Ischemic Encephalopathy Research Articles

Hypoglycemic encephalopathy mimicking acute ischemic stroke in clinical presentation and magnetic resonance imaging: a case report

BackgroundThe imaging findings of hypoglycemic encephalopathy can be considerably similar to those of ischemic infarction or toxic leukoencephalopathy. We demonstrated unusual magnetic resonance (MR) imaging features of hypoglycemic encephalopathy which can be confused with other pathology both on imaging and acute clinical presentation. The diffusion-weighted imaging (DWI) and apparent diffusion coefficients (ADC) map findings in our case further supports the hypothesis of hypoglycemia-induced “excitotoxic injury” of glial cells and myelin sheath that might protect neuron axons from intracellular edema and irreversible damage.Case presentationA 72-year-old woman presented with poor appetite and was initially drowsy at home; the symptoms progressed to loss of consciousness accompanied by mild incontinence. The initial glucose level was 44 mg/dL, but no nausea, vomiting, fever, or cold sweating was reported. Physical examination after intravenous glucose supplementation revealed the absence of focal neurological signs, facial palsy, and tongue or eye deviations. The images obtained 24 h after symptoms onset revealed symmetrical hyperintensities on DWI (b-value: 1000) associated with hypointensities on ADC map along the corticospinal tract, from the levels of the cerebral peduncle and the posterior limbs of the internal capsule to the level of the corona radiata, which may mimic the imaging findings of acute ischemic infarction or amyotrophic lateral sclerosis. The patient received sliding-scale insulin therapy and rehabilitation, and she recovered consciousness without motor function deficits after 1 month. Moreover, repeat DWI and ADC map showed the complete disappearance of the lesions.ConclusionsIn the phenomenon of excitotoxic injury, axons could be protected from intracellular edema and irreversible damage, which may explain the reversible clinical symptoms and imaging abnormality after controlling for blood glucose because of the preserved motor axon. The diagnosis of acute symptomatic hypoglycemic encephalopathy through clinical and imaging features can be challenging. It is crucial to differentiate it from ischemic encephalopathy since the management and clinical outcome are different.

Neurodevelopmental Outcomes for Infants Treated with Whole Body Cooling After Hypoxic- Ischemic Encephalopathy with and without Clinical Seizures: Retrospective Chart Review

Neurodevelopmental Outcomes for Infants Treated with Whole Body Cooling After Hypoxic- Ischemic Encephalopathy with and without Clinical Seizures: Retrospective Chart Review

THE CHANGES IN THE PERIVENTRICULAR ZONE AND BRAIN CORTEX IN PRETERM NEWBORN WITH VERY LOW BIRTH WEIGHT AND EXTREME LOW BIRTH WEIGHT

The results of autopsy material of preterm newborns very low birth weight (VLBW) and extremely low birth weight (ELBW) brains are presented. In life the brains lesions were detected in the examined newborns with cranial ultrasound and MRI (intraventricular herminal hemorrhages/IVH and hypoxic — ischemic encephalopathy /HIE). In this researching were been using method of microscopy. Postmortem examination confirmed brain cell migration continues after birth in all examined newborns. This study have detailed the directions, positions, thickness cells migration columns. There were found that cells migration thickness and length depend on gestation age of preterm newborn with IVH and HIE. Besides we found the age morphologic differences in cell structures cerebral cortex in preterm newborns.

Clinical Profile of Hypoxic- Ischemic Encephalopathy in Neonates with Birth Asphyxia in a Rural Tertiary Care Hospital in Central India

Clinical Profile of Hypoxic- Ischemic Encephalopathy in Neonates with Birth Asphyxia in a Rural Tertiary Care Hospital in Central India

Neuronal Growth After Treatment with Human Adipose Stem Cells in Rat Pups Post Hypoxic – Ischemic Encephalopathy

Neuronal Growth After Treatment with Human Adipose Stem Cells in Rat Pups Post Hypoxic – Ischemic Encephalopathy

Routine addition of diffusion-weighted imaging to pediatric brain imaging with acute presentation: An initial experience

Context: A number of disorders affecting the pediatric brain pose a diagnostic challenge. Magnetic resonance imaging (MRI) is widely accepted as a sensitive technique for the diagnosis of ischemia, encephalitis, and leukodystrophies. Conventional MR sequences used in routine practice include T1-weighted (T1-W), T2-weighted, and fluid-attenuation inversion recovery (FLAIR) sequences. However usually, the presentation in small children is confusing and presents a diagnostic challenge even after the use of these various MR sequences requiring repeated MRI examinations. Detecting pathological changes occurring at microenvironment level is vital for early diagnosis, effective treatment, and obviating the need of repeated MRI. Aims: The purpose of our study was to assess the additional role of diffusion-weighted imaging (DWI) in better detection of these various pathologies of brain. Settings and Design: This was a prospective study. Subjects and Methods: Thirty children of ages ranging from neonate to 12 years of age with various complaints of central nervous system involvement were evaluated with MRI brain within 72 h of initial clinical presentation. T1 and T2 spin-echo sequences FLAIR and postcontrast T1-W imaging were done. DWI was performed with echoplanar imaging using depth-resolved surface coil spectroscopy sequence. The lesions were evaluated on DWI and conventional sequences. The final diagnosis was established on the basis of clinical evaluation, electroencephalographic findings, imaging, cerebrospinal fluid analysis, serologic tests, and fatty acid evaluation in plasma assay. Statistical Analysis Used: This was a descriptive study. Results: The patients were divided into three groups. Group A included patients in whom DWI detected more lesions or showed a greater extent of lesions on apparent diffusion coefficient (ADC) map than conventional MRI. This group had 11 cases including 7 cases of ischemic encephalopathy, one case of adrenoleukodystrophy (ADL) showing increased extent of lesion with restricted diffusion at the advancing edge and 3 cases of viral encephalitis. In Group B, 12 cases had similar results in both DWI and conventional MRI imaging. Of these, 7 cases with no specific diagnosis and subsequent spontaneous recovery showed no lesion on both conventional and DWI; 5 cases showed equal extent and number of lesions on DWI; 1 case was diagnosed as ADL, 2 as viral encephalitis, and 2 as ischemic encephalopathy on final workup. In Group C, T2 and FLAIR showed more lesions than DWI and had 7 cases. 5 had normal ADC maps but 1–2 small hyperintense lesions on T2 and FLAIR imaging, while the remaining two diagnosed with ischemic encephalopathy had hyperintense areas on T2 and FLAIR sequences with associated ventricular enlargement and cortical atrophy while DWI revealed them to be T2 shine through areas with increased ADC value focally. The 5 cases with hyperintensity on T2 and FLAIR, but normal ADC maps were labeled as nonspecific white matter hyperintensities. These children showed neither any progress of lesion nor any further clinical symptoms during the duration of study. Conclusions: We concluded that DWI was more sensitive than the other MR sequences in detecting early pathological changes even in cases of viral encephalitis and leukodystrophy apart from ischemia. It was also helpful in delineating the area more accurately at the microscopic level. We were also able to rule out actual pathology from nonspecific hyperintensities on T2 and FLAIR in some cases on DWI.

INTEGRATED MODEL FOR THE PREDICTION OF ORGANIC DYSFUNCTIONS DEVELOPMENT IN NEWBORNS WITH ASPHYXIA AND APPLIED POINTS OF ITS IMPLEMENTATION

Relevance of the research. The causes of asphyxia are well known, but the debates about the importance of antenatal and intranatal factors in its development are still ongoing. Identification of clear predictors for the development of the dysfunction in vital and non-vital organs will improve the existing algorithms for monitoring neonates who are subject to hypoxia/asphyxia, and will enable the doctors to make decisions on the timely use of personalized therapeutic and diagnostic measures aimed at reducing mortality, morbidity, childhood disability and enhancing the quality of their life.The aims of the research are substantiation and development of the integrated model for prediction of organ dysfunctions, and improvement of the algorithm for monitoring newborns with asphyxia in the early neonatal period.Materials and methods. The study included 72 full-term infants with asphyxia and 35 healthy newbornswho were born at the perinatal centre of M.V. Sklifosovsky Poltava Regional Clinical Hospital and Poltava City Clinical Maternity Hospital in 2011-2013. We studied the associations between the development of organ dysfunction and risk factors characterizing the somatic, obstetric, antenatal/intranatal history of the mother, the condition of the infant, the volume of primary resuscitation, as well as the metabolic, inflammatory and vascular biomarkers. The prediction of lesions of organs and systems of the newborn is considered from the point of view of pathophysiological mechanisms of circulatory and non-circulatory adaptation reactions in newborns with asphyxia, when against the background of increased cerebral, coronary and adrenal blood flow, there is a decrease in perfusion in the kidneys, lungs, gastrointestinal tract, liver and their dysfunctions.Results of the research. The proposed integrated model for the prediction of lesions of vital and non-vital organs demonstrates the insignificant role of ante and intranatal factors in the prognosis of multiorgan dysfunction development. It was determined that the prognostic model for the development of hypoxic and ischemic encephalopathy, which includes poor uterine contraction strength (odds ratio 13.2), administering 0.9% solution of sodium chloride during primary intensive care (OR 9.2), LDH level >1700 units/l (OR 7.4) and creatinine>110 mmol/l (OR 15.9) for 1 day of life has an area under the ROC curve of 0.8711. The development of myocardial dysfunction is reliably associated with glucose levels <3.3 mmol/l (OR 11.6), urea >7.0 mmol/l (OR 21.3) and NO2¯+ NO3¯ <21 mmol/l in urine (OR 15.2) and the prognostic model of its development has an area under the ROC curve of 0.8368. The prognostic models for the development of lesions of non-vital organs, in particular, the dysfunction of the gastrointestinal tract (Apgar score of <5 points on the 5th min., administering 4% NaHCO3 solution during the course of reanimation measures, glucose level <3.3 mmol/l, urea <6.0 mmol/l) and acute myocardial infarction (Apgar score <4 points on the 5th min. of life, meconial aspiration), have the corresponding areas under the ROC curves − 0.8424 and 0.8054.Taking into account the pathophysiological mechanisms of organ dysfunction development in newborns with asphyxia, 4 possible clinical scenarios were suggested for the aforementioned disease, which allow to assume the time hypoxic / asphyxial episode.The algorithm for monitoring infants with possible or present hypoxic episode has been improved, in particular, if a child has at least one of the following symptoms: sentinel event, Apgar score less than 7 points on the 5th min. of life, pH of umbilical cord blood less than 7.25, use of artificial lung ventilation during resuscitation. In addition to the recommendations provided by the Order of the Ministry of Healthcare No. 255 as of 2014, it is advisable to prescribe the following studies: complete blood count, blood glucose level, creatinine, urea in blood serum at the obstetrical inpatient establishments of the 2nd level, and in addition to the abovesaid − NO2¯ + NO3¯ in the urine − for obstetric hospitals of the 3rd level.Conclusions. The integrated model for the prediction of organ dysfunctions development in newborns with asphyxia has been substantiated; the applied points of its implementation have been determined; and the algorithm for monitoring the newborns with a score less than 7 points on the 5th min. of life has been suggested.

Canine primary encephalopathies: a retrospective study of 48 cases (2008-2012)

A retrospective study was performed on 48 dogs with primary encephalopathies, admitted during a 5-year period (2008-2012). Their age ranged from 2 months to 19 years, the majority being older than 10 years. Genders were almost equally distributed and most animals were purebreds or crossbreds. Onset of neurological signs was acute (11/48), subacute (12/48) or chronic (24/48). Lesion localization was focal in 31 and multifocal in 17 dogs. The cerebrum and brainstem were the most common focal localizations, while cerebellar lesions were recorded only in 4 dogs. An aetiologic diagnosis was established in 29 dogs and included primary (8/29) or metastatic neoplasia (2/29), encephalitis of variable etiology (9/29), congenital or inherited diseases (6/29), senile cognitive dysfunction (3/29) and ischaemic encephalopathy (1/29). In the remaining 19 dogs, aetiology of intracranial dysfunction was not determined; however a tentative diagnosis was speculated in eight of these cases and included breed specific and viral encephalitis, neoplasia, ischaemic encephalopathy and inherited disease. Most dogs were euthanized due to the debilitating neurological signs (24/48) or died from complications of their illness (13/48). Six animals are still alive with symptomatic medical treatment and supportive nursing care and 5 were lost to follow up.

Зміни метаболізму амінокислот при перинатальній гіпоксично-ішемічній енцефалопатії та їх залежність від ступеня морфологічних змін головного мозку за даними нейросонографії

Зміни метаболізму амінокислот при перинатальній гіпоксично-ішемічній енцефалопатії та їх залежність від ступеня морфологічних змін головного мозку за даними нейросонографії

Prenatal and Early Postnatal Environmental Enrichment Reduce Acute Cell Death and Prevent Neurodevelopment and Memory Impairments in Rats Submitted to Neonatal Hypoxia Ischemia.

Environmental enrichment (EE) is an experimental strategy to attenuate the negative effects of different neurological conditions including neonatal hypoxia ischemia encephalopathy (HIE). The aim of the present study was to investigate the influence of prenatal and early postnatal EE in animals submitted to neonatal HIE model at postnatal day (PND) 3. Wistar rats were housed in EE or standard conditions (SC) during pregnancy and lactation periods. Pups of both sexes were assigned to one of four experimental groups, considering the early environmental conditions and the injury: SC-Sham, SC-HIE, EE-sham, and EE-HIE. The offspring were euthanized at two different time points: 48h after HIE for biochemical analyses or at PND 67 for histological analyses. Behavioral tests were performed at PND 7, 14, 21, and 60. Offspring from EE mothers had better performance in neurodevelopmental and spatial memory tests when compared to the SC groups. HIE animals showed a reduction of IGF-1 and VEGF in the parietal cortex, but no differences in BDNF and TrkB levels were found. EE-HIE animals showed reduction in cell death, lower astrocyte reactivity, and an increase in AKTp levels in the hippocampus and parietal cortex. In addition, the EE was also able to prevent the hippocampus tissue loss. Altogether, present findings point to the protective potential of the prenatal and early postnatal EE in attenuating molecular and histological damage, as well as the neurodevelopmental impairments and the cognitive deficit, caused by HIE insult at PND 3.

Clinical research of Xingnaojing injection combined with naloxone in the treatment of hypoxic ischemic encephalopathy

Objective To observe the clinical effect of Xingnaojing injection combined with naloxone in the treatment of hypoxic ischemic encephalopathy. Methods 62 patients with hypoxia ischemia encephalopathy were randomly assigned into the control group(31 cases) and the treatment group(31 cases). The control group used naloxone treatment on the basis of the conventional treatment.The treatment group received Xingnaojing injection combined with naloxone treatment on the basis of routine treatment.The changes in different time of Glasgow Coma Scale(GCS) scores of the two groups after treatment were compared. Results After treatment for 1, 5, 10, 15d, the GCS scores in the control group were (5.27±0.87)points, (9.03±0.72)points, (10.03±0.72)points, (13.03±0.72)points respectively, which in the treatment group were (5.14±1.03)points, (9.24±1.06)points, (13.31±2.83)points, (15.31±0.93)points.The differences of GCS scores after treatment for 15, 10d between the two groups were statistically significant(t=15.113, 10.501, P=0.00, 0.00). In the control group, the total effective rate was 50.0%, which of the treatment group was 82.7%, the total effective rate between the two groups had statistically significant difference(χ2=6.437, P<0.05). Conclusion On the basis of routine treatment, Xingnaojing injection combined with naloxone in the treatment of hypoxic ischemic encephalopathy has better effect than the single use of naloxone treatment. Key words: Hypoxia-ischemia, brain; Xingnaojing; Naloxone

Neural Stem Cell Transplantation and CNS Diseases.

In neurological disorders, pathological lesions in the central nervous system (CNS) may be globally dispersed throughout the brain or localized to specific regions. Although native neural stem cells (NSCs) are present in the adult mammalian brain, intrinsic self-repair of injured adult CNS tissue is inadequate or ineffective. The brain's poor regenerative ability may be due to the fact that NSCs are restricted to discrete locations, are few in number, or are surrounded by a microenvironment that does not support neuronal differentiation. Therapeutic potential of NSC transplantation in CNS diseases characterized by global degeneration requires that gene products and/or replaced cells be widely distributed. Global degenerative CNS diseases include inherited pediatric neurodegenerative diseases (inborn errors of metabolism, including lysosomal storage disorders (LSDs), such as Tay-Sachs-related Sandhoff disease), hypoxic or ischemic encephalopathy, and some adult CNS diseases (such as multiple sclerosis). Both mouse and human NSCs express many chemokines and chemokine receptors (including CXCR4 and adhesion molecules, such as integrins, selectins, and immunoglobulins) that mediate homing to sources of inflammatory chemokines, such as SDF-1α. In mammalian brains of all ages, NSCs may be attracted even at a great distance to regions of neurodegeneration. Consequently, NSC transplantation presents a promising strategy for treating many CNS diseases.

87. Median nerve SEPs predict motor outcome in neonatal ipossic-ischemic encephalopathy treated with hypothermia

The role of SEPs in motor prognosis of hypoxic–ischemic neonatal encephalopathy has been evaluated in pre-hypothermia era (Suppiej, 2010) but their role in babies treated with hypothermia has not been studied yet. We investigated motor outcome at 12 months of age in 38 children who suffered from hypoxic–ischemic neonatal encephalopathy and were treated with hypothermia at the NICU of the Paediatric University Hospital of Padua. All performed median nerve SEPs in the neonatal period, traces were scored as bilaterally present (group1) or as bilaterally/unilaterally absent (group2) cortical N20 response. At follow up 4/38 children had the diagnosis of cerebral palsy (all of them had bilaterally absent cortical SEP). Of the remaining 34, 7 had abnormal (

Legal Briefs: Prolonged Labor and Ischemic Encephalopathy

A 4,232-g 40-3/7-week-gestation male infant was delivered by a 38-year-old gravida 1, para 0 woman after 4 days of uterine contractions. Eighteen hours before delivery when the cervix was 5 cm dilated, 100% effaced, and the fetus was at –2 station, the obstetrician artificially ruptured the membranes and placed an intrauterine pressure catheter (IUPC). The plaintiff obstetrical expert pointed out that the IUPC was not calibrated and this was below the standard of care. A caput was discovered at this point. The plaintiff obstetrical expert pointed out that much pressure must have been exerted on the fetal head thus far to have produced a caput before the second stage of labor. The presence of the caput did not allow the obstetrical team, which consisted of a midwife, a remotely distant supervising obstetrician, and several shifts of bedside nurses, to accurately assess the station and position of the fetus. The midwife noted variable decelerations with increasing frequency and severity 24 hours before delivery, prompting her to perform an amnioinfusion. The anesthesiologist provided an epidural. The plaintiff obstetrical expert maintained that because there were multiple and deep variables during the first stage of labor, it was very probable that the fetus would not be able to tolerate the contractions during the second stage. He further contended that delivery was remote, considering the slow progress of labor up to this point, and it was unlikely that a safe vaginal delivery could be reasonably expected. In fact, multiple attempts were made with intravenous boluses, position changes, and supplemental oxygen to help the fetus recover from the deep decelerations during the first stage of labor. The recovery to the prior baseline heart rate (HR) after decelerations initially was good. However, as time went on, by 16 hours before delivery, the fetus was not recovering well …

Hyperhomocysteinemia in developing age and nutritional aspects of folates: an early cardiovascular risk factor

During the last decade, scientific evidence is mounting that elevated plasma levels of homocysteine are associated with an increased risk of atherosclerosis and cardiovascular ischemic events. Despite this evidence, however, there are still concerns about the mechanisms(s) by which homocysteine exerts its pro-atherogenic effect, and it is unclear whether the decreased plasma levels of homocysteine through diet or drugs may be paralleled by a reduction in cardiovascular risk. Experimental studies have shown that many possible mechanisms are implicated in the pro-atherogenic effect of homocysteine. Endothelial function is altered in subjects with hyperhomocysteinemia, and endothelial dysfunction is correlated with plasma levels of homocysteine. Exercise training reduces plasma levels of homocysteine and improves endothelial function, however without evidence of a better outcome. Larger studies are needed in order to demonstrate that the reduction of plasma levels of homocysteine by oral supplementation with folates and vitamins B6 and B12 translates into a decreased incidence of ischemic events, in particular in patients with documented coronary artery disease and ischemic encephalopathy.

Poster 395 Adrenoleukodystrophy Diagnosed in a Patient Admitted to a Pediatric Inpatient Rehabilitation Hospital for Hypoxic, Ischemic Encephalopathy: A Case Report

PM&RVolume 7, Issue 9S p. S220-S221 Pediatric Poster 395 Adrenoleukodystrophy Diagnosed in a Patient Admitted to a Pediatric Inpatient Rehabilitation Hospital for Hypoxic, Ischemic Encephalopathy: A Case Report Fabiola I. Reyes MD, Fabiola I. Reyes MD New York Presbyterian Hospital, New York, NY, United StatesSearch for more papers by this authorHeakyung Kim MD, Heakyung Kim MD New York Presbyterian Hospital, New York, NY, United StatesSearch for more papers by this authorRuth E. Alejandro MD, Ruth E. Alejandro MD New York Presbyterian Hospital, New York, NY, United StatesSearch for more papers by this authorHannah A. Shoval, Hannah A. Shoval New York Presbyterian Hospital, New York, NY, United StatesSearch for more papers by this author Fabiola I. Reyes MD, Fabiola I. Reyes MD New York Presbyterian Hospital, New York, NY, United StatesSearch for more papers by this authorHeakyung Kim MD, Heakyung Kim MD New York Presbyterian Hospital, New York, NY, United StatesSearch for more papers by this authorRuth E. Alejandro MD, Ruth E. Alejandro MD New York Presbyterian Hospital, New York, NY, United StatesSearch for more papers by this authorHannah A. Shoval, Hannah A. Shoval New York Presbyterian Hospital, New York, NY, United StatesSearch for more papers by this author First published: 08 September 2015 https://doi.org/10.1016/j.pmrj.2015.06.432Read the full textAboutPDF ToolsRequest permissionExport citationAdd to favoritesTrack citation ShareShare Give accessShare full text accessShare full-text accessPlease review our Terms and Conditions of Use and check box below to share full-text version of article.I have read and accept the Wiley Online Library Terms and Conditions of UseShareable LinkUse the link below to share a full-text version of this article with your friends and colleagues. Learn more.Copy URL Share a linkShare onFacebookTwitterLinked InRedditWechat No abstract is available for this article. Volume7, Issue9SSeptember 2015Pages S220-S221 RelatedInformation

Amplitude-integrated EEG abnormalities in two neonates with encephalopathy due to mitochondrial dysfunction (respiratory chain complex I deficiency)

Amplitude-integrated electroencephalography (aEEG) findings in hypoxic-ischemic encephalopathy characterized by secondary energy failure have been described in detail. In contrast, reports of use of aEEG in patients with encephalopathy due to primary energy failure as seen in inherited metabolic disorders are sparse. We report two cases of lethal mitochondrial encephalopathy due to mitochondrial respiratory chain complex I deficiency. We present clinical course, laboratory evaluations, aEEG, conventional electroencephalography, magnetic resonance imaging and magnetic resonance spectroscopy findings of two cases identified with mitochondrial encephalopathy between 2002 and 2007. Both infants were born at term. Both presented with intractable seizures and mild hypotonia within the first days of life, in the absence of any evidence suggestive of hypoxic- ischemic encephalopathy. Both cases were treated with multiple anticonvulsants and in neither case were seizures fully controlled. Magnetic resonance imaging in both cases revealed a structurally normal brain and case one showed subtle diffuse deep white matter signal abnormality. Magnetic resonance spectroscopy revealed no elevation of lactate. In both cases, aEEG tracings were markedly abnormal, confirmed by electroencephalography. Case one showed status epilepticus on an abnormally high amplitude background and case two presented with a mainly discontinuous background pattern with intermittent burst-suppression pattern activity. Complex I activity in skeletal muscle homogenate was abnormally low in both patients. The use of aEEG as a valuable assessment and monitoring tool in patients with metabolic encephalopathy should be further promoted.

LONG - TERM OUTCOMES OF HYPOXIC - ISCHEMIC ENCEPHALOPATHY OF NEWBORNS

Neonatal encephalopathy is a major cause of disability of term infants and one of the most universally recognized causes of severe, long-term neurological deficits. The aim was to study the neurological and mental development at age 1 year and 6 year old children who were born full term and had hypoxic-ischemic encephalopathy. Analysis of early neonatal period 36 term infants was compared with the results of neuropsychological development at the age of 1 year and 6 years of age. Adverse effects of the neonatal hypoxic-ischemic encephalopathy associated with resuscitation, not inadequate of protocol recommendations in 25% of patients, later transportation to a tertiary level of care, the need for prolonged mechanical ventilation. Adverse effects in the approximate age of 1 year recorded in about 50% of children who have suffered hypoxic - ischemic encephalopathy. Adverse long-term consequences aged 6 years is every fifth baby, including 30% cerebral palsy and 8% of a complex pathology. Children who at the 1 year age are diagnosed moderate delayed neuro-mental development after the rehabilitation process have the opportunity to neuro - psychological development disorders have not aged 6 years.

Neurological Sequels and Their Causes in Patients Hospitalized in the Toxicology Intensive Care Unit of Bahraloo Hospital, Tehran, Iran

Background: The occurrence of neurologic complications in the intensive care units (ICUs) is one of the major risks in management of patients. These sequels may be caused by structural or metabolic disorders. The same phenomenon can be seen in the toxicology ICUs, although the toxicological effects of drugs and poisons may also cause the neurological complications. Objectives: This study aimed to determine the frequency of neurological sequels and their causes in patients hospitalized in the toxicology ICUs. Patients and Methods: In this descriptive study, the data of patients admitted in toxicology ICU of Baharloo Hospital, Tehran, Iran, were investigated during a 2-year period (2010 ‒ 2011) and the patients with neurological sequels, based on neurological examination or brain computed tomography (CT) scan findings, were included. Data recorded in questionnaires were analyzed by means of SPSS software, with a significance level at P < 0.05. Results: Out of 1571 patients admitted in toxicology ICU during this period, 56 patients (3.56%), with the mean ± SD age of 36 ± 13.01 years, were included. The most common finding in neurological examination was the Babinski sign (67.9%). Ischemic encephalopathy with brain edema was the most common finding on the brain CT scans of these patients (33.9%). The mortality rate was 58.9% (33 out of 56). Thirteen patients (23.2%) were discharged with vegetative state. The most common cause of neurological sequel, in this study, was hypoxia (64.3%) Conclusions: This study, for the first time in Iran, investigated the frequency and cause of neurological sequels in toxicology ICUs. The findings can improve the prophylaxis and diagnostic programs for the patients in this field.

Gender-specific effects of CGP 55845, GABAB receptor antagonist, on neuromuscular coordination, learning and memory formation in albino mouse following neonatal hypoxia-ischemia insult.

GABAB receptor antagonists are experimentally proved as spatial memory enhancers in mouse models but their role has not been described following hypoxic-ischemic insult. 10-day-old albino mice were subjected to Murine model of hypoxia and ischemia. Following brain damage, mice were fed on normal rodent diet till they were 13 weeks old. At this time point, mice were divided into two groups. Group 1 received saline and group 2 received intraperitoneally CGP 55845 (1 mg/ml solvent/Kg body weight) for 12 days. Behavioural observations were made during rota rod, open field and Morris water maze test along with brain infarct measurement in both CGP 55845 treated and untreated groups. It was observed that application of GABAB receptor antagonist improved the over all motor function in male and female albino mice but effects were more pronounced in males. In open field, CGP 55845-treated female mice showed poor performance. CGP 55845 had no significant effect on learning and memory formation during Morris water maze test and also on brain infract size in both genders following hypoxia ischemia encephalopathy. Effects of CGP 55845 can be further explored in a dose and duration dependent manner to improve the learning and memory in albino mice following neonatal brain damage.