07-01

On April 21, 2015, the first SCN8A Encephalopathy Research Group convened in Washington, DC, to assess current research into clinical and pathogenic features of the disorder and prepare an agenda for future research collaborations. The group comprised clinical and basic scientists and representatives of patient advocacy groups. SCN8A encephalopathy is a rare disorder caused by de novo missense mutations of the sodium channel gene SCN8A, which encodes the neuronal sodium channel Nav 1.6. Since the initial description in 2012, approximately 140 affected individuals have been reported in publications or by SCN8A family groups. As a result, an understanding of the severe impact of SCN8A mutations is beginning to emerge. Defining a genetic epilepsy syndrome goes beyond identification of molecular etiology. Topics discussed at this meeting included (1) comparison between mutations of SCN8A and the SCN1A mutations in Dravet syndrome, (2) biophysical properties of the Nav 1.6 channel, (3) electrophysiologic effects of patient mutations on channel properties, (4) cell and animal models of SCN8A encephalopathy, (5) drug screening strategies, (6) the phenotypic spectrum of SCN8A encephalopathy, and (7) efforts to develop a bioregistry. A panel discussion of gaps in bioregistry, biobanking, and clinical outcomes data was followed by a planning session for improved integration of clinical and basic science research. Although SCN8A encephalopathy was identified only recently, there has been rapid progress in functional analysis and phenotypic classification. The focus is now shifting from identification of the underlying molecular cause to the development of strategies for drug screening and prioritized patient care. Wiley Periodicals, Inc. © 2016 International League Against Epilepsy.

Magneto-aerotactic bacteria deliver drug-containing nanoliposomes to tumour hypoxic regions

Science.gov (United States)

Felfoul, Ouajdi; Mohammadi, Mahmood; Taherkhani, Samira; de Lanauze, Dominic; Zhong Xu, Yong; Loghin, Dumitru; Essa, Sherief; Jancik, Sylwia; Houle, Daniel; Lafleur, Michel; Gaboury, Louis; Tabrizian, Maryam; Kaou, Neila; Atkin, Michael; Vuong, Té; Batist, Gerald; Beauchemin, Nicole; Radzioch, Danuta; Martel, Sylvain

2016-11-01

Oxygen-depleted hypoxic regions in the tumour are generally resistant to therapies. Although nanocarriers have been used to deliver drugs, the targeting ratios have been very low. Here, we show that the magneto-aerotactic migration behaviour of magnetotactic bacteria, Magnetococcus marinus strain MC-1 (ref. 4), can be used to transport drug-loaded nanoliposomes into hypoxic regions of the tumour. In their natural environment, MC-1 cells, each containing a chain of magnetic iron-oxide nanocrystals, tend to swim along local magnetic field lines and towards low oxygen concentrations based on a two-state aerotactic sensing system. We show that when MC-1 cells bearing covalently bound drug-containing nanoliposomes were injected near the tumour in severe combined immunodeficient beige mice and magnetically guided, up to 55% of MC-1 cells penetrated into hypoxic regions of HCT116 colorectal xenografts. Approximately 70 drug-loaded nanoliposomes were attached to each MC-1 cell. Our results suggest that harnessing swarms of microorganisms exhibiting magneto-aerotactic behaviour can significantly improve the therapeutic index of various nanocarriers in tumour hypoxic regions.

Can the tyrosine kinase inhibitors trigger metabolic encephalopathy in cirrhotic patients?

Science.gov (United States)

Brandi, Giovanni; de Rosa, Francesco; Calzà, Laura; Girolamo, Stefania Di; Tufoni, Manuel; Ricci, Carmen Serena; Cirignotta, Fabio; Caraceni, Paolo; Biasco, Guido

2013-03-01

Sorafenib is the standard treatment of advanced hepatocarcinoma (HCC) in cirrhotic patients with preserved liver function. It shares many adverse effects with other tyrosine-kinase (TK) inhibitors and antiangiogenic drugs. TK inhibitors could have a direct toxicity on CNS, both by interfering with TK-related pathways and by inhibiting angiogenesis. The aim of this study was to investigate whether sorafenib administration can be associated to metabolic encephalopathy in patients with cirrhosis. We retrospectively reviewed medical records of all cirrhotic patients treated with sorafenib for HCC afferent at our Department from January 2009 to December 2011. Among 62 patients, we identified 10 patients with clinically significant cognitive impairment. Seven of these were clearly diagnosed with overt hepatic encephalopathy (HE), one with brain metastases and two with drug-related toxic-metabolic encephalopathy. These last two cases were characterized by severe cognitive impairment, mood alteration and memory deficit. Clinical exam, blood tests and brain CT excluded organic causes of encephalopathy and precipitating factors of HE. Sorafenib discontinuation was associated with complete reversal of the syndrome, which recurred on drug re-administration in one case. Our study suggests that sorafenib may be a precipitating factor of metabolic encephalopathy in cirrhotic patients with advanced HCC. This neurological syndrome appears to be not responsive to the conventional treatment for HE, but it is fully reversible by drug discontinuation. It can be speculated that the potential direct neuronal action of sorafenib may represent a trigger for the onset of metabolic encephalopathy in a subset of cirrhotic patients. © 2012 John Wiley & Sons A/S.

Hepatic Encephalopathy

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Benefits of starting hypothermia treatment within 6 h vs. 6-12 h in newborns with moderate neonatal hypoxic-ischemic encephalopathy.

Science.gov (United States)

Jia, Wen; Lei, Xiaoping; Dong, Wenbin; Li, Qingping

2018-02-12

It has been suggested that mild hypothermia treatment of hypoxia-ischemic encephalopathy (HIE) should start within 6 h after HIE, but many children are admitted to the hospital > 6 h, particularly in developing areas. We aimed to determine whether hypothermia treatment could remain effective within 12 h after birth. According to their admission, 152 newborns were enrolled in the newborns received conventional treatment combined with mild head hypothermia therapy, according to our routine clinical practice. Some newborns only received conventional treatment (lacking informed consent). All newborns received amplitude-integrated electroencephalography (aEEG) monitoring for 4 h and neuron-specific enolase (NSE) measurement before and after 3 days of therapy. Compared to the conventional treatment, hypothermia significantly improved the aEEG scores and NSE values in all newborns of the newborns with moderate HIE. Hypothermia treatment seems to have no effect in newborns with severe HIE after 6 h (P > 0.05). Hypothermia improved the rates of neonatal death and 18-month disability (all P newborns with moderate HIE, starting hypothermia therapy < 6 h and 6-12 h after HIE showed curative effects. In those with severe HIE, only starting hypothermia therapy within 6 h showed curative effects.

[Star fruit (Averrhoa carambola) toxic encephalopathy].

Science.gov (United States)

Signaté, A; Olindo, S; Chausson, N; Cassinoto, C; Edimo Nana, M; Saint Vil, M; Cabre, P; Smadja, D

2009-03-01

Ingestion of star fruit (Averrhoa carambola) can induce severe intoxication in subjects with chronic renal failure. Oxalate plays a key role in the neurotoxicity of star fruit. We report the cases of two patients with unknown chronic renal insufficiency who developed severe encephalopathy after ingestion of star fruit. The two patients developed intractable hiccups, vomiting, impaired consciousness and status epilepticus. Diffusion-weighted MR imaging showed cortical and thalamic hyperintense lesions related to epileptic status. They improved after being submitted to continuous hemofiltration which constitutes the most effective treatment during the acute phase.

CDKL5 alterations lead to early epileptic encephalopathy in both genders.

Science.gov (United States)

Liang, Jao-Shwann; Shimojima, Keiko; Takayama, Rumiko; Natsume, Jun; Shichiji, Minobu; Hirasawa, Kyoko; Imai, Kaoru; Okanishi, Tohru; Mizuno, Seiji; Okumura, Akihisa; Sugawara, Midori; Ito, Tomoshiro; Ikeda, Hiroko; Takahashi, Yukitoshi; Oguni, Hirokazu; Imai, Katsumi; Osawa, Makiko; Yamamoto, Toshiyuki

2011-10-01

Genetic mutations of the cyclin-dependent kinase-like 5 gene (CDKL5) have been reported in patients with epileptic encephalopathy, which is characterized by intractable seizures and severe-to-profound developmental delay. We investigated the clinical relevance of CDKL5 alterations in both genders. A total of 125 patients with epileptic encephalopathy were examined for genomic copy number aberrations, and 119 patients with no such aberrations were further examined for CDKL5 mutations. Five patients with Rett syndrome, who did not show methyl CpG-binding protein 2 gene (MECP2) mutations, were also examined for CDKL5 mutations. One male and three female patients showed submicroscopic deletions including CDKL5, and two male and six female patients showed CDKL5 nucleotide alterations. Development of early onset seizure was a characteristic clinical feature for the patients with CDKL5 alterations in both genders despite polymorphous seizure types, including myoclonic seizures, tonic seizures, and spasms. Severe developmental delays and mild frontal lobe atrophies revealed by brain magnetic resonance imaging (MRI) were observed in almost all patients, and there was no gender difference in phenotypic features. We observed that 5% of the male patients and 14% of the female patients with epileptic encephalopathy had CDKL5 alterations. These findings indicate that alterations in CDKL5 are associated with early epileptic encephalopathy in both female and male patients. Wiley Periodicals, Inc. © 2011 International League Against Epilepsy.

A case of recurrent encephalopathy with SCN2A missense mutation.

Science.gov (United States)

Fukasawa, Tatsuya; Kubota, Tetsuo; Negoro, Tamiko; Saitoh, Makiko; Mizuguchi, Masashi; Ihara, Yukiko; Ishii, Atsushi; Hirose, Shinichi

2015-06-01

Voltage-gated sodium channels regulate neuronal excitability, as well as survival and the patterning of neuronal connectivity during development. Mutations in SCN2A, which encodes the Na(+) channel Nav1.2, cause epilepsy syndromes and predispose children to acute encephalopathy. Here, we report the case of a young male with recurrent acute encephalopathy who carried a novel missense mutation in the SCN2A gene. He was born by normal delivery and developed repetitive apneic episodes at 2days of age. Diffusion-weighted imaging revealed high-intensity areas in diffuse subcortical white matter, bilateral thalami, and basal nuclei. His symptoms improved gradually without any specific treatment, but he exhibited a motor milestone delay after the episode. At the age of 10months, he developed acute cerebellopathy associated with a respiratory syncytial viral infection. He received high-dose intravenous gammaglobulin and methylprednisolone pulse therapy and seemed to have no obvious sequelae after the episode. He then developed severe diffuse encephalopathy associated with gastroenteritis at the age of 14months. He received high-dose intravenous gammaglobulin and methylprednisolone pulse therapy but was left with severe neurological sequelae. PCR-based analysis revealed a novel de novo missense mutation, c.4979T>G (p.Leu1660Trp), in the SCN2A gene. This case suggests that SCN2A mutations might predispose children to repetitive encephalopathy with variable clinical and imaging findings. Copyright © 2014 The Japanese Society of Child Neurology. Published by Elsevier B.V. All rights reserved.

PREDICTIVE VALUE OF GENERAL MOVEMENTS IN ASPHYXIATED FULL-TERM INFANTS

NARCIS (Netherlands)

PRECHTL, HFR; FERRARI, F; CIONI, G

1993-01-01

The developmental course of spontaneous motility was investigated in a group of 26 fullterm infants, affected by mild to severe hypoxic-ischaemic encephalopathy. Serial 1-h videorecordings were carried out from birth to 15-22 weeks and a quality assessment of general movements (GMs) was made from a

The Clinical Value of Intensive Monitoring in Term Asphyxiated Newborns

NARCIS (Netherlands)

R.M.C. Swarte (Renate)

2010-01-01

textabstractPerinatal asphyxia is an important cause of brain injury. It may lead to hypoxic-ischaemic encephalopathy (HIE) which occurs in one to six of every 1000 full term births. The risk of death or severe handicap is 0.5-2.0 out of 1000. Following intrapartum asphyxia cerebral

"Symptomatic" infection-associated acute encephalopathy in children with underlying neurological disorders.

Science.gov (United States)

Hirayama, Yoshimichi; Saito, Yoshiaki; Maegaki, Yoshihiro

2017-03-01

Development of infection-associated acute encephalopathy (AE) is precipitated by several factors, including viral agents, age, and genetic polymorphisms. In addition, children with prior underlying neurological disorders can also present with AE. We reviewed 55 children with AE who were referred to hospitals participating in the Status Epilepticus Study Group from 1988 to 2013. AE was classified into eight subtypes: acute encephalopathy with biphasic seizures and late reduced diffusion (AESD); hemiconvulsion-hemiplegia syndrome (HH); acute necrotizing encephalopathy; hemorrhagic shock and encephalopathy syndrome (HSES); clinically mild encephalitis/encephalopathy with a reversible splenial lesion; acute encephalitis with refractory, repetitive partial seizures; Reye-like syndrome; and unclassified. Of the 55 AE cases, 14 (25.4%) had underlying neurological disorders, including perinatal insults (n=6) and genetic syndrome and/or brain malformations (n=8). These preceding morbidities were relatively common in AESD (6/18, 33.3%), HH (3/9, 33.3%), and HSES (3/6, 50.0%). History of epilepsy or febrile seizures were frequent in HH cases (4/9, 44.4%), whereas they were rare in other AE subtypes. Among the AE subgroups, HH, HSES, and AESD frequently emerged in preceding etiologies with augmented neuronal excitability. These subgroups may have distinct pathomechanism from the "cytokine storm" mediated AEs during childhood. Copyright © 2016 The Japanese Society of Child Neurology. Published by Elsevier B.V. All rights reserved.

Interleukin-17 limits hypoxia-inducible factor 1α and development of hypoxic granulomas during tuberculosis.

Science.gov (United States)

Domingo-Gonzalez, Racquel; Das, Shibali; Griffiths, Kristin L; Ahmed, Mushtaq; Bambouskova, Monika; Gopal, Radha; Gondi, Suhas; Muñoz-Torrico, Marcela; Salazar-Lezama, Miguel A; Cruz-Lagunas, Alfredo; Jiménez-Álvarez, Luis; Ramirez-Martinez, Gustavo; Espinosa-Soto, Ramón; Sultana, Tamanna; Lyons-Weiler, James; Reinhart, Todd A; Arcos, Jesus; de la Luz Garcia-Hernandez, Maria; Mastrangelo, Michael A; Al-Hammadi, Noor; Townsend, Reid; Balada-Llasat, Joan-Miquel; Torrelles, Jordi B; Kaplan, Gilla; Horne, William; Kolls, Jay K; Artyomov, Maxim N; Rangel-Moreno, Javier; Zúñiga, Joaquín; Khader, Shabaana A

2017-10-05

Mycobacterium tuberculosis (Mtb) is a global health threat, compounded by the emergence of drug-resistant strains. A hallmark of pulmonary tuberculosis (TB) is the formation of hypoxic necrotic granulomas, which upon disintegration, release infectious Mtb. Furthermore, hypoxic necrotic granulomas are associated with increased disease severity and provide a niche for drug-resistant Mtb. However, the host immune responses that promote the development of hypoxic TB granulomas are not well described. Using a necrotic Mtb mouse model, we show that loss of Mtb virulence factors, such as phenolic glycolipids, decreases the production of the proinflammatory cytokine IL-17 (also referred to as IL-17A). IL-17 production negatively regulates the development of hypoxic TB granulomas by limiting the expression of the transcription factor hypoxia-inducible factor 1α (HIF1α). In human TB patients, HIF1α mRNA expression is increased. Through genotyping and association analyses in human samples, we identified a link between the single nucleotide polymorphism rs2275913 in the IL-17 promoter (-197G/G), which is associated with decreased IL-17 production upon stimulation with Mtb cell wall. Together, our data highlight a potentially novel role for IL-17 in limiting the development of hypoxic necrotic granulomas and reducing disease severity in TB.

Diagnostic and prognostic factors for acute encephalopathy.

Science.gov (United States)

Motojima, Yukiko; Nagura, Michiaki; Asano, Yoshitaka; Arakawa, Hiroshi; Takada, Eiko; Sakurai, Yoshio; Moriwaki, Koichi; Tamura, Masanori

2016-11-01

Acute encephalopathy has the possibility of sequelae. While early treatment is required to prevent the development of sequelae, differential diagnosis is of the utmost priority. The aim of this study was therefore to identify parameters that can facilitate early diagnosis and prediction of outcome of acute encephalopathy. We reviewed the medical charts of inpatients from 2005 to 2011 and identified 33 patients with febrile status epilepticus. Subjects were classified into an acute encephalopathy group (n = 20) and a febrile convulsion group (n = 13), and the parameters serum aspartate aminotransferase (AST), alanine aminotransferase (ALT), lactate dehydrogenase (LDH), ammonia (NH 3 ), cerebrospinal fluid (CSF) tau protein, and CSF interleukin-6 compared between them. Furthermore, the relationship between each parameter and prognosis was investigated in the encephalopathy group. Significant differences in serum AST, ALT, and LDH were observed between the febrile convulsion and acute encephalopathy group. Moreover, a significant difference in serum LDH was noted between the patients with and without developmental regression at the time of hospital discharge in the encephalopathy group. In particular, CSF tau protein was found to be highly likely to indicate progress, with CSF tau protein >1000 pg/dL associated with poor prognosis leading to developmental regression. Serum AST, ALT and LDH may be related to early diagnosis and prognosis, and should be carefully investigated in patients with encephalopathy. CSF tau protein could also be used as an indicator of poor prognosis in acute encephalopathy. © 2016 Japan Pediatric Society.

Hypoxic-cell sensitizers

International Nuclear Information System (INIS)

Dische, S.

1983-01-01

There is now 6 years of clinical experience with misonidazole as a hypoxic-cell sensitizer. Neurotoxicity limits the total dose which may be given, and so relatively low concentrations of radiosensitizing drugs are likely to be achieved in hypoxic cells in man as compared with those in animal tumors. It is likely that benefit will only be shown in those situations where radioresistant hypoxic cells strongly dominate as a cause of radiation failure. Many clinical trials are underway, and thus far some show no benefit while in others there is a definite advantage to the patients given the drug. These trials must be continued to their conclusion, but misonidazole must be regarded as the first of a series of radiosensitizers to reach the clinic for trial. There is a promise of more effective drugs becoming available within the next few years. Those showing a lower lipophilicity than misonidazole have been found to have a shorter half-life and a lower uptake in neural tissue in animal studies. One such drug, desmethylmisonidazole, is presently undergoing clinical trial

Mutations in UNC80, Encoding Part of the UNC79-UNC80-NALCN Channel Complex, Cause Autosomal-Recessive Severe Infantile Encephalopathy

Science.gov (United States)

Shamseldin, Hanan E.; Faqeih, Eissa; Alasmari, Ali; Zaki, Maha S.; Gleeson, Joseph G.; Alkuraya, Fowzan S.

2016-01-01

Brain channelopathies represent a growing class of brain disorders that usually result in paroxysmal disorders, although their role in other neurological phenotypes, including the recently described NALCN-related infantile encephalopathy, is increasingly recognized. In three Saudi Arabian families and one Egyptian family all affected by a remarkably similar phenotype (infantile encephalopathy and largely normal brain MRI) to that of NALCN-related infantile encephalopathy, we identified a locus on 2q34 in which whole-exome sequencing revealed three, including two apparently loss-of-function, recessive mutations in UNC80. UNC80 encodes a large protein that is necessary for the stability and function of NALCN and for bridging NALCN to UNC79 to form a functional complex. Our results expand the clinical relevance of the UNC79-UNC80-NALCN channel complex. PMID:26708753

Hypoxic cell turnover in different solid tumor lines

International Nuclear Information System (INIS)

Ljungkvist, Anna S.E.; Bussink, Johan; Kaanders, Johannes H.A.M.; Rijken, Paulus F.J.W.; Begg, Adrian C.; Raleigh, James A.; Kogel, Albert J. van der

2005-01-01

Purpose: Most solid tumors contain hypoxic cells, and the amount of tumor hypoxia has been shown to have a negative impact on the outcome of radiotherapy. The efficacy of combined modality treatments depends both on the sequence and timing of the treatments. Hypoxic cell turnover in tumors may be important for optimal scheduling of combined modality treatments, especially when hypoxic cell targeting is involved. Methods and Materials: Previously we have shown that a double bioreductive hypoxic marker assay could be used to detect changes of tumor hypoxia in relation to the tumor vasculature after carbogen and hydralazine treatments. This assay was used in the current study to establish the turnover rate of hypoxic cells in three different tumor models. The first hypoxic marker, pimonidazole, was administered at variable times before tumor harvest, and the second hypoxic marker, CCI-103F, was injected at a fixed time before harvest. Hypoxic cell turnover was defined as loss of pimonidazole (first marker) relative to CCI-103F (second marker). Results: The half-life of hypoxic cell turnover was 17 h in the murine C38 colon carcinoma line, 23 h and 49 h in the human xenograft lines MEC82 and SCCNij3, respectively. Within 24 h, loss of pimonidazole-stained areas in C38 and MEC82 occurred concurrent with the appearance of pimonidazole positive cell debris in necrotic regions. In C38 and MEC82, most of the hypoxic cells had disappeared after 48 h, whereas in SCCNij3, viable cells that had been labeled with pimonidazole were still observed after 5 days. Conclusions: The present study demonstrates that the double hypoxia marker assay can be used to study changes in both the proportion of hypoxic tumor cells and their lifespan at the same time. The present study shows that large differences in hypoxic cell turnover rates may exist among tumor lines, with half-lives ranging from 17-49 h

Diagnostic criterions of the postradiation encephalopathy in remote period of the acute radiation syndrome

International Nuclear Information System (INIS)

Nyagu, A.I.; Loganovskij, K.N.; Vashchenko, E.A.

1998-01-01

Development of post-radiation encephalopathy diagnostic criteria on the base of neuro psychic, neuro- and psychofisiological research in patients who suffered with acute radiation disease after Chernobyl catastrophe was the aim of this work. 110 persons of 20-75 years age were investigated. 55 refs., 6 tab., 6 figs

Hashimoto's encephalopathy

DEFF Research Database (Denmark)

Montagna, Giacomo; Imperiali, Mauro; Agazzi, Pamela

2016-01-01

Hashimoto's encephalopathy (HE) is a rare not well understood, progressive and relapsing multiform disease, characterized by seizures, movement disorders, subacute cognitive dysfunction, psychiatric symptoms and responsiveness to steroid therapy. The disorder is generally associated with thyroid ...... diseases and the most common feature is the presence of anti-thyroperoxidase antibodies (TPOAb). Patients are usually euthyroid or mildly hypothyroid at presentation. All age groups can be affected. The pathophysiology is still unclear, especially the link between elevated serum TPOAb...... and the encephalopathy. Most reported cases occurred in women and girls. Unspecific symptoms, non-pathognomonic laboratory neurophysiology and neuroimaging features make its diagnosis a real challenge for clinicians.The case of a 16 year old boy, with a clinical picture of HE associated with hypothyroidism...

Hypoxic survival strategies in two fishes: extreme anoxia tolerance in the North European crucian carp and natural hypoxic preconditioning in a coral-reef shark.

Science.gov (United States)

Nilsson, Göran E; Renshaw, Gillian M C

2004-08-01

Especially in aquatic habitats, hypoxia can be an important evolutionary driving force resulting in both convergent and divergent physiological strategies for hypoxic survival. Examining adaptations to anoxic/hypoxic survival in hypoxia-tolerant animals may offer fresh ideas for the treatment of hypoxia-related diseases. Here, we summarise our present knowledge of two fishes that have evolved to survive hypoxia under very different circumstances. The crucian carp (Carassius carassius) is of particular interest because of its extreme anoxia tolerance. During the long North European winter, it survives for months in completely oxygen-deprived freshwater habitats. The crucian carp also tolerates a few days of anoxia at room temperature and, unlike anoxia-tolerant freshwater turtles, it is still physically active in anoxia. Moreover, the crucian carp does not appear to reduce neuronal ion permeability during anoxia and may primarily rely on more subtle neuromodulatory mechanisms for anoxic metabolic depression. The epaulette shark (Hemiscyllium ocellatum) is a tropical marine vertebrate. It lives on shallow reef platforms that repeatedly become cut off from the ocean during periods of low tides. During nocturnal low tides, the water [O(2)] can fall by 80% due to respiration of the coral and associated organisms. Since the tides become lower and lower over a period of a few days, the hypoxic exposure during subsequent low tides will become progressively longer and more severe. Thus, this shark is under a natural hypoxic preconditioning regimen. Interestingly, hypoxic preconditioning lowers its metabolic rate and its critical P(O(2)). Moreover, repeated anoxia appears to stimulate metabolic depression in an adenosine-dependent way.

Cardiac biomarkers in neonatal hypoxic ischaemia.

LENUS (Irish Health Repository)

Sweetman, D

2012-04-01

Following a perinatal hypoxic-ischaemic insult, term infants commonly develop cardiovascular dysfunction. Troponin-T, troponin-I and brain natriuretic peptide are sensitive indicators of myocardial compromise. The long-term effects of cardiovascular dysfunction on neurodevelopmental outcome following perinatal hypoxic ischaemia remain controversial. Follow-up studies are warranted to ensure optimal cardiac function in adulthood. CONCLUSION: Cardiac biomarkers may improve the diagnosis of myocardial injury, help guide management, estimate mortality risk and may also aid in longterm neurodevelopmental outcome prediction following neonatal hypoxic-ischaemia.

Wernicke’s encephalopathy following hyperemesis gravidarum: A case report

Directory of Open Access Journals (Sweden)

leila pourali

2016-06-01

Full Text Available Introduction: Wernicke’s Korsakoff syndrome is the most important complication of severe thiamine deficiency. Confusion and gait ataxia are the most prevalent symptoms, respectively. The aim of this study was report of a case of Wernicke’s encephalopathy following hyperemesis gravidarum. Case report: A 28-years-old pregnant woman in 19th weeks of gestation referred to the hospital with hyperemesis, gait ataxia, and dysarthria. MRI showed hyperdense lesion which was characteristic of wernicke’s encephalopathy. Rapid improvement in patient’s condition occurred after thiamine infusion. Conclusion: In hyperemesis gravidarum, presence of either symptoms of ocular or mental disorder or ataxia must be considered to rull out Wernicke’s syndrome which can cause maternal death.

Association between Helicobacter pylori seropositivity and Hepatic Encephalopathy

International Nuclear Information System (INIS)

Behroozian, R.; Faramarzpur, M.; Rahimi, E.

2010-01-01

Objective: The knowledge on Helicobacter pylori (H. pylori) contribution in the pathology of the liver and biliary tract diseases in human is very limited. The aim of this study was to assess the probable association between H. pylori seropositivity and hepatic encephalopathy. Methodology: This is a case control study conducted through three groups, cirrhotics with hepatic encephalopathy (HE), cirrhotics without HE and healthy controls. All subjects were examined serologically for determination of IgG class antibodies to H. pylori based on ELISA technique. Results: H. pylori seropositivity was present in 88% cirrhotic patients with hepatic encephalopathy, 86% cirrhotics without hepatic encephalopathy and 66% healthy controls. Conclusion: According to our results, H. pylori seropositivity rate in cirrhotic patients with or without hepatic encephalopathy was higher than healthy controls. But H. pylori seropositivity rate was not significantly different among cirrhotics with hepatic encephalopathy and those without it.

Hepatic Encephalopathy

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Benzodiazepine receptor antagonists for acute and chronic hepatic encephalopathy

DEFF Research Database (Denmark)

Als-Nielsen, B; Kjaergard, L L; Gluud, C

2001-01-01

The pathogenesis of hepatic encephalopathy is unknown. It has been suggested that liver failure leads to the accumulation of substances that bind to a receptor-complex in the brain resulting in neural inhibition which may progress to coma. Several trials have assessed benzodiazepine receptor...

Metronidazole-induced encephalopathy in a patient with liver cirrhosis.

Science.gov (United States)

Cheong, Hyeong Cheol; Jeong, Taek Geun; Cho, Young Bum; Yang, Bong Joon; Kim, Tae Hyeon; Kim, Haak Cheoul; Cho, Eun-Young

2011-06-01

Encephalopathy is a disorder characterized by altered brain function, which can be attributed to various causes. Encephalopathy associated with metronidazole administration occurs rarely and depends on the cumulative metronidazole dose, and most patients with this condition recover rapidly after discontinuation of therapy. Because metronidazole is metabolized in the liver and can be transported by the cerebrospinal fluid and cross the blood-brain barrier, it may induce encephalopathy even at a low cumulative dose in patients with hepatic dysfunction. We experienced a patient who showed ataxic gait and dysarthric speech after receiving metronidazole for the treatment of hepatic encephalopathy that was not controlled by the administration of lactulose. The patient was diagnosed as metronidazole-induced encephalopathy, and stopping drug administration resulted in a complete recovery from encephalopathy. This case shows that caution should be exercised when administering metronidazole because even a low dose can induce encephalopathy in patients with liver cirrhosis.

Application of rare variant transmission disequilibrium tests to epileptic encephalopathy trio sequence data

DEFF Research Database (Denmark)

2017-01-01

The classic epileptic encephalopathies, including infantile spasms (IS) and Lennox-Gastaut syndrome (LGS), are severe seizure disorders that usually arise sporadically. De novo variants in genes mainly encoding ion channel and synaptic proteins have been found to account for over 15% of patients...... with IS or LGS. The contribution of autosomal recessive genetic variation, however, is less well understood. We implemented a rare variant transmission disequilibrium test (TDT) to search for autosomal recessive epileptic encephalopathy genes in a cohort of 320 outbred patient-parent trios that were generally...... not find evidence of a role for individual autosomal recessive genes, our current sample is insufficiently powered to assess the overall role of autosomal recessive genotypes in an outbred epileptic encephalopathy population....

[Subacute encephalopathy with epileptic seizures in an alcoholic patient].

Science.gov (United States)

Kozian, R; Otto, F G

2000-09-01

We introduce a case of a 66 year-old male with chronic alcoholism who suffered from confusion, Wernicke-aphasia and epileptic seizures. Several EEG revealed periodic lateralized epileptiform discharges. The patient's case resembles the symptoms of a subacute encephalopathy with epileptic seizures which can occur in alcoholics.

Hepatic encephalopathy. Imaging Findings

International Nuclear Information System (INIS)

Carrillo, Maria Claudia; Bermudez Munoz, Sonia; J Morillo, Anibal

2007-01-01

Hepatic encephalopathy occurs in patients with chronic hepatic insufficiency and can produce abnormalities in the central nervous system, which can be observed in MRI studies. Traditionally, these imaging findings include symmetrical hyper intensities in T1-weighted sequences in the basal ganglia (mainly globus pallidus), involving also the substantia nigra, mesencephalic tegmentum, frontal and occipital cortex. These areas appear of normal intensity in T2-weighted imaging sequences. Other entities that can lead to similar findings include manganese intoxication and type-1 neurofibromatosis. Currently, with the advent of MR spectroscopy, abnormalities in patients with clinical and subclinical hepatic encephalopathy have been described. After hepatic transplantation, hyper intensities of the basal ganglia and the MR spectroscopic findings may disappear within 3 months to 1 year, suggesting a functional, more than a structural damage. This article will demonstrate the MR findings of patients with hepatic encephalopathy due to chronic hepatic insufficiency.

Hepatic Encephalopathy

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Full Text Available ... to continue to work to my full capacity? Will I be able to drive? Patient Stories Angie M. Caregiver for Brother Charles DiAngelo Hepatic Encephalopathy Jason Dedmon Alcohol-related Cirrhosis ...

Hepatic Encephalopathy

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Full Text Available ... responsible for the daily needs of another person. Caregivers can be a friend, spouse, life partner, parent, sibling or other family member. What is HE? Hepatic Encephalopathy, sometimes referred to as ...

Computerized tomography in acute toxic encephalopathy

International Nuclear Information System (INIS)

Aoki, Nobuhiko; Kaneshi, Kunio; Mizuguchi, Masashi; Kurihara, Eiji.

1983-01-01

We experienced three cases of acute toxic encephalopathy, including a case of probable Reye syndrome, which had similar and unique CT findings in their acute stage; symmetrical low density area in the thalamus and the dentate nucleus, followed by changes in cerebellar hemispheres and around lateral ventricles. The CT findings, common to probable Reye syndrome and other acute toxic encephalopathy, may suggest the possibility of similar pathogenesis of brain damage in both disorders. The authors propose that present cases are a new subgroup in acute toxic encephalopathy, because of their similar and unique CT features. (author)

Hepatic Encephalopathy

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Full Text Available ... to Treatment Who treats HE? Preparing for your Medical Appointment Hepatic Encephalopathy Treatment Options Treatment Basics Treatment ... treatment. Being a fully-informed participant in your medical care is an important factor in staying as ...

Hepatic Encephalopathy

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Full Text Available ... your body when your liver isn’t working well, it may affect your brain and cause HE. ... it apparent that the liver is not doing well. These could be the symptoms of Hepatic Encephalopathy ( ...

Hepatic Encephalopathy

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Full Text Available ... build-up and painful swelling of the legs (edema) and abdomen (ascites) or hepatic encephalopathy. For more ... build up and painful swelling of the legs (edema) and abdomen (ascites) Bruising and bleeding easily Enlarged ...

Hepatic Encephalopathy

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Full Text Available ... People ALF Near You Events ALF Blogs Financial Information Policies Advocacy Patient Advisory Council Media Center Careers ... and abdomen (ascites) or hepatic encephalopathy. For more information about cirrhosis of the liver and symptoms, call ...

Hepatic Encephalopathy

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Full Text Available ... Your Story Spread the Word Give While You Shop Contact Us Donate Now Hepatic Encephalopathy Back Hepatic ... Your Story Spread the Word Give While You Shop Contact Us Donate Now Help ALF Improve This ...

Hepatic Encephalopathy

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Full Text Available ... Related Liver Disease Alpha-1 Antitrypsin Deficiency Autoimmune Hepatitis Benign Liver Tumors Biliary Atresia Cirrhosis of the ... Disease Type 1 (von Gierke) Hemochromatosis Hepatic Encephalopathy Hepatitis A Hepatitis B Hepatitis C Intrahepatic Cholestasis of ...

Hepatic Encephalopathy

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Full Text Available ... Patient Advisory Council Media Center Careers How You Can Help OVERVIEW Donate Now Join an Event Volunteer ... Hepatic Encephalopathy is a short-term problem that can be corrected . It may also occur as part ...

Hepatic Encephalopathy

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Full Text Available ... Hemochromatosis Hepatic Encephalopathy Hepatitis A Hepatitis B Hepatitis C Intrahepatic Cholestasis of Pregnancy (ICP) Jaundice In Newborns ... are the common causes of cirrhosis? Hepatitis B & C Alcohol-related Liver Disease Non-alcoholic Fatty Liver ...

Hepatic Encephalopathy

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Full Text Available ... friend, spouse, life partner, parent, sibling or other family member. What is HE? Hepatic Encephalopathy, sometimes referred ... disease is. It’s important for you and your family to become familiar with the signs of Hepatic ...

Hepatic Encephalopathy

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Full Text Available ... important for you and your family to become familiar with the signs of Hepatic Encephalopathy so you ... team evaluates the person’s overall physical and mental health, plan to pay for transplant related medical expenses, ...

Hepatic Encephalopathy

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Full Text Available ... become familiar with the signs of Hepatic Encephalopathy so you can tell your doctor right away if ... with continuous treatment, HE can usually be controlled. So it’s important to tell your doctor about any ...

Hepatic Encephalopathy

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Full Text Available ... Hepatic Encephalopathy so you can tell your doctor right away if you think you may have it. ... Site Map © COPYRIGHT 2017 AMERICAN LIVER FOUNDATION. ALL RIGHTS RESERVED. Your Liver Overview

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Hepatic Encephalopathy

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Full Text Available ... Hepatic Encephalopathy Treatment Options Treatment Basics Treatment Medications Importance of Adhering to Your Treatment Plan Long-Term Considerations Patient Support Finding Support Services Peer Support Groups Financial Assistance Support for My Loved Ones Resources Find ...

Anti-hypoxic activity of the ethanol extract from Portulaca oleracea in mice.

Science.gov (United States)

Chen, Cheng-Jie; Wang, Wan-Yin; Wang, Xiao-Li; Dong, Li-Wei; Yue, Yi-Tian; Xin, Hai-Liang; Ling, Chang-Quan; Li, Min

2009-07-15

To investigate the effects of the ethanol extract from Portulaca oleracea (EEPO) on hypoxia models mice and to find the possible mechanism of its anti-hypoxic actions so as to elucidate the anti-hypoxia activity and provide scientific basis for the clinical use of Portulaca oleracea. EEPO was evaluated on anti-hypoxic activity in several hypoxia mice models, including closed normobaric hypoxia and sodium nitrite or potassium cyanide toxicosis. To verify the possible mechanism(s), we detected the activities of pyruvate kinase (PK), phosphofructokinase (PFK), lactate dehydrogenase (LDH) and the level of adenosine triphosphate (ATP) in mice cortices. Given orally, the EEPO at doses of 100, 200, 400 mg/kg could dose-dependently enhance the survival time of mice in both of the normobaric and chemical hypoxia models. The activity of the glycolysis enzymes and the level of ATP were higher than those of the control. In the pentobarbital sodium-induced sleeping time test and the open-field test, EEPO neither significantly enhanced the pentobarbital sodium-induced sleeping time nor impaired the motor performance, indicating that the observed anti-hypoxic activity was unlikely due to sedation or motor abnormality. These results demonstrated that the EEPO possessed notable anti-hypoxic activity, which might be related to promoting the activity of the key enzymes in glycolysis and improving the level of ATP in hypoxic mice.

Qualifying and quantifying minimal hepatic encephalopathy

DEFF Research Database (Denmark)

Morgan, Marsha Y; Amodio, Piero; Cook, Nicola A

2016-01-01

Minimal hepatic encephalopathy is the term applied to the neuropsychiatric status of patients with cirrhosis who are unimpaired on clinical examination but show alterations in neuropsychological tests exploring psychomotor speed/executive function and/or in neurophysiological variables. There is ......Minimal hepatic encephalopathy is the term applied to the neuropsychiatric status of patients with cirrhosis who are unimpaired on clinical examination but show alterations in neuropsychological tests exploring psychomotor speed/executive function and/or in neurophysiological variables...... analytical techniques may provide better diagnostic information while the advent of portable wireless headsets may facilitate more widespread use. A large number of other diagnostic tools have been validated for the diagnosis of minimal hepatic encephalopathy including Critical Flicker Frequency......, the Inhibitory Control Test, the Stroop test, the Scan package and the Continuous Reaction Time; each has its pros and cons; strengths and weaknesses; protagonists and detractors. Recent AASLD/EASL Practice Guidelines suggest that the diagnosis of minimal hepatic encephalopathy should be based on the PHES test...

Chronic traumatic encephalopathy: The unknown disease.

Science.gov (United States)

Martínez-Pérez, R; Paredes, I; Munarriz, P M; Paredes, B; Alén, J F

2017-04-01

Chronic traumatic encephalopathy is a neurodegenerative disease produced by accumulated minor traumatic brain injuries; no definitive premortem diagnosis and no treatments are available for chronic traumatic encephalopathy. Risk factors associated with chronic traumatic encephalopathy include playing contact sports, presence of the apolipoprotein E4, and old age. Although it shares certain histopathological findings with Alzheimer disease, chronic traumatic encephalopathy has a more specific presentation (hyperphosphorylated tau protein deposited as neurofibrillary tangles, associated with neuropil threads and sometimes with beta-amyloid plaques). Its clinical presentation is insidious; patients show mild cognitive and emotional symptoms before progressing to parkinsonian motor signs and finally dementia. Results from new experimental diagnostic tools are promising, but these tools are not yet available. The mainstay of managing this disease is prevention and early detection of its first symptoms. Copyright © 2014 Sociedad Española de Neurología. Publicado por Elsevier España, S.L.U. All rights reserved.

Hepatic Encephalopathy

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Hepatic Encephalopathy

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Full Text Available ... bad. It sends the good things – such as vitamins and nutrients – into your bloodstream for your body ... for Wife Joyce O. Caregiver for Mother Lynette K. Hepatic Encephalopathy Samantha W. Caregiver for Husband Stan ...

Hepatic Encephalopathy

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Full Text Available ... 1 (von Gierke) Hemochromatosis Hepatic Encephalopathy Hepatitis A Hepatitis B Hepatitis C Intrahepatic Cholestasis of Pregnancy (ICP) Jaundice ... diseases. What are the common causes of cirrhosis? Hepatitis B & C Alcohol-related Liver Disease Non-alcoholic Fatty ...

Hyperammonemia: What Urea-lly Need to Know: Case Report of Severe Noncirrhotic Hyperammonemic Encephalopathy and Review of the Literature

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Ruby Upadhyay

2016-01-01

Full Text Available Purpose. A 66-year-old man who presented with coma was found to have isolated severe hyperammonemia and diagnosed with a late-onset urea-cycle disorder. He was treated successfully and had full recovery. Methods. We report a novel case of noncirrhotic hyperammonemia and review the literature on this topic. Selected literature for review included English-language articles concerning hyperammonemia using the search terms “hyperammonemic encephalopathy”, “non-cirrhotic encephalopathy”, “hepatic encephalopathy”, “urea-cycle disorders”, “ornithine transcarbamylase (OTC deficiency”, and “fulminant hepatic failure”. Results. A unique case of isolated hyperammonemia diagnosed as late-onset OTC deficiency is presented. Existing evidence about hyperammonemia is organized to address pathophysiology, clinical presentation, diagnosis, and treatment. The case report is discussed in context of the reviewed literature. Conclusion. Late-onset OTC deficiency presenting with severe hyperammonemic encephalopathy and extensive imaging correlate can be fully reversible if recognized promptly and treated aggressively.

Hypoxic training: Clinical benefits on cardiometabolic risk factors.

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Wee, Justin; Climstein, Mike

2015-01-01

The main aim of this review was to evaluate the effectiveness of hypoxic training on the modulation of cardiometabolic risk factors. Literature review. An electronic search encompassing five databases (PUBMED, EMBASE, MEDLINE, CINAHL, and SPORTDiscus) was conducted. A total of 2138 articles were retrieved. After excluding non-relevant articles, duplications and outcomes not related to cardiometabolic risk factors, 25 articles were chosen for review. Body weight and body composition were reported to be significantly improved when hypoxic training (≥1700 m) was used in conjunction with exercise regimes, at least three times a week, however extreme altitudes (>5000 m) resulted in a loss of fat-free muscle mass. Fasting blood glucose levels generally improved over time (≥21 days) at moderate levels of altitude (1500 m-3000 m), although reductions in blood glucose tolerance were observed when subjects were exposed to extreme hypoxia (>4000 m). Resting systolic and diastolic blood pressure levels improved as much as 26 mmHg and 13 mmHg respectively, with hypoxic training (1285 m-2650 m) in medicated, stable hypertensive subjects. Effects of hypoxic training when used in combination with exercise training on cholesterol levels were mixed. While there were improvements in total cholesterol (-4.2% to -30%) and low-density lipoprotein (-2.6% to -14.3%) reported as a result of hypoxic training, available evidence does not substantiate hypoxic training for the improvement of high-density lipoprotein and triglycerides. In conclusion, hypoxic training may be used as an adjunct treatment to modify some cardiometabolic risk factors. Measurement of hypoxic load may be used to individualize and ascertain appropriate levels of hypoxic training. Copyright © 2013 Sports Medicine Australia. Published by Elsevier Ltd. All rights reserved.

Occipital lobe epilepsy secondary to posterior reversible encephalopathy syndrome (PRES) during a post-partum eclampsia in Mali (West Africa).

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Youssoufa, Maïga; Callixte, Kuate Tegueu; Christian, Napon

2013-08-13

Eclampsia is known to cause posterior reversible encephalopathy syndrome (PRES) that is often associated with an extensive neurovascular damage affecting preferably posterior regions, often leading to reversible cortical blindness. In spite the magnitude of these lesions, post eclamptic symptomatic epilepsy is rare. We therefore report a case of symptomatic occipital lobe epilepsy secondary to PRES. A 39-year-old female right handed teacher who presented with headache of progressive onset, phosphenes, rapid decline of visual acuity to blindness, vomiting, repeated generalized tonic-clonic seizures followed by altered consciousness and very high blood pressure (HBP) of 240/120 mmHg, all of which started about 12 hours following a normal delivery. Nine months later, the patient presented with paroxysmal visual symptoms predominating in the right visual field followed by partial tonic clonic seizures with secondary generalization and recurrence of partial occipital lobe seizures. The pathophysiologic mechanism of irreversible tissue damage during PRES syndrome could result from a combination of events including the delay for early treatment, inadequate antihypertensive drugs that could worsen the brain damage by hypo perfusion, inadequate or delayed treatment for seizures or status epilepticus. Despite its high incidence in the third world, eclampsia is not a usual cause of epilepsy. Our case is the first description of post eclamptic occipital lobe epilepsy in Africa. With this report, we draw practitioners' attention on this rare complication.

MRI finding of ethylmalonic encephalopathy: case report

International Nuclear Information System (INIS)

Kim, Jin Yong; Lee, Shi Kyung; Han, Chun Hwan; Rho, Eun Jin

2002-01-01

Ethylmalonic encephalopathy is a rare syndrom characterized by developmental delay, acrocyanosis, petechiae, chronic diarrhea, and ethylmalonic, lactic, and methylsuccinic aciduria. We report the MRI finding of ethylmalonic encephalopathy including previously unreported intracranial hematoma

Hyperammonemic encephalopathy due to suture line breakdown after bladder operation.

Science.gov (United States)

Boogerd, W; Zoetmulder, F A; Moffie, D

1990-01-01

A patient is described with a severe encephalopathy and hyperammonemia in absence of liver dysfunction, attributed to urine absorption into the systemic circulation due to suture line breakdown after bladder dome resection. At autopsy characteristic Alzheimer type II astrocytes were found in the basal ganglia.

Time Domains of the Hypoxic Ventilatory Response and Their Molecular Basis

Science.gov (United States)

Pamenter, Matthew E.; Powell, Frank L.

2016-01-01

Ventilatory responses to hypoxia vary widely depending on the pattern and length of hypoxic exposure. Acute, prolonged, or intermittent hypoxic episodes can increase or decrease breathing for seconds to years, both during the hypoxic stimulus, and also after its removal. These myriad effects are the result of a complicated web of molecular interactions that underlie plasticity in the respiratory control reflex circuits and ultimately control the physiology of breathing in hypoxia. Since the time domains of the physiological hypoxic ventilatory response (HVR) were identified, considerable research effort has gone toward elucidating the underlying molecular mechanisms that mediate these varied responses. This research has begun to describe complicated and plastic interactions in the relay circuits between the peripheral chemoreceptors and the ventilatory control circuits within the central nervous system. Intriguingly, many of these molecular pathways seem to share key components between the different time domains, suggesting that varied physiological HVRs are the result of specific modifications to overlapping pathways. This review highlights what has been discovered regarding the cell and molecular level control of the time domains of the HVR, and highlights key areas where further research is required. Understanding the molecular control of ventilation in hypoxia has important implications for basic physiology and is emerging as an important component of several clinical fields. PMID:27347896

[The bioelectric activity of the brain in dyscirculatory encephalopathy and arterial hypertension developed in the Chernobyl nuclear disaster liquidators].

Science.gov (United States)

Podsonnaia, I V; Efremushkin, G G; Zhelobetskaia, E D

2012-01-01

The long-term effects of the ionizing radiation on the bioelectric brain activity in the Chernobyl nuclear disaster liquidators with discirculatory encephalopathy and arterial hypertension were studied. We examined 195 male patients, aged from 30 to 65 years, with the clinical presentations of discirculatory encephalopathy, using electroencephalography: 105 patients were liquidators of the Chernobyl nuclear disaster (the main group) and 90 patients had no radiation anamnesis (the comparison group). It has been found that the development of discirculatory encephalopathy in liquidators of the Chernobyl nuclear disaster is mainly associated with the dysfunction of diencephalic and cortical structures. The specificity of the neurofunctional brain abnormalities in liquidators with discirculatory encephalopathy is characterized by the predominance of the low-amplitude and low-frequency alpha-activity or by the lack of alpha-rhythm and by its substitution for the high-frequency beta-rhythm with the presence of theta- and delta-activity and by the more significant flatness of the alpha-rhythm zonation. The presence of the radiation factor in the past history is correlated with the failure of the bioelectric brain activity in the alpha band (r=0.42) that increases risk of abnormal changes by a factor of 10 (pChernobyl nuclear disaster in the post-radiation period during the development of discirculatory encephalopathy and arterial hypertension.

Seizure characteristics of epilepsy in childhood after acute encephalopathy with biphasic seizures and late reduced diffusion.

Science.gov (United States)

Ito, Yuji; Natsume, Jun; Kidokoro, Hiroyuki; Ishihara, Naoko; Azuma, Yoshiteru; Tsuji, Takeshi; Okumura, Akihisa; Kubota, Tetsuo; Ando, Naoki; Saitoh, Shinji; Miura, Kiyokuni; Negoro, Tamiko; Watanabe, Kazuyoshi; Kojima, Seiji

2015-08-01

The aim of this study was to clarify characteristics of post-encephalopathic epilepsy (PEE) in children after acute encephalopathy with biphasic seizures and late reduced diffusion (AESD), paying particular attention to precise diagnosis of seizure types. Among 262 children with acute encephalopathy/encephalitis registered in a database of the Tokai Pediatric Neurology Society between 2005 and 2012, 44 were diagnosed with AESD according to the clinical course and magnetic resonance imaging (MRI) findings and were included in this study. Medical records were reviewed to investigate clinical data, MRI findings, neurologic outcomes, and presence or absence of PEE. Seizure types of PEE were determined by both clinical observation by pediatric neurologists and ictal video-electroencephalography (EEG) recordings. Of the 44 patients after AESD, 10 (23%) had PEE. The period between the onset of encephalopathy and PEE ranged from 2 to 39 months (median 8.5 months). Cognitive impairment was more severe in patients with PEE than in those without. Biphasic seizures and status epilepticus during the acute phase of encephalopathy did not influence the risk of PEE. The most common seizure type of PEE on clinical observation was focal seizures (n = 5), followed by epileptic spasms (n = 4), myoclonic seizures (n = 3), and tonic seizures (n = 2). In six patients with PEE, seizures were induced by sudden unexpected sounds. Seizure types confirmed by ictal video-EEG recordings were epileptic spasms and focal seizures with frontal onset, and all focal seizures were startle seizures induced by sudden acoustic stimulation. Intractable daily seizures remain in six patients with PEE. We demonstrate seizure characteristics of PEE in children after AESD. Epileptic spasms and startle focal seizures are common seizure types. The specific seizure types may be determined by the pattern of diffuse subcortical white matter injury in AESD and age-dependent reorganization of the brain

Hypoxic hypoxia as a means of modifying radiosensibility

International Nuclear Information System (INIS)

Neumeister, K.; Niemiec, C.; Bolck, M.; Jahns, J.; Kamprad, F.; Arnold, P.; Johannsen, U.; Koch, F.; Mehlhorn, G.

1977-01-01

Following an overview of the various possibilities of creating hypoxia in mammals, the problem of reducing radioresistance of hypoxic tumor cells is treated. Furthermore, the results of irradiation experiments with mice, rats and pigs breathing hypoxic mixtures of O 2 and N 2 are given and discussed with a view to applying hypoxic hypoxia in the radiotherapy of human tumors. (author)

Radioresistance and hypoxic cells

International Nuclear Information System (INIS)

Ando, Koichi

1989-01-01

Current progress to explore further understanding of tumor hypoxia was reviewed. At subcellular level, hypoxia induces specific proteins, inhibits DNA synthesis as well as initiation of DNA replicon. Radioresistant characteristics of hypoxic cells is questioned in condition where irradiated cells were kept hypoxia during colony formation. Chronically hypoxic cells recovered from the inner layer of V79 multicellular spheroids are more sensitive to radiation than those from the oxic, outer layer. A novel sandwich culture method, which enables to reoxygenate chronic hypoxia, implies that chronically hypoxic cells are less sensitive to radiation after reoxygenation than oxic cells. For in vivo tumor, two types of tumor hypoxia are reported: diffusion-limited, chronic hypoxia and perfusion-limited, acute hypoxia. Evidence supporting the existence of perfusion-limited hypoxia is provided by an elegant method using vital staining and cell sorter. Data of our own laboratory also implies 2 types of tumor hypoxia; fractional hypoxia and incomplete hypoxia. Fractional hypoxia corresponds to a radioresistant tail on a biphasic tumor cell survival curves while tumors with incomplete hypoxia demonstrate only single component with radioresistant characteristics, instead. (author)

Malignant hypertension and hypertensive encephalopathy in primary aldosteronism caused by adrenal adenoma

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Bortolotto Luiz Aparecido

2003-01-01

Full Text Available Two cases are reported as follows: 1 1 female patient with accelerated-malignant hypertension secondary to an aldosterone-producing adrenal adenoma; and 2 1 female patient with adrenal adenoma, severe hypertension, and hypertensive encephalopathy. This association is a rare clinical finding, and malignant hypertension may modify the hormonal characteristic of primary aldosteronism, making its diagnosis more difficult. The diagnosis of primary aldosteronism should be considered in patients with malignant hypertension or hypertensive encephalopathy if persistent hypokalemia occurs. Identification of primary aldosteronism is of paramount importance for the patient's evolution, because the surgical treatment makes the prognosis more favorable.

The potential of erythropoietin to treat asphyxia in newborns

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Pet GC

2014-11-01

Full Text Available Gillian C Pet, Sandra E Juul Department of Pediatrics, Division of Neonatology, University of Washington, Seattle, WA, USA Abstract: Perinatal asphyxia is a cause of significant neonatal morbidity worldwide. Lack of oxygenation and perfusion to the neonatal brain leads to energy failure and cell death. Currently, therapeutic hypothermia is the standard of care for term infants with hypoxic-ischemic encephalopathy, but as it has shown only modest effects on survival and morbidity, additional neuroprotective agents are needed. Erythropoietin has been extensively studied as a neuroprotective agent for infants who suffer a hypoxic-ischemic brain injury. It has multiple mechanisms of action, in both preventing cell death and promoting tissue repair. Studies have progressed over time from in vitro to in vivo studies, first in animals and now in humans, with several Phase I/II trials completed and Phase III trials underway. As therapeutic hypothermia has become the standard of care in treating term infants with hypoxic-ischemic encephalopathy, studies must now evaluate other neuroprotective agents, including erythropoietin, used in concert with therapeutic hypothermia. Erythropoietin has shown promise as a neuroprotective agent in animal and human models, both alone and together with hypothermia. Keywords: neonate, brain injury

Portal hemodynamics in chronic portal-systemic encephalopathy

International Nuclear Information System (INIS)

Takashi, Motohide; Igarashi, Masahiko; Hino, Shinichi; Takayasu, Kenichi; Goto, Nobuaki; Musha, Hirotaka; Ohnishi, Kunihiko; Okuda, Kunio

1985-01-01

A portal hemodynamic study was made in 7 consecutive patients with chronic portal-systemic encephalopathy by percutaneous transhepatic catheterization of the portal vein and injecting contrast medium into the superior mesenteric vein or by superior mesenteric arterial portography in comparison with patients without encephalopathy studied by percutaneous catheterization of these veins. It is suggested that chronic portal-systemic encephalopathy is a result of a large collateral route shunting a large proportion of the superior mesenteric venous blood into systemic circulation, and that development of such collaterals precludes formation of large esophageal varices. (Auth.)

No oxygen delivery limitation in hepatic encephalopathy

DEFF Research Database (Denmark)

Gjedde, Albert; Keiding, Susanne; Vilstrup, Hendrik

2010-01-01

to choose between cause and effect in three groups of volunteers, including healthy control subjects (HC), patients with cirrhosis of the liver without hepatic encephalopathy (CL), and patients with cirrhosis with acute hepatic encephalopathy. Compared to HC subjects, blood flow and energy metabolism had......Hepatic encephalopathy is a condition of reduced brain functioning in which both blood flow and brain energy metabolism declined. It is not known whether blood flow or metabolism is the primary limiting factor of brain function in this condition. We used calculations of mitochondrial oxygen tension...

MR imaging of term infants with hypoxic-ischaemic encephalopathy as a predictor of neurodevelopmental outcome and late MRI appearances

International Nuclear Information System (INIS)

Twomey, Eilish; Ryan, Stephanie; Twomey, Anne; Murphy, John; Donoghue, Veronica B.

2010-01-01

Morbidity attributable to hypoxic-ischaemic injury (HIE) in the perinatal period remains problematic, and timely and accurate assessment of the degree of injury is required for clinical management and prognosis. Conventional MR sequences typically appear normal in the first 48 h post HIE. While diffusion-weighted imaging (DWI) and apparent diffusion coefficient (ADC) maps register the injury earlier, perhaps within the first 24 h, it has been suggested that there may be a propensity at that early stage to underestimate the lesion severity or extent. To assess whether MR imaging that included DWI, measured ADC values and T1- and T2-weighted sequences ultimately correlated with either neurodevelopmental outcome or with late MR imaging at 2 years of age. In addition, we wished to compare the performance of MR imaging with cranial US imaging. All infants presenting with HIE who had an MRI within 10 days of life were eligible for enrollment and subsequently underwent a full neurodevelopmental assessment at 2 years of age. All children underwent repeat MRI at this time. All neonates had at least one cranial US study. The US findings were categorized as normal, abnormalities confined to the cerebral cortex and subcortical white matter, isolated central grey matter hyperechogenicity, and central hyperechogenicity combined with cerebral cortical/subcortical changes. All MRI studies were retrospectively reviewed by three radiologists. The patterns of injury on the early DWI and ADC maps and early T1- and T2-W studies were recorded as diffuse, central, watershed or atypical. The patterns of signal abnormality were assessed using a scoring system that yielded four separate scores [basal ganglia (BG), watershed (W), BG/W and summation (S)] for the three sets of images, a total of 12 scores in all. The appearance of the posterior limb of the internal capsule (PLIC) on T1-W inversion recovery sequences and of the corpus callosum on all sequences was also documented. After

MR imaging of term infants with hypoxic-ischaemic encephalopathy as a predictor of neurodevelopmental outcome and late MRI appearances

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Twomey, Eilish; Ryan, Stephanie [Children' s University Hospital, Department of Radiology, Dublin (Ireland); Twomey, Anne; Murphy, John [National Maternity Hospital, Department of Neonatology, Dublin (Ireland); Donoghue, Veronica B. [National Maternity Hospital, Department of Radiology, Dublin (Ireland); Children' s University Hospital, Department of Radiology, Dublin (Ireland)

2010-09-15

Morbidity attributable to hypoxic-ischaemic injury (HIE) in the perinatal period remains problematic, and timely and accurate assessment of the degree of injury is required for clinical management and prognosis. Conventional MR sequences typically appear normal in the first 48 h post HIE. While diffusion-weighted imaging (DWI) and apparent diffusion coefficient (ADC) maps register the injury earlier, perhaps within the first 24 h, it has been suggested that there may be a propensity at that early stage to underestimate the lesion severity or extent. To assess whether MR imaging that included DWI, measured ADC values and T1- and T2-weighted sequences ultimately correlated with either neurodevelopmental outcome or with late MR imaging at 2 years of age. In addition, we wished to compare the performance of MR imaging with cranial US imaging. All infants presenting with HIE who had an MRI within 10 days of life were eligible for enrollment and subsequently underwent a full neurodevelopmental assessment at 2 years of age. All children underwent repeat MRI at this time. All neonates had at least one cranial US study. The US findings were categorized as normal, abnormalities confined to the cerebral cortex and subcortical white matter, isolated central grey matter hyperechogenicity, and central hyperechogenicity combined with cerebral cortical/subcortical changes. All MRI studies were retrospectively reviewed by three radiologists. The patterns of injury on the early DWI and ADC maps and early T1- and T2-W studies were recorded as diffuse, central, watershed or atypical. The patterns of signal abnormality were assessed using a scoring system that yielded four separate scores [basal ganglia (BG), watershed (W), BG/W and summation (S)] for the three sets of images, a total of 12 scores in all. The appearance of the posterior limb of the internal capsule (PLIC) on T1-W inversion recovery sequences and of the corpus callosum on all sequences was also documented. After

Diffusion MR findings in cyclosporin-A induced encephalopathy

International Nuclear Information System (INIS)

Aydin, Kubilay; Minareci, Ozenc; Donmez, Fuldem; Tuzun, Umit; Atamer, Tanju

2004-01-01

Cyclosporin encephalopathy is a well-known entity, which is clinically characterized by altered mental status, vision problems, focal neurological deficits and seizures. The exact pathophysiology of the cyclosporin encephalopathy has not yet been defined. We report the diffusion-weighted MR imaging and proton MR spectroscopy findings in a case of cyclosporin encephalopathy. The white-matter lesions with reversible restricted diffusion supported the hypothesis of reversible vasospasm induced by the cyclosporin. (orig.)

[Autonomic regulation at emotional stress under hypoxic conditions in the elderly with physiological and accelerated aging: effect of hypoxic training].

Science.gov (United States)

Os'mak, E D; Asanov, É O

2014-01-01

The effect of hypoxic training on autonomic regulation in psycho-emotional stress conditions in hypoxic conditions in older people with physiological (25 people) and accelerated (28 people) aging respiratory system. It is shown that hypoxic training leads to an increase in vagal activity indicators (HF) and reduced simpatovagal index (LF/HF), have a normalizing effect on the autonomic balance during stress loads in older people with different types of aging respiratory system.

MR findings of wernicke encephalopathy

International Nuclear Information System (INIS)

Yoon, Hyun Ki; Chang, Kee Hyun; Lee, Goo; Han, Moon Hee; Park, Sung Ho; Na, Duk Yull; Song, Chi Sung

1991-01-01

Seven patients (33 to 58 years old) with clinical diagnoses of Wernicke encephalopathy were examined with MR on either a 2.0T (5 cases) or a 0.5T scanner (2 cases) using spin-echo pulse sequences. In 2 patients, follow-up MR studies were performed 1 and 5 weeks after thiamine (vitamine B1) treatment. Five patients (4 chronic alcoholics and 1 with hyperemesis gravidarum) showed atrophy of both mamillary bodies, along with patchy lesions around the third ventricle, medial thalami, tectum of the midbrain, and periaqueductal gray matter. Another patient with hyperemesis of gravidrum demonstrated only slightly atrophic mamillary bodies, and the last patient with severe vomiting after gastrojejunostomy showed only diencephaic/mesencephalic lesions with apparently normal mamillary bodies. A follow-up MR showed a decrease in previously-noted diencephalic/-/mesencephalic lesions but no change in the size of the mamillary bodies. Diencephalic/mesencephalic lesions were well seen as a high-signal intensity on proton-and T2-weighted axial images, while atrophy of the mamillary bodies was seen best on T1-weighted sagittal images. MR imaging is very useful in demonstrating the characteristic lesions of Wernicke encephalopathy and in evaluating the result of treatment on follow-up study

Biomarkers of brain injury in neonatal encephalopathy treated with hypothermia.

Science.gov (United States)

Massaro, An N; Chang, Taeun; Kadom, Nadja; Tsuchida, Tammy; Scafidi, Joseph; Glass, Penny; McCarter, Robert; Baumgart, Stephen; Vezina, Gilbert; Nelson, Karin B

2012-09-01

To determine if early serum S100B and neuron-specific enolase (NSE) levels are associated with neuroradiographic and clinical evidence of brain injury in newborns with encephalopathy. Patients who received therapeutic whole-body hypothermia were prospectively enrolled in this observational study. Serum specimens were collected at 0, 12, 24, and 72 hours of cooling. S100B and NSE levels were measured by enzyme linked immunosorbent assay. Magnetic resonance imaging was performed in surviving infants at 7-10 days of life. Standardized neurologic examination was performed by a child neurologist at 14 days of life. Multiple linear regression analyses were performed to evaluate the association between S100B and NSE levels and unfavorable outcome (death or severe magnetic resonance imaging injury/significant neurologic deficit). Cutoff values were determined by receiver operating curve analysis. Newborns with moderate to severe encephalopathy were enrolled (n = 75). Median pH at presentation was 6.9 (range, 6.5-7.35), and median Apgar scores of 1 at 1 minute, 3 at 5 minutes, and 5 at 10 minutes. NSE and S100B levels were higher in patients with unfavorable outcomes across all time points. These results remained statistically significant after controlling for covariables, including encephalopathy grade at presentation, Apgar score at 5 minutes of life, initial pH, and clinical seizures. Elevated serum S100B and NSE levels measured during hypothermia were associated with neuroradiographic and clinical evidence of brain injury in encephalopathic newborns. These brain-specific proteins may be useful immediate biomarkers of cerebral injury severity. Copyright © 2012 Mosby, Inc. All rights reserved.

Pheochromocytoma: a rare cause of childhood hypertensive encephalopathy

International Nuclear Information System (INIS)

Aftab, S.; Yasmeen, T.; Hamid, M.H.; Sarwar, M.; Sipra, H.; Sheikh, A.; Haider, N.; Hanif, G.

2012-01-01

Pheochromocytomas are rare neuroendocrine tumours of chromaffin tissues. They are catecholamine secreting tumours which cause severe hypertension and other systemic disturbances. Of all the causes of childhood hypertension, pheochromocytoma constitutes less than 1%. We report the case of a 12 years old child who presented with hypertensive encephalopathy, confirmed histologically to be secondary to pheochromocytoma, and cured with meticulous critical care and surgical resection. (author)

Reversible cortical blindness in a case of hepatic encephalopathy

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Amlan Kanti Biswas

2016-01-01

Full Text Available Hepatic encephalopathy is a frequent and often fatal manifestation of chronic liver disease. The pathogenesis of hepatic encephalopathy is believed to be multifactorial including impaired blood-brain barrier function, imbalance between the excitatory and inhibitory neurotransmitters in cortex, accumulation of various toxic and false neurotransmitters, and lack of nutrients like oxygen and glucose. Signs and symptoms of hepatic encephalopathy varies and commonly ranges from personality changes, disturbed consciousness, sleep pattern alternation, intellectual deterioration, speech disturbances, asterixis to frank coma and even death. Reversible or transient cortical blindness is rare manifestation of hepatic encephalopathy. It may even precede the phase of altered consciousness in such patients. Very few similar cases have been reported worldwide. Hence, we would like to report a case of transient cortical blindness in a patient of hepatic encephalopathy.

Chylous ascites post open cholecystectomy after severe pancreatitis.

LENUS (Irish Health Repository)

Cheung, Cherry X

2012-05-01

Chylous ascites a rare complication post cholecystectomy. There are to our knowledge only 3 reported cases in the literature. We describe a case of chylous ascites post open cholecystectomy in a patient with recent severe pancreatitis. We propose a potential relationship between acute biliary pancreatitis and the development of chylous ascites.

Does CT scan performed at one week of age help predict neurodevelopmental outcome following perinatal hypoxic-ischaemic injury in term infants?

International Nuclear Information System (INIS)

Gunn, M.; Battin, M.R.; Teele, R.L.; O'Connor, K.; Hope, J.A.

2002-01-01

Full text: Cerebral imaging may be used as an adjunct to clinical assessment to help prognostician following a perinatal hypoxic ischaemic insult. A good correlation has been shown between MRI and neurologic outcome but data obtained using CT is less clear. The aim of this study was to determine whether CT of the brain performed at one week of age was prognostic for neurodevelopmental outcome in term infants with hypoxic ischaemic encephalopathy. Term infants with an umbilical artery pH<7.1 or Apgar score <6 at 5 minutes plus evidence of encephalopathy and no evidence of major congenital anomalies were reviewed and data obtained. Nearly all of the infants in the study (35) were part of a trial of selective head cooling. CT scans were randomised and reviewed independently by three practising neuroradiologists on two occasions. The CTs were graded as 0) normal; 1) white matter oedema; 2a) mild watershed infarction; 2b) moderate watershed infarction; 3) severe generalised infarction; 4) involvement of basal ganglia. Follow up neurological examination was performed at regular intervals, until 18 months of age, by a neonatologist. Developmental testing at 18 months using the revised Bailey Scales of Infant Development was performed by a psychologist. The study group consisted of 36 infants. Mean birth weight was 3555 (SD+/- 510)g, gestational age was 39.7 (+/- 1.4) weeks, umbilical or first arterial pH was 6.9 (+/- 0.2) and 5 min Apgar scores was 4.3 (+/- 1.9). Neurological outcome was designated as cerebral palsy (7), tone abnormalities before 12 months but only mild abnormality or normal examination at 18 months (2), developmental delay but normal physical examination (1) and functionally normal at 18 months (24). In 27% of infants the images were with normal limits. In only 17% there was overt basal ganglia damage and in 56% there was some degree of white matter abnormality. Overall, an abnormal CT had a sensitivity of 78%, and a specificity of 91% for the prediction

Frequency of helicobacter pylori antibodies in porto-systemic encephalopathy,

International Nuclear Information System (INIS)

Sethar, G.H.; Ahmed, R.; Afsar, S.; Zuberi, B.F.

2004-01-01

Objective: To study the frequency of Helicobacter pylori antibodies in patients presenting with porto-systemic encephalopathy due to liver disease. Patients and Methods: During the study period, seventy-six patients of porto-systemic encephalopathy due to liver diseases was selected. These subjects were evaluated for hepatic encephalopathy grade, modified Child-Pugh classification and were managed according to the standard practices. These patients were evaluated for Helicobacter (H. pylori) antibody status by ELlSA (Abbott Laboratories) method. Results: Out of 76 patients studied and tested for H. pylori antibodies, 48(63.2%) were males and 28(36.8%) were females with age ranging between 17 and 85 years. Out of 76 patients who presented with porto-systemic encephalopathy, 59(77.6%) had a positive H. pylori antibody test. Thirty-five of these were males and 24 were females. A significant number of patients who presented with higher grade of encephalopathy were H. pylori antibody positive (p<0.001). Conclusion: In this study, frequency of H. pylori antibodies was significantly high in patients of porto-systematic encephalopathy. (author)

Hepatic encephalopathy in a liver transplant recipient with stable liver function.

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Arab, Juan Pablo; Meneses, Luis; Pérez, Rosa M; Arrese, Marco; Benítez, Carlos

2013-04-01

Postshunt hepatic encephalopathy after liver transplantation (LT) is an infrequent condition and is commonly associated with portal occlusion or stenosis and the presence of a patent portosystemic shunt. Portal vein stenosis (PVS) or thrombosis (PVT) are uncommon complications after LT. The overall frequency of both complications is reported to be less than 3%. When PVS or PVT develop early after LT, the occlusion of the portal vein can have catastrophic consequences to the graft including acute liver failure and graft loss. Late PVT/PVS are asymptomatic in approximately 50% of the cases and mainly diagnosed by a routine ultrasound. Symptomatic postshunt hepatic encephalopathy (HE) is a very infrequent condition after LT that has been scarcely reported in the literature. We present here the case of a liver recipient with normal graft function who presented with hepatic encephalopathy 3 months after LT with stable liver function but a severe portal stenosis and the presence of a spontaneous portosystemic shunt whose successful endovascular treatment was followed by the complete resolution of the HE.

Temperature control during therapeutic hypothermia for newborn encephalopathy using different Blanketrol devices.

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Laptook, Abbot R; Kilbride, Howard; Shepherd, Edward; McDonald, Scott A; Shankaran, Seetha; Truog, William; Das, Abhik; Higgins, Rosemary D

2014-12-01

Therapeutic hypothermia improves the survival and neurodevelopmental outcome of infants with newborn encephalopathy of a hypoxic-ischemic origin. The NICHD Neonatal Research Network (NRN) Whole Body Cooling trial used the Cincinnati Sub-Zero Blanketrol II to achieve therapeutic hypothermia. The Blanketrol III is now available and provides additional cooling modes that may result in better temperature control. This report is a retrospective comparison of infants undergoing hypothermia using two different cooling modes of the Blanketrol device. Infants from the NRN trial were cooled with the Blanketrol II using the Automatic control mode (B2 cohort) and were compared with infants from two new NRN centers that adopted the NRN protocol and used the Blanketrol III in a gradient mode (B3 cohort). The primary outcome was the percent time the esophageal temperature stayed between 33°C and 34°C (target 33.5°C) during maintenance of hypothermia. Cohorts had similar birth weight, gestational age, and level of encephalopathy at the initiation of therapy. Baseline esophageal temperature differed between groups (36.6°C ± 1.0°C for B2 vs. 33.9°C ± 1.2°C for B3, p<0.0001) reflecting the practice of passive cooling during transport prior to initiation of active device cooling in the B3 cohort. This difference prevented comparison of temperatures during induction of hypothermia. During maintenance of hypothermia the mean and standard deviation of the percent time between 33°C and 34°C was similar for B2 compared to B3 cohorts (94.8% ± 0.1% vs. 95.8% ± 0.1%, respectively). Both the automatic and gradient control modes of the Blanketrol devices appear comparable in maintaining esophageal temperature within the target range during maintenance of therapeutic hypothermia.

Current Theory on the Cerebral Mechanisms of Hypoxic PRE- and Postconditioning.

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Rybnikova, E A; Samoilov, M O

2016-01-01

An exposure of the organism to several episodes of mild hypoxia results in the development of brain hypoxic/ischemic tolerance, as well as cross-tolerance to the stressful factors of psychoemotional nature. Such kind of preconditioning by mild hypoxia functions as “alarm signalization” by I.P. Pavlov, preparing the organism and, in particularly, brain to the forthcoming harmful event. Dose-dependent action of hypoxia on the brain can be considered as one particular case of the general phenomenon termed hormesis, or neurohormesis. Endogenous defense processes launched by the hypoxic preconditioning and leading to the development of cerebral tolerance are associated with activation of intracellular signal cascades, transcriptional factors, regulatory proteins and expression of pro-adaptive genes and their products in the susceptible brain regions. Important mechanism of systemic adaptation induced by hypoxic preconditioning includes modifications of pituitary-adrenal axis aimed at enhancement of its adaptive resources. All these components are involved in the neuroprotective processes in three sequential phases - initiation, induction, and expression. Important role belongs also to epigenetic mechanisms controlling the activity of pro-adaptive genes. In contrast to the preconditioning, hypoxic postconditioning is comparatively novel phenomenon and therefore its mechanisms are less studied. The involvement of hypoxia-inducible factor HIF-1, and non-specific protective processes as up-regulation of anti-apoptotic factors and neurotrophines.

Type and etiology of liver cirrhosis are not related to the presence of hepatic encephalopathy or health-related quality of life: a cross-sectional study

Directory of Open Access Journals (Sweden)

Björnsson Einar

2008-10-01

Full Text Available Abstract Background Hepatic encephalopathy has a negative impact on health-related quality of life (QoL in liver cirrhosis. There are scarce and conflicting data on whether type or etiology of liver cirrhosis could be related to hepatic encephalopathy in patients with cirrhosis. We aimed to determine the impact of cirrhosis etiology on hepatic encephalopathy and whether hepatic encephalopathy affects health-related QoL among patients with cirrhosis of different etiologies. Methods A total of 156 cirrhotic patients were prospectively evaluated for the presence of hepatic encephalopathy according to the West-Haven criteria as well as by means of two psychometric tests. Patients with cryptogenic cirrhosis or cirrhosis due to mixed hepatocellular/cholestatic etiologies were excluded. Fasting plasma glucose levels were also measured. QoL was evaluated by means of a validated questionnaire (SF-36. Results Diabetes mellitus was more common in patients with hepatocellular cirrhosis compared to those with cholestatic cirrhosis but the two groups did not differ in cirrhosis severity or the prevalence of hepatic encephalopathy (p > 0.05. The groups of patients with cirrhosis due to alcohol, hepatitis C, or cholestatic liver disease did not differ in severity of liver cirrhosis or the prevalence of hepatic encephalopathy (p > 0.05. Patients with cirrhosis of different etiologies did not differ in any SF-36 domain (p > 0.05. In multivariate analysis, performance at neuropsychological testing was independently related only to age, diabetes mellitus, and the Child-Pugh score whereas the SF-36 physical component summary only to the Child-Pugh score and hepatic encephalopathy. Conclusion Cirrhosis etiology does not seem to be related to hepatic encephalopathy or health-related QoL. Cognitive impairment is associated mainly with age, liver disease severity and diabetes mellitus.

Analysis of Multiple B-Value Diffusion-Weighted Imaging in Pediatric Acute Encephalopathy

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Tachibana, Yasuhiko; Aida, Noriko; Niwa, Tetsu; Nozawa, Kumiko; Kusagiri, Kouki; Mori, Kana; Endo, Kazuo; Obata, Takayuki; Inoue, Tomio

2013-01-01

Acute encephalopathy is a disease group more commonly seen in children. It is often severe and has neurological sequelae. Imaging is important for early diagnosis and prompt treatment to ameliorate an unfavorable outcome, but insufficient sensitivity/specificity is a problem. To overcome this, a new value (fraction of high b-pair (FH)) that could be processed from clinically acceptable MR diffusion-weighted imaging (DWI) with three different b-values was designed on the basis of a two-compartment model of water diffusion signal attenuation. The purpose of this study is to compare FH with the apparent diffusion coefficient (ADC) regarding the detectability of pediatric acute encephalopathy. We retrospectively compared the clinical DWI of 15 children (1–10 years old, mean 2.34, 8 boys, 7 girls) of acute encephalopathy with another 16 children (1–11 years old, mean 4.89, 9 boys, 7 girls) as control. A comparison was first made visually by mapping FH on the brain images, and then a second comparison was made on the basis of 10 regions of interest (ROIs) set on cortical and subcortical areas of each child. FH map visually revealed diffusely elevated FH in cortical and subcortical areas of the patients with acute encephalopathy; the changes seemed more diffuse in FH compared to DWI. The comparison based on ROI revealed elevated mean FH in the cortical and subcortical areas of the acute encephalopathy patients compared to control with significant difference (Pencephalopathy may be superior in FH compared to ADC. PMID:23755112

Electroencephalography and Brain MRI Patterns in Encephalopathy.

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Wabulya, Angela; Lesser, Ronald P; Llinas, Rafael; Kaplan, Peter W

2016-04-01

Using electroencephalography (EEG) and histology in patients with diffuse encephalopathy, Gloor et al reported that paroxysmal synchronous discharges (PSDs) on EEG required combined cortical gray (CG) and "subcortical" gray (SCG) matter pathology, while polymorphic delta activity (PDA) occurred in patients with white matter pathology. In patients with encephalopathy, we compared EEG findings and magnetic resonance imaging (MRI) to determine if MRI reflected similar pathological EEG correlations. Retrospective case control study of 52 cases with EEG evidence of encephalopathy and 50 controls without evidence of encephalopathy. Review of clinical, EEG and MRI data acquired within 4 days of each other. The most common EEG finding in encephalopathy was background slowing, in 96.1%. We found PSDs in 0% of cases with the combination of CG and SCG abnormalities. Although 13.5% (n=7) had PSDs on EEG; 3 of these had CG and 4 had SCG abnormalities. A total of 73.1% (38/52) had white matter abnormalities-of these 28.9% (11/38) had PDA. PSDs were found with either CG or "SCG" MRI abnormalities and did not require a combination of the two. In agreement with Gloor et al, PDA occurred with white matter MRI abnormalities in the absence of gray matter abnormalities. © EEG and Clinical Neuroscience Society (ECNS) 2015.

Preclinical assessment of hypoxic marker specificity and sensitivity

International Nuclear Information System (INIS)

Iyer, Renuka V.; Engelhardt, Edward L.; Stobbe, Corinne C.; Schneider, Richard F.; Chapman, J. Donald

1998-01-01

Purpose: In the search for a sensitive, accurate, and noninvasive technique for quantifying human tumor hypoxia, our laboratory has synthesized several potential radiodiagnostic agents. The purpose of this study was to assess and compare the hypoxic marking properties of both radioiodinated and Tc-99m labeled markers in appropriate test systems which can predict for in vivo activity. Materials and Methods: Preclinical assessment of hypoxic marker specificity and sensitivity employed three laboratory assays with tumor cells in vitro and in vivo. Radiolabeled marker uptake and/or binding to whole EMT-6 tumor cells under extremely hypoxic and aerobic conditions was measured and their ratio defined hypoxia-specific factor (HSF). Marker specificity to hypoxic tumor tissue was estimated from its selective avidity to two rodent tumors in vivo, whose radiobiologic hypoxic fractions (HF) had been measured. The ratios of % injected dose/gram (%ID/g) of marker at various times in EMT-6 tumor tissue relative to that in the blood and muscle of scid mice were used to quantify hypoxia-specific activity. This tumor in this host exhibited an average radiobiologic HF of ∼35%. As well, nuclear medicine images were acquired from R3327-AT (HF ≅15%) and R3327-H (no measurable HF) prostate carcinomas growing in rats to distinguish between marker avidity due to hypoxia versus perfusion. Results: The HSF for FC-103 and other iodinated markers were higher (5-40) than those for FC-306 and other Tc-99m labeled markers. The latter did not show hypoxia-specific uptake into cells in vitro. Qualitative differences were observed in the biodistribution and clearance kinetics of the iodinated azomycin nucleosides relative to the technetium chelates. The largest tumor/blood (T/B) and tumor/muscle (T/M) ratios were observed for compounds of the azomycin nucleoside class in EMT-6 tumor-bearing scid mice. These markers also showed a 3-4 x higher uptake into R3327-AT tumors relative to the well

Malnutrition-induced Wernicke's encephalopathy following a water-only fasting diet.

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Hutcheon, Deborah A

2015-02-01

Wernicke's encephalopathy is a critical condition of neurological dysfunction resulting from a deficiency in thiamine. Chronic alcoholism is recognized as the most common cause of Wernicke's encephalopathy, but other causes, including fasting/starvation and malnutrition, have been documented within the scientific literature. These causes may not be readily recognized by healthcare professionals and may lead to Wernicke's encephalopathy being overlooked as a diagnosis when a nonalcoholic patient presents with classic signs and symptoms of the disorder. A narrative review of thiamine and its relationship to the development, diagnosis, and treatment of Wernicke's encephalopathy is presented based on a review of evidence-based guidelines and published research. To heighten awareness of the development of Wernicke's encephalopathy in fasted/starved and malnourished patients and to contribute to the scientific body of knowledge for the identification and management of Wernicke's encephalopathy in these patients, the clinical course and treatment of an adult woman who developed Wernicke's encephalopathy following a 40-day water-only fasting diet is outlined. Clinical suspicion was required to identify the patient's condition and initiate immediate intervention through parenteral thiamine administration. Oral thiamine supplementation of 100 to 800 mg per day for 6 months was required to aid recovery. The patient's clinical course and response to treatment illustrate the necessity for clinical awareness and suspicion of Wernicke's encephalopathy among healthcare professionals, timely and adequate parenteral thiamine administration, and oral thiamine supplementation at therapeutic doses to correct the nutrient deficiency, halt the progression of Wernicke's encephalopathy, and promote recovery. © 2014 American Society for Parenteral and Enteral Nutrition.

Radiographical findings in patients with liver cirrhosis and hepatic encephalopathy.

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Elwir, Saleh; Hal, Hassan; Veith, Joshua; Schreibman, Ian; Kadry, Zakiyah; Riley, Thomas

2016-08-01

Hepatic encephalopathy is a common complication encountered in patients with liver cirrhosis. Hepatic encephalopathy is not reflected in the current liver transplant allocation system. Correlation was sought between hepatic encephalopathy with findings detected on radiographic imaging studies and the patient's clinical profile. A retrospective analysis was conducted of patients with cirrhosis, who presented for liver transplant evaluation in 2009 and 2010. Patients with hepatocellular carcinoma, ejection fraction less than 60% and who had a TIPS (transjugular intrahepatic portosystemic shunting) procedure or who did not complete the evaluation were excluded. Statistical analysis was performed and variables found to be significant on univariate analysis (P encephalopathy group (n = 58) and a control group (n = 59). Univariate analysis found that a smaller portal vein diameter, smaller liver antero-posterior diameter, liver nodularity and use of diuretics or centrally acting medications showed significant correlation with hepatic encephalopathy. This association was confirmed for smaller portal vein, use of diuretics and centrally acting medications in the multivariate analysis. A decrease in portal vein diameter was associated with increased risk of encephalopathy. Identifying patients with smaller portal vein diameter may warrant screening for encephalopathy by more advanced psychometric testing, and more aggressive control of constipation and other factors that may precipitate encephalopathy. © The Author(s) 2015. Published by Oxford University Press and the Digestive Science Publishing Co. Limited.

Bovine Spongiform Encephalopathy (BSE), or Mad Cow Disease

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... the CDC Bovine Spongiform Encephalopathy (BSE), or Mad Cow Disease Note: Javascript is disabled or is not ... spongiform encephalopathy) is a progressive neurological disorder of cattle that results from infection by an unusual transmissible ...

Brain hypoxia imaging

Energy Technology Data Exchange (ETDEWEB)

Song, Ho Chun [Chonnam National University Medical School, Gwangju (Korea, Republic of)

2007-04-15

The measurement of pathologically low levels of tissue pO{sub 2} is an important diagnostic goal for determining the prognosis of many clinically important diseases including cardiovascular insufficiency, stroke and cancer. The target tissues nowadays have mostly been tumors or the myocardium, with less attention centered on the brain. Radiolabelled nitroimidazole or derivatives may be useful in identifying the hypoxic cells in cerebrovascular disease or traumatic brain injury, and hypoxic-ischemic encephalopathy. In acute stroke, the target of therapy is the severely hypoxic but salvageable tissue. {sup 18}F-MISO PET and {sup 99m}Tc-EC-metronidazole SPECT in patients with acute ischemic stroke identified hypoxic tissues and ischemic penumbra, and predicted its outcome. A study using {sup 123}I-IAZA in patient with closed head injury detected the hypoxic tissues after head injury. Up till now these radiopharmaceuticals have drawbacks due to its relatively low concentration with hypoxic tissues associated with/without low blood-brain barrier permeability and the necessity to wait a long time to achieve acceptable target to background ratios for imaging in acute ischemic stroke. It is needed to develop new hypoxic marker exhibiting more rapid localization in the hypoxic region in the brain. And then, the hypoxic brain imaging with imidazoles or non-imidazoles may be very useful in detecting the hypoxic tissues, determining therapeutic strategies and developing therapeutic drugs in several neurological disease, especially, in acute ischemic stroke.

Approach to Clinical Syndrome of Jaundice and Encephalopathy in Tropics

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Anand, Anil C.; Garg, Hitendra K.

2015-01-01

A large number of patients present with jaundice and encephalopathy in tropical country like India and acute liver failure is the usual cause. Clinical presentation like ALF is also a complication of many tropical infections, and these conditions may mimic ALF but may have subtle differences from ALF. Moreover, what hepatologists see as acute liver failure in tropics is different from what is commonly described in Western Textbooks. Paracetamol overdose, which is possibly the commonest cause of ALF in UK and USA, is hardly ever seen in India. Most common etiology here is viral hepatitis (hepatitis E > hepatitis B> hepatitis A). Apart from ALF, one may also come across subacute hepatic failure (SAHF) as well as acute-on-chronic liver failure (ACLF) due to viral hepatitis. Interestingly, a host of other conditions can mimic ALF because clinical presentation in these conditions can be dominated by jaundice and encephalopathy. Malarial hepatopathy is possibly the best-known condition out of these and is not an uncommon manifestation of severe malaria. A similar presentation can also be seen in other common infections in tropics such as dengue fever, typhoid fever, leptospirosis, scrub typhus, amoebic liver abscesses, tuberculosis and other bacterial and fungal infections with or without human immunodeficiency virus (HIV) related disease. In many of these conditions, liver failure may not be underlying pathophysiology. Some pregnancy related liver diseases could also present with jaundice and encephalopathy. This review summarizes the commonly seen presentations in tropical country like India, where jaundice and encephalopathy dominate the clinical picture. PMID:26041951

Involvement of SIRT1 in hypoxic down-regulation of c-Myc and β-catenin and hypoxic preconditioning effect of polyphenols

Energy Technology Data Exchange (ETDEWEB)

Hong, Kyung-Soo [Department of Biochemistry, Pusan National University School of Medicine, Yangsan (Korea, Republic of); Research Center for Ischemic Tissue regeneration, Pusan National University School of Medicine, Yangsan (Korea, Republic of); Park, Jun-Ik [Department of Biochemistry, Pusan National University School of Medicine, Yangsan (Korea, Republic of); Kim, Mi-Ju; Kim, Hak-Bong; Lee, Jae-Won [Department of Biochemistry, Pusan National University School of Medicine, Yangsan (Korea, Republic of); Research Center for Ischemic Tissue regeneration, Pusan National University School of Medicine, Yangsan (Korea, Republic of); Dao, Trong Tuan; Oh, Won Keun [BK21 Project Team, College of Pharmacy, Chosun University, Gwangju (Korea, Republic of); Kang, Chi-Dug, E-mail: kcdshbw@pusan.ac.kr [Department of Biochemistry, Pusan National University School of Medicine, Yangsan (Korea, Republic of); Kim, Sun-Hee, E-mail: ksh7738@pusan.ac.kr [Department of Biochemistry, Pusan National University School of Medicine, Yangsan (Korea, Republic of); Research Center for Ischemic Tissue regeneration, Pusan National University School of Medicine, Yangsan (Korea, Republic of)

2012-03-01

SIRT1 has been found to function as a Class III deacetylase that affects the acetylation status of histones and other important cellular nonhistone proteins involved in various cellular pathways including stress responses and apoptosis. In this study, we investigated the role of SIRT1 signaling in the hypoxic down-regulations of c-Myc and β-catenin and hypoxic preconditioning effect of the red wine polyphenols such as piceatannol, myricetin, quercetin and resveratrol. We found that the expression of SIRT1 was significantly increased in hypoxia-exposed or hypoxic preconditioned HepG2 cells, which was closely associated with the up-regulation of HIF-1α and down-regulation of c-Myc and β-catenin expression via deacetylation of these proteins. In addition, blockade of SIRT1 activation using siRNA or amurensin G, a new potent SIRT1 inhibitor, abolished hypoxia-induced HIF-1α expression but increased c-Myc and β-catenin expression. SIRT1 was also found to stabilize HIF-1α protein and destabilize c-Myc, β-catenin and PHD2 under hypoxia. We also found that myricetin, quercetin, piceatannol and resveratrol up-regulated HIF-1α and down-regulated c-Myc, PHD2 and β-catenin expressions via SIRT1 activation, in a manner that mimics hypoxic preconditioning. This study provides new insights of the molecular mechanisms of hypoxic preconditioning and suggests that polyphenolic SIRT1 activators could be used to mimic hypoxic/ischemic preconditioning. -- Graphical abstract: Polyphenols mimicked hypoxic preconditioning by up-regulating HIF-1α and SIRT1 and down-regulating c-Myc, PHD2, and β-catenin. HepG2 cells were pretreated with the indicated doses of myricetin (MYR; A), quercetin (QUR; B), or piceatannol (PIC; C) for 4 h and then exposed to hypoxia for 4 h. Levels of HIF-1α, SIRT1, c-Myc, β-catenin, and PHD2 were determined by western blot analysis. The data are representative of three individual experiments. Highlights: ► SIRT1 expression is increased in hypoxia

Involvement of SIRT1 in hypoxic down-regulation of c-Myc and β-catenin and hypoxic preconditioning effect of polyphenols

International Nuclear Information System (INIS)

Hong, Kyung-Soo; Park, Jun-Ik; Kim, Mi-Ju; Kim, Hak-Bong; Lee, Jae-Won; Dao, Trong Tuan; Oh, Won Keun; Kang, Chi-Dug; Kim, Sun-Hee

2012-01-01

SIRT1 has been found to function as a Class III deacetylase that affects the acetylation status of histones and other important cellular nonhistone proteins involved in various cellular pathways including stress responses and apoptosis. In this study, we investigated the role of SIRT1 signaling in the hypoxic down-regulations of c-Myc and β-catenin and hypoxic preconditioning effect of the red wine polyphenols such as piceatannol, myricetin, quercetin and resveratrol. We found that the expression of SIRT1 was significantly increased in hypoxia-exposed or hypoxic preconditioned HepG2 cells, which was closely associated with the up-regulation of HIF-1α and down-regulation of c-Myc and β-catenin expression via deacetylation of these proteins. In addition, blockade of SIRT1 activation using siRNA or amurensin G, a new potent SIRT1 inhibitor, abolished hypoxia-induced HIF-1α expression but increased c-Myc and β-catenin expression. SIRT1 was also found to stabilize HIF-1α protein and destabilize c-Myc, β-catenin and PHD2 under hypoxia. We also found that myricetin, quercetin, piceatannol and resveratrol up-regulated HIF-1α and down-regulated c-Myc, PHD2 and β-catenin expressions via SIRT1 activation, in a manner that mimics hypoxic preconditioning. This study provides new insights of the molecular mechanisms of hypoxic preconditioning and suggests that polyphenolic SIRT1 activators could be used to mimic hypoxic/ischemic preconditioning. -- Graphical abstract: Polyphenols mimicked hypoxic preconditioning by up-regulating HIF-1α and SIRT1 and down-regulating c-Myc, PHD2, and β-catenin. HepG2 cells were pretreated with the indicated doses of myricetin (MYR; A), quercetin (QUR; B), or piceatannol (PIC; C) for 4 h and then exposed to hypoxia for 4 h. Levels of HIF-1α, SIRT1, c-Myc, β-catenin, and PHD2 were determined by western blot analysis. The data are representative of three individual experiments. Highlights: ► SIRT1 expression is increased in hypoxia

Hepatic Encephalopathy

Medline Plus

Full Text Available ... of brain function in people with advanced liver disease. When your liver is damaged it can no longer remove toxic substances from your blood. These toxins build up and can travel through your body until they reach your brain, causing mental and physical symptoms of HE. Hepatic Encephalopathy often ...

Molecular & Genetic Investigation of Tau in Chronic Traumatic Encephalopathy

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2015-10-01

AWARD NUMBER: W81XWH-14-1-0399 TITLE: Molecular & Genetic Investigation of Tau in Chronic Traumatic Encephalopathy PRINCIPAL INVESTIGATOR: John F...Include area code) October 2015 Annual Report 30 Sep 2014 - 29 Sep 2015 Molecular & Genetic Investigation of Tau in Chronic Traumatic Encephalopathy John... encephalopathy (CTE), but the underlying molecular changes remain unclear. Here, biochemical and genetic studies that deepen our understanding of the

Development of a real-time imaging system for hypoxic cell apoptosis

Directory of Open Access Journals (Sweden)

Go Kagiya

2016-01-01

Full Text Available Hypoxic regions within the tumor form due to imbalances between cell proliferation and angiogenesis; specifically, temporary closure or a reduced flow due to abnormal vasculature. They create environments where cancer cells acquire resistance to therapies. Therefore, the development of therapeutic approaches targeting the hypoxic cells is one of the most crucial challenges for cancer regression. Screening potential candidates for effective diagnostic modalities even under a hypoxic environment would be an important first step. In this study, we describe the development of a real-time imaging system to monitor hypoxic cell apoptosis for such screening. The imaging system is composed of a cyclic luciferase (luc gene under the control of an improved hypoxic-responsive promoter. The cyclic luc gene product works as a caspase-3 (cas-3 monitor as it gains luc activity in response to cas-3 activation. The promoter composed of six hypoxic responsible elements and the CMV IE1 core promoter drives the effective expression of the cyclic luc gene in hypoxic conditions, enhancing hypoxic cell apoptosis visualization. We also confirmed real-time imaging of hypoxic cell apoptosis in the spheroid, which shares properties with the tumor. Thus, this constructed system could be a powerful tool for the development of effective anticancer diagnostic modalities.

Wernicke's encephalopathy as a complication of gastroparesis after ...

African Journals Online (AJOL)

Wernicke's encephalopathy is a common complication of malnutrition, alcohol abuse and gastric outlet obstruction. We describe a patient who developed Wernicke's encephalopathy secondary to gastroparesis, with no significant evidence of malnutrition, alcohol abuse, or gastric outlet obstruction.

Genetics Home Reference: STXBP1 encephalopathy with epilepsy

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... Resources (8 links) Boston Children's Hospital: Epilepsy and Seizure Disorder in Children Centers for Disease Control and Prevention: ... stxbp1 encephalopathy with epilepsy Merck Manual Consumer Version: Seizure Disorders Orphanet: Early infantile epileptic encephalopathy Patient Support and ...

CT findings and prognosis of 70 full-term infants having spasm due to hypoxic ischemic encephalography following asphyxia

International Nuclear Information System (INIS)

Ogita, Yasutoki; Kawakami, Tadashi; Tsunei, Mikio; Ohta, Yuko; Sone, Yoshiharu; Akamatsu, Hiroshi

1984-01-01

Relationship between cranial CT findings and prognosis at 12 months or more after birth was studied in 70 full-term (appropriate for date and large for date) infants who had spasm due to hypoxic ischemic encephalopathy following neonatal asphyxia. There was correlation between the prognosis of the infants and neonatal CT findings showing slight and marked low density areas in the brain parenchyma. However, it was sometimes difficult to estimate the prognosis when the low density area was moderate on CT. Therefore, follow-up CT at one and six months and one year after birth was required to examine changes in low density areas for the estimation of prognosis. The prognosis was unfavorable in cases of the disease accompanied by hemorrhage in the brain parenchyma or cerebral ventricle, persistent cerebral edema on neonatal CT, and low density areas in the atrophied brain by the follow-up CT. There was no consistent relationship between subarachnoid hemorrhage and the prognosis. (Namekawa, K.)

Reversible dementia with psychosis: Hashimoto's encephalopathy.

Science.gov (United States)

Mocellin, Ramon; Lubman, Dan I; Lloyd, John; Tomlinson, E Bruce; Velakoulis, Dennis

2006-12-01

A case of presumed Hashimoto's encephalopathy (HE) is presented. The presentation included memory loss, delusions, functional decline and culminated in a generalized seizure. Anti-thyroid antibodies were detected and symptoms resolved with prednisolone. Patients with HE may present with prominent neuropsychiatric symptoms, attract psychiatric diagnoses and present to psychiatric services. Primarily a diagnosis of exclusion, HE should be considered in cases of encephalopathy in which standard investigations are negative.

Cerebral ultrasound in newborns with severs asphyxia: correlation with the neurological status at 12 months

International Nuclear Information System (INIS)

Esparza, J.; Gonzalez, A.; Inchusta, M.I.; Pina, L.

1997-01-01

To establish the prognostic value of cerebral ultrasound performed in newborns (NB) with severe asphyxia. A retrospective study of the ultrasound (US) findings during the acute phase of severe perinatal asphyxia was carried out in a series of 182 NB. The US images were correlated with the neurological status of the infants at the age of 12 months. Of the 122 NB with normal US findings, 94,2% presented no sequelae or a slightly impaired psychomotor performance attributable to prematurity, thus conferring a high prognostic value to this technique. Subependymal cerebral hemorrhage was diagnosed in 35 cases (22 grades I and II, 9 grade III and 4 grade IV), in whom the prognosis was related to the grade of hemorrhage. Twenty-five NB were diagnosed as having some type of hypoxic or ischemic encephalopathy, eith the prognosis differing according to the topography of the lesion and the reversibility of the ultrasonographic signs: poor prognosis in ten NB with diffuse cerebral involvement and in four with periventricular leukomalacia, uncertain prognosis in seven NB with focal brain damage and a good prognosis in four with reversible cerebral edema. (Author) 35 refs

Concentric structure of thalamic lesions in acute necrotizing encephalopathy

International Nuclear Information System (INIS)

Mizuguchi, M.; Nakano, I.; Hayashi, M.; Kuwashima, M.; Yoshida, K.; Nakai, Y.; Itoh, M.; Takashima, S.

2002-01-01

Acute necrotizing encephalopathy of childhood (ANE) is characterized by multiple, symmetrical brain lesions affecting the bilateral thalami, putamina and cerebral white matter, which often show a concentric structure on CT and MRI. To reveal the pathological substrate of this finding, comparison was made between CT and necropsy findings of three fatal cases of ANE. Cranial CT demonstrated a concentric structure of the thalamocerebral lesions in one patient who died 3.5 days after the onset of encephalopathy, but not in the other two patients who died within 30 h. Neuropathological examination of postmortem brains revealed laminar changes of vascular and parenchymal pathology in all the cases. Excessive permeability of blood vessels and resultant vasogenic edema became more prominent with increasing depth from the cerebral surface. The deep portion of the lesions showed severe perivascular hemorrhage, accounting for the central high density on the CT images of one patient. (orig.)

Repair of neonatal brain injury : bringing stem cell-based therapy into clinical practice

NARCIS (Netherlands)

Wagenaar, Nienke; Nijboer, Cora H.; van Bel, Frank

2017-01-01

Hypoxic-ischaemic brain injury is one of most important causes of neonatal mortality and long-term neurological morbidity in infants born at term. At present, only hypothermia in infants with perinatal hypoxic-ischaemic encephalopathy has shown benefit as a neuroprotective strategy. Otherwise,

Hypertensive brainstem encephalopathy involving deep supratentorial regions: does only blood pressure matter?

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Jong-Ho Park

2010-04-01

Full Text Available We report on a 42-year-old female patient who presented with high arterial blood pressure of 245/150 mmHg and hypertensive brainstem encephalopathy that involved the brainstem and extensive supratentorial deep gray and white matter. The lesions were nearly completely resolved several days after stabilization of the arterial blood pressure. Normal diffusion-weighted imaging findings and high apparent diffusion coefficient values suggested that the main pathomechanism was vasogenic edema owing to severe hypertension. On the basis of a literature review, the absolute value of blood pressure or whether the patient can control his/her blood pressure seems not to be associated with the degree of the lesions evident on magnetic resonance imaging. It remains to be determined if the acceleration rate and the duration of elevated arterial blood pressure might play a key role in the development of the hypertensive encephalopathy pattern.

Hemolytic Uremic Syndrome-associated Encephalopathy Successfully Treated with Corticosteroids.

Science.gov (United States)

Hosaka, Takashi; Nakamagoe, Kiyotaka; Tamaoka, Akira

2017-11-01

The encephalopathy that occurs in association with hemolytic uremic syndrome (HUS), which is caused by enterohemorrhagic Escherichia coli (E. coli), has a high mortality rate and patients sometimes present sequelae. We herein describe the case of a 20-year-old woman who developed encephalopathy during the convalescent stage of HUS caused by E.coli O26. Hyperintense lesions were detected in the pons, basal ganglia, and cortex on diffusion-weighted brain MRI. From the onset of HUS encephalopathy, we treated the patient with methylprednisolone (mPSL) pulse therapy alone. Her condition improved, and she did not present sequelae. Our study shows that corticosteroids appear to be effective for the treatment of some patients with HUS encephalopathy.

Transient widespread cortical and splenial lesions in acute encephalitis/encephalopathy associated with primary Epstein–Barr virus infection

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Shuo Zhang

2016-01-01

Full Text Available Infection with Epstein–Barr virus (EBV is very common and usually occurs in childhood or early adulthood. Encephalitis/encephalopathy is an uncommon but serious neurological complication of EBV. A case of EBV-associated encephalitis/encephalopathy with involvement of reversible widespread cortical and splenial lesions is presented herein. An 8-year-old Chinese girl who presented with fever and headache, followed by seizures and drowsiness, was admitted to the hospital. Magnetic resonance imaging revealed high signal intensities on diffusion-weighted imaging in widespread cortical and splenial lesions. The clinical and laboratory examination results together with the unusual radiology findings suggested acute encephalitis/encephalopathy due to primary EBV infection. After methylprednisolone pulse therapy together with ganciclovir, the patient made a full recovery without any brain lesions. The hallmark clinical–radiological features of this patient included severe encephalitis/encephalopathy at onset, the prompt and complete recovery, and rapidly reversible widespread involvement of the cortex and splenium. Patients with EBV encephalitis/encephalopathy who have multiple lesions, even with the widespread involvement of cortex and splenium of the corpus callosum, may have a favorable outcome with complete disappearance of all brain lesions.

Post-Traumatic Stress Disorder and severe maternal morbidity: is there an association?

Science.gov (United States)

Angelini, Carina R; Pacagnella, Rodolfo C; Parpinelli, Mary A; Silveira, Carla; Andreucci, Carla B; Ferreira, Elton C; Santos, Juliana P; Zanardi, Dulce M; Souza, Renato T; Cecatti, Jose G

2018-01-01

To evaluate the occurrence of Post-Traumatic Stress Disorder among women experiencing a severe maternal morbidity event and associated factors in comparison with those without maternal morbidity. In a retrospective cohort study, 803 women with or without severe maternal morbidity were evaluated at 6 months to 5 years postpartum for the presence of Post-Traumatic Stress Disorder. Interviews were conducted by telephone and electronic data was stored. Data analysis was carried out by using χ2, Fisher's Exact test, and logistic regression analysis. There was no significant change in the prevalence of Post-Traumatic Stress Disorder related to a previous severe maternal morbidity experience. There were also no differences in diagnostic criteria for severe maternal morbidity (hypertensive syndromes, hemorrhage, surgical intervention or intensive care unit admission required, among other management criteria). Low parity (2.5-fold risk) and increasing age were factors associated with Post-Traumatic Stress Disorder. A severe maternal morbidity episode is not associated with Post-Traumatic Stress Disorder symptoms within five years of the severe maternal morbidity event and birth. However, a more advanced maternal age and primiparity increased the risk of Post-Traumatic Stress Disorder. This does not imply that women who had experienced a severe maternal morbidity event did not suffer or need differentiated care.

Rare and unusual ... or are they? Less commonly diagnosed encephalopathies associated with systemic disease.

Science.gov (United States)

Weathers, Allison L; Lewis, Steven L

2009-04-01

Encephalopathy due to hepatic or renal failure, electrolyte disturbances, or the administration of benzodiazepines and narcotics is commonly encountered, well reviewed in the literature, and, therefore, not usually missed. This article focuses on encephalopathies that were previously well described but may be overlooked by modern clinicians, as well as those that are still taught in the classroom but seldom thought of in practice. Due to the presumed relative rarity of these cases and emphasis on the well-memorized "classic" clinical presentations, these often treatable, and perhaps not so rare, encephalopathies due to systemic medical illness may go undiagnosed and untreated. Pancreatic encephalopathy, Wernicke's encephalopathy, and pellagra encephalopathy are reviewed in detail; cefepime and ifosfamide encephalopathies are discussed as examples of specific medication-induced encephalopathies. Septic encephalopathy, central pontine myelinolysis, and fat embolism syndrome are briefly reviewed. The encephalopathies reviewed have the potential for devastating neurological consequences if recognition and, therefore, treatment are delayed. Clinical improvement for many of these syndromes depends on prompt intervention. This article highlights some representative examples of less-commonly diagnosed metabolic and toxic encephalopathies.

Ceftriaxone attenuates hypoxic-ischemic brain injury in neonatal rats

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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.

Research progress of BOLD-fMRI in minimal hepatic encephalopathy

International Nuclear Information System (INIS)

Zhou Zhiming; Zhao Jiannong

2013-01-01

The minimal hepatic encephalopathy is the early stage of hepatic encephalopathy. It has few apparent clinical symptoms and specific manifestations, and is difficult to diagnose. In the recent years, BOLD-fMRI has been used to study hepatic encephalopathy gradually. Through detection of the brain neuron activities in different states, it can not only locate the abnormal activity of brain functional areas, but also can find the changes of brain functional connectivity. BOLD- fMRI combining with other MR technologies can explore the pathology and pathogenesis of minimal hepatic encephalopathy from micro to macro and from structure to function. (authors)

Potentially modifiable factors contributing to sepsis-associated encephalopathy.

Science.gov (United States)

Sonneville, Romain; de Montmollin, Etienne; Poujade, Julien; Garrouste-Orgeas, Maïté; Souweine, Bertrand; Darmon, Michael; Mariotte, Eric; Argaud, Laurent; Barbier, François; Goldgran-Toledano, Dany; Marcotte, Guillaume; Dumenil, Anne-Sylvie; Jamali, Samir; Lacave, Guillaume; Ruckly, Stéphane; Mourvillier, Bruno; Timsit, Jean-François

2017-08-01

Identifying modifiable factors for sepsis-associated encephalopathy may help improve patient care and outcomes. We conducted a retrospective analysis of a prospective multicenter database. Sepsis-associated encephalopathy (SAE) was defined by a score on the Glasgow coma scale (GCS) sepsis at ICU admission, of whom 1341 (53%) had sepsis-associated encephalopathy. After adjusting for baseline characteristics, site of infection, and type of admission, the following factors remained independently associated with sepsis-associated encephalopathy: acute renal failure [adjusted odds ratio (aOR) = 1.41, 95% confidence interval (CI) 1.19-1.67], hypoglycemia 10 mmol/l (aOR = 1.37, 95% CI 1.09-1.72), hypercapnia >45 mmHg (aOR = 1.91, 95% CI 1.53-2.38), hypernatremia >145 mmol/l (aOR = 2.30, 95% CI 1.48-3.57), and S. aureus (aOR = 1.54, 95% CI 1.05-2.25). Sepsis-associated encephalopathy was associated with higher mortality, higher use of ICU resources, and longer hospital stay. After adjusting for age, comorbidities, year of admission, and non-neurological SOFA score, even mild alteration of mental status (i.e., a score on the GCS of 13-14) remained independently associated with mortality (adjusted hazard ratio = 1.38, 95% CI 1.09-1.76). Acute renal failure and common metabolic disturbances represent potentially modifiable factors contributing to sepsis-associated encephalopathy. However, a true causal relationship has yet to be demonstrated. Our study confirms the prognostic significance of mild alteration of mental status in patients with sepsis.

Hypoxic stress-induced changes in ribosomes of maize seedling roots

International Nuclear Information System (INIS)

Bailey-Serres, J.; Freeling, M.

1990-01-01

The hypoxic stress response of Zea mays L. seedling roots involves regulation of gene expression at transcriptional and posttranscriptional levels. We investigated the effect of hypoxia on the translational machinery of seedling roots. The levels of monoribosomes and ribosomal subunits increased dramatically within 1 hour of stress. Prolonged hypoxia resulted in continued accumulation of nontranslating ribosomes, as well as increased levels of small polyribosomes. The return of seedlings to normal aerobic conditions resulted in recovery of normal polyribosome levels. Comparison of ribosomal proteins from control and hypoxic roots revealed differences in quantity and electrophoretic mobility. In vivo labeling of roots with [ 35 S]methionine revealed variations in newly synthesized ribosomal proteins. In vivo labeling of roots with [ 32 P]orthophosphate revealed a major reduction in the phosphorylation of a 31 kilodalton ribosomal protein in hypoxic stressed roots. In vitro phosphorylation of ribosomal proteins by endogenous kinases was used to probe for differences in ribosome structure and composition. The patterns of in vitro kinased phosphoproteins of ribosomes from control and hypoxic roots were not identical. Variation in phosphoproteins of polyribosomes from control and hypoxic roots, as well as among polyribosomes from hypoxic roots were observed. These results indicate that modification of the translational machinery occurs in response to hypoxic stress

Effect of systemic inflammatory response in the development of encephalopathy in severe thermal injury

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Sorokina O.Y.

2015-11-01

Full Text Available The article discusses the burn encephalopathy as a manifestation of organ dysfunction. Purpose: to determine the impact of the systemic inflammatory response to the development of en­cephalopathy in thermal injury. The study involved 104 patients, who were divided into two groups depending on the severity of the burn injury. The development of SIRS in patients was confirmed by high levels of IL-6 during the whole period of observation. The level of IL-6 did not affect the development, timing and duration of sleep disorders in both groups. The level of LII on the day 1 affects the development of sleep disorders in group 1 (R=0.499, p=0.041. Development of insomnia correlated with the shift of leukocyte formula to the left in group 2 on the day 5 (R=0.349, p=0.020. We found a relationship between the development of delirium, its duration and the level of young forms of neutrophils in patients of 1 (R=0.563, p=0.001 and 2 (R=0.3488, p=0.003 groups. Development of delirium, its timing and duration correlated with the level of IL-6 on day 3 (R=0.812, p=0,049, R=0.5903, p=0.079 and R=0.615, p=0.059, respectively in the group 2. The extent of the inflammatory reaction determined the disorders of thought (R=-0.545, p=0.036, memory (R=-0.547, p=0.023 and the dynamic of the recovery of cognitive functions in patients of group 1. Cognitive deficit correlated with the level of IL-6 (R=0.760, p=0.079 and the level of young forms of neutrophils (R=-0.603, p=0,013 in group 2. Thus, SIRS is a defining moment in the development of nervous system dysfunction in severe thermal injury.

Dengue viral infections as a cause of encephalopathy

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Malavige G

2007-01-01

Full Text Available The aim of this study was to determine the clinical characteristics and poor prognostic factors associated with high mortality in dengue encephalopathy. Fifteen patients with confirmed dengue infections, who developed encephalopathy, were recruited from two tertiary care hospitals in Colombo, Sri Lanka. Among the factors that contributed to encephalopathy were: Acute liver failure (73%, electrolyte imbalances (80% and shock (40%. Five (33.3% patients developed seizures. Disseminated intravascular coagulation was seen in five (33.3%. Secondary bacterial infections were observed in 8 (53.3% of our patients. The overall mortality rate was 47%.

CDKL5 Mutations in Boys With Encephalopathy and Early-Onset Intractable Epilepsy

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J Gordon Millichap

2008-10-01

Full Text Available Clinical and EEG data of 3 Italian boys (ages 3, 9, and 13 years with severe early-onset encephalopathy, mental retardation, facial dysmorphisms, and intractable epilepsy were found to carry missense mutations in the CDKL5 gene, in a report from Troina, Italy.

Hypoxic Preconditioning Promotes the Bioactivities of Mesenchymal Stem Cells via the HIF-1?-GRP78-Akt Axis

OpenAIRE

Lee, Jun Hee; Yoon, Yeo Min; Lee, Sang Hun

2017-01-01

Mesenchymal stem cells (MSC) are ideal materials for stem cell-based therapy. As MSCs reside in hypoxic microenvironments (low oxygen tension of 1% to 7%), several studies have focused on the beneficial effects of hypoxic preconditioning on MSC survival; however, the mechanisms underlying such effects remain unclear. This study aimed to uncover the potential mechanism involving 78-kDa glucose-regulated protein (GRP78) to explain the enhanced MSC bioactivity and survival in hindlimb ischemia. ...

Minimal hepatic encephalopathy characterized by parallel use of the continuous reaction time and portosystemic encephalopathy tests

DEFF Research Database (Denmark)

Lauridsen, M M; Schaffalitzky de Muckadell, O B; Vilstrup, H

2015-01-01

Minimal hepatic encephalopathy (MHE) is a frequent complication to liver cirrhosis that causes poor quality of life, a great burden to caregivers, and can be treated. For diagnosis and grading the international guidelines recommend the use of psychometric tests of different modalities (computer...... based vs. paper and pencil). To compare results of the Continuous Reaction time (CRT) and the Portosystemic Encephalopathy (PSE) tests in a large unselected cohort of cirrhosis patients without clinically detectable brain impairment and to clinically characterize the patients according to their test...

Compare Of the West Syndrome with Other Syndromes in the Epileptic Encephalopathy - Kosovo Experience

Science.gov (United States)

Zeka, Naim; Gërguri, Abdurrahim; Bejiqi, Ramush; Retkoceri, Ragip; Vuciterna, Armend

2017-01-01

BACKGROUND: West Syndrome (WS) represents as a specific epileptic encephalopathy characterised with a unique type of attacks, called infantile spasms, severe forms of abnormalities in electroencephalographic (EEG) records as a hypsarythmias and delays in the psychomotoric development. The characteristics of the disease, mostly affecting male gender, are infantile spasms and typical findings in EEG as a hypsarythmia. Infantile spasms are a consequence of many factors in the undeveloped brain. AIM: We aimed: (1) to see the incidence of the illness and the spreading out because of gender in rapport with other syndromes in the epileptic encephalopathies group; (2) to show principles of the treatment for the illness; and (3) to present the effects of the disease in the psycho-motoric development of affected children. METHODS: The study was designed as a cross-sectional study of the patients with epileptic encephalopathies, treated in Paediatric Clinic in Prishtina, from 1st of January 2013 until the 31st of December 2015. RESULTS: From the cohort group of 97 children diagnosed with epileptic encephalopathies, in 14 of them clinical and EEG signs of WS were noted. The earliest age of disease manifestation was 74 days (± 63.8 days). On the group of children with WS, 13 of them with Natrium Valpropat were treated, with the doses of 301.9 mg (± 64.1). From the cohort group, in 89 children (91.8%) psychomotoric retardation was documented, within the higher reoccurrence in the undifferentiated epileptic encephalopathies (96%) and the WS (78.6%). CONCLUSION: WS is a frequent disease of the encephalopathies with the epileptogenic framework. The resistance in anticonvulsive therapy is huge, and psychomotoric retardation follows a big percentage of children with this syndrome. PMID:29362620

Preliminary report of the Hepatic Encephalopathy Assessment Driving Simulator (HEADS) score.

Science.gov (United States)

Baskin-Bey, Edwina S; Stewart, Charmaine A; Mitchell, Mary M; Bida, John P; Rosenthal, Theodore J; Nyberg, Scott L

2008-01-01

Audiovisual simulations of real-life driving (ie, driving simulators) have been used to assess neurologic dysfunction in a variety of medical applications. However, the use of simulated driving to assess neurologic impairment in the setting of liver disease (ie, hepatic encephalopathy) is limited. The aim of this analysis was to develop a scoring system based on simulated driving performance to assess mild cognitive impairment in cirrhotic patients with hepatic encephalopathy. This preliminary analysis was conducted as part of the Hepatic Encephalopathy Assessment Driving Simulator (HEADS) pilot study. Cirrhotic volunteers initially underwent a battery of neuropsychological tests to identify those cirrhotic patients with mild cognitive impairment. Performance during an audiovisually simulated course of on-road driving was then compared between mildly impaired cirrhotic patients and healthy volunteers. A scoring system was developed to quantify the likelihood of cognitive impairment on the basis of data from the simulated on-road driving. Mildly impaired cirrhotic patients performed below the level of healthy volunteers on the driving simulator. Univariate logistic regression and correlation models indicated that several driving simulator variables were significant predictors of cognitive impairment. Five variables (run time, total map performance, number of collisions, visual divided attention response, and average lane position) were incorporated into a quantitative model, the HEADS scoring system. The HEADS score (0-9 points) showed a strong correlation with cognitive impairment as measured by area under the receiver-operator curve (.89). The HEADS system appears to be a promising new tool for the assessment of mild hepatic encephalopathy.

Normalization of the psychometric hepatic encephalopathy score for ...

African Journals Online (AJOL)

Aim: To construct normal values for the tests of the psychometric hepatic encephalopathy score (PHES) and evaluate the prevalence of minimal hepatic encephalopathy (MHE) among Turkish patients with liver cirrhosis. Materials and Methods: One hundred and eighty-five healthy subjects and sixty patients with liver ...

Reduced miR-659-3p levels correlate with progranulin increase in hypoxic conditions: implications for frontotemporal dementia.

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Paola ePiscopo

2016-05-01

Full Text Available Progranulin (PGRN is a secreted protein expressed ubiquitously throughout the body, including the brain, where it localizes in neurons and activated microglia. Loss-of-function mutations in the GRN gene are an important cause of familial Frontotemporal Lobar Degeneration (FTLD. PGRN has a neurotrophic and anti-inflammatory activity, and it is neuroprotective in several injury conditions, such as oxygen or glucose deprivation, oxidative injury, and hypoxic stress. Indeed, we have previously demonstrated that hypoxia induces the up-regulation of GRN transcripts. Several studies have shown microRNAs involvement in hypoxia. Moreover, in FTLD patients with a genetic variant of GRN (rs5848, the reinforcement of miR-659-3p binding site has been suggested to be a risk factor. Here, we report that miR-659-3p interacts directly with GRN 3’UTR as shown by luciferase assay in HeLa cells and ELISA and Western Blot analysis in HeLa and Kelly cells. Moreover, we demonstrate the physical binding between GRN mRNA and miR-659-3p employing a miRNA capture-affinity technology in SK-N-BE and Kelly cells. In order to study miRNAs involvement in hypoxia-mediated up-regulation of GRN, we evaluated miR-659-3p levels in SK-N-BE cells after 24h of hypoxic treatment, finding them inversely correlated to GRN transcripts. Furthermore, we analyzed an animal model of asphyxia, finding that GRN mRNA levels increased at post-natal day (pnd 1 and pnd 4 in rat cortices subjected to asphyxia in comparison to control rats and miR-659-3p decreased at pnd 4 just when GRN reached the highest levels. Our results demonstrate the interaction between miR-659-3p and GRN transcript and the involvement of miR-659-3p in GRN up-regulation mediated by hypoxic/ischemic insults.

Retinal neuroprotection by hypoxic preconditioning is independent of hypoxia-inducible factor-1 alpha expression in photoreceptors.