Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0038220 (status epilepticus)
 7,272 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Eleven of 89 dogs (12 per cent) developed neurological signs within six days of surgical attenuation of a congenital extrahepatic portosystemic shunt. Neurological signs were not associated with hepatic encephalopathy or hypoglycaemia. Signs varied in severity from non-progressive ataxia (three dogs) to generalised motor seizures (four dogs), progressing to status epilepticus (three dogs). In a further four cases, ataxia and disorientation were treated vigorously with anticonvulsant medication, presumably preventing the development of seizures. Two dogs that developed status epilepticus died or were eventually euthanased. All other animals survived, although some had persistent neurological deficits. Postligation neurological complications were not prevented by gradual shunt attenuation. Prophylactic treatment with phenobarbitone (5 to 10 mg/kg preoperatively, followed by 3 to 5 mg/kg every 12 hours for three weeks) did not significantly reduce the incidence of neurological sequelae (2/31 [6 per cent] dogs with phenobarbitone vs 9/58 [16 per cent] without phenobarbitone; P = 0.2). However, no animal receiving phenobarbitone experienced generalised motor seizures or status epilepticus. In conclusion, these observations suggest that postligation neurological syndrome comprises a spectrum of neurological signs of variable severity. Perioperative treatment with phenobarbitone may not reduce the risk of neurological sequelae, but may reduce their severity.
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PMID:Neurological dysfunction in dogs following attenuation of congenital extrahepatic portosystemic shunts. 1113 52

Acute neurodegeneration in man is encountered during and following stroke, transient cardiac arrest, brain trauma, insulin-induced hypoglycemia and status epilepticus. All these severe clinical conditions are characterized by neuronal calcium overload, aberrant cell signaling, generation of free radicals and elevation of cellular free fatty acids, conditions that favor activation of the mitochondrial permeability transition pore (mtPTP). Cyclosporin A (CsA) and its analog N-methyl-valine-4-cyclosporin A (MeValCsA) are potent blockers of the mtPTP and protect against neuronal death following excitotoxicity and oxygen glucose deprivation. Also, CsA and MeValCsA diminish cell death following cerebral ischemia, trauma, and hypoglycemia. Here we present data that strongly imply the mtPT in acute neurodegeneration in vivo. Compounds that readily pass the blood-brain-barrier (BBB) and block the mtPT may be neuroprotective in stroke.
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PMID:Mitochondrial permeability transition in acute neurodegeneration. 1202 55

Excitatory amino acid-induced death of central neurons may be mediated by at least two receptor types, the so-called NMDA (N-methyl-d-aspartate) and AMPA (alpha-amino-3-hydroxy-5-methyl-4-isoxazoleproprionate) receptors. We have studied the neurodegenerative mechanisms set in motion by AMPA receptor activation using incubated slices of 8-day-old rat cerebellum and hippocampus. In both preparations, AMPA induced a pattern of degeneration that differed markedly from the one previously shown to be elicited by NMDA. In cerebellar slices, AMPA induced the degeneration of most Purkinje cells together with a population of Golgi cells; in hippocampal slices the neurons were affected in the order CA3 > CA1 > dentate granule cells. Three mechanisms could be discerned: an acute one in which neurons (e.g. cerebellar Golgi cells) underwent a rapid degeneration; a delayed one in which the neurons (Purkinje cells and hippocampal neurons) appeared to be only mildly affected immediately after a 30 min exposure but then underwent a protracted degeneration during the postincubation period (1.5 - 3 h); and finally a slow toxicity, which took place during long (2 h) exposures to AMPA (3 - 30 microM). Although Purkinje cells were vulnerable in both cases, the efficacy of AMPA was higher for the delayed mechanism than for the slow one. The pathology displayed by the acutely destroyed Golgi neurons was a classical oedematous necrosis, whereas most neurons vulnerable to the delayed and slow mechanisms displayed a 'dark cell degeneration', whose cytological features bore a close resemblance to those of neurons irreversibly damaged by ischaemia, hypoglycaemia or status epilepticus in vivo.
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PMID:AMPA Neurotoxicity in Rat Cerebellar and Hippocampal Slices: Histological Evidence for Three Mechanisms. 1210 58

Isolated status epilepticus or severe hypoglycemia rarely causes irreversible focal neurologic deficits in children. We describe three children who presented with status epilepticus and prolonged hypoglycemia resulting in hemiplegia due to unilateral hemispheric damage. The non-vascular cortical topography of the lesions is consistent with selective neuronal necrosis, confirmed by histopathology in one patient. This suggests increased neuronal vulnerability to necrosis secondary to energy failure resulting from combination of hypoglycemia and status epilepticus.
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PMID:Unilateral cortical necrosis following status epilepticus with hypoglycemia. 1258 6

This study determined whether stroke and other types of insults produced a gene expression profile in blood that correlated with the presence of neuronal injury. Adult rats were subjected to ischemic stroke, intracerebral hemorrhage, status epilepticus, and insulin-induced hypoglycemia and compared with untouched, sham surgery, and hypoxia animals that had no brain injury. One day later, microarray analyses showed that 117 genes were upregulated and 80 genes were downregulated in mononuclear blood cells of the "injury" (n = 12) compared with the "no injury" (n = 9) animals. A second experiment examined the whole blood genomic response of adult rats after global ischemia and kainate seizures. Animals with no brain injury were compared with those with brain injury documented by TUNEL and PANT staining. One day later, microarray analyses showed that 37 genes were upregulated and 67 genes were downregulated in whole blood of the injury (n = 4) animals compared with the no-injury (n = 4) animals. Quantitative reverse transcription-polymerase chain reaction confirmed that the vesicular monoamine transporter-2 increased 2.3- and 1.6-fold in animals with severe and mild brain injury, respectively, compared with no-injury animals. Vascular tyrosine phosphatase-1 increased 2.0-fold after severe injury compared with no injury. The data support the hypothesis that there is a peripheral blood genomic response to neuronal injury, and that this blood response is associated with a specific blood mRNA gene expression profile that can be used as a marker of the neuronal damage.
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PMID:Blood genomic expression profile for neuronal injury. 1262 6

A 24-year-old woman of Somali origin delivered at term after an uncomplicated pregnancy. Post-partum haemorrhage resulted in hypovolaemic shock which was treated by hysterectomy. Five days later she became comatose due to unrecognised hypoglycaemia which caused severe irreversible brain damage and status epilepticus. Treatment in the intensive care unit with artificial respiration, prednisolone, desmopressin, inotropic support, barbiturates and an anaesthetic under EEG guidance was unsuccessful. The patient died 28 days post-partum. The hypoglycaemia was due to a combination of (a) inadequate glucose intake and (b) lack of counter-regulatory mechanisms due to a deficiency of steroids and growth hormone as a result of loss of pituitary function (Sheehan syndrome) together with adrenocortical insufficiency. The combination of Sheehan syndrome and primary adrenocortical insufficiency has not been described previously in the literature.
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PMID:[Irreversible coma following hypoglycemia in Sheehan syndrome with adrenocortical insufficiency]. 1464 66

This report describes a previously healthy 28 year old patient with a 5 month period of intractable generalised status epilepticus (SE) of unknown aetiology with fatal outcome. Repeated magnetic resonance imaging (MRI) showed no pre-existing abnormality, but did show progressive cortical and hippocampal atrophy and T2 hyperintensity in both hippocampal formations, suggestive of progressive tissue damage. Post-mortem histopathological analysis revealed substantial neuronal cell loss including CA1 and CA4 sectors of the hippocampus compatible with bilateral hippocampal sclerosis. There was no evidence of systemic complications including arterial hypotension and hypoxia, hypoglycaemia, hyperpyrexia, or other confounding factors to account for these findings. This case provides further evidence of SE induced hippocampal damage in humans.
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PMID:Evolution of MRI changes and development of bilateral hippocampal sclerosis during long lasting generalised status epilepticus. 1514 10

Diffusion-weighted nuclear magnetic resonance (NMR) imaging (DWI) is sensitive to the random translational motion of water molecules due to Brownian motion. Although the mechanism is still not completely understood, the cellular swelling that accompanies cell membrane depolarization results in a reduction in the net displacement of diffusing water molecules and thus a concomitant reduction in the apparent diffusion coefficient (ADC) of tissue water. Cerebral regions of reduced ADC appear hyperintense in a DWI and this technique has been used extensively to study acute stroke. In addition to cerebral ischemia, reductions in the ADC of cerebral water have been observed following cortical spreading depression, ischemic depolarizations (IDs), transient ischemic attack (TIA), status epilepticus, and hypoglycemia. Although the mechanism responsible for initiating membrane depolarization varies in each case, the ensuing cell volume changes follow a similar pattern. Water ADC values are also affected by the presence and orientation of barriers to translational motion (such as cell membranes and myelin fibers) and thus NMR measures of anisotropic diffusion are sensitive to more chronic pathological states where the integrity of these structures is modified by disease. Both theoretical prediction and experimental evidence suggest that the ADC of tissue water is related to the volume fraction of the interstitial space via the electrical conductivity of the tissue. The implication is that acute neurological disorders that exhibit electrical conductivity changes should also exhibit ADC changes that are detectable by DWI. A qualitative correlation between electrical conductivity and the ADC of water has been demonstrated in a number of animal model studies and the results indicate that reduced ADC values are associated with reductions in the extracellular volume fraction and increased extracellular tortuosity. The close relationship between ADC changes and cell volume changes in various pathological states suggests that NMR measurements are also sensitive to chemical communication between cells through the extracellular space (i.e., extrasynaptic or volume transmission, VT).
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PMID:Nuclear magnetic resonance (NMR) measurement of the apparent diffusion coefficient (ADC) of tissue water and its relationship to cell volume changes in pathological states. 1518 24

Axonal pathology is increasingly identified by beta-amyloid precursor protein (betaAPP) immunohistochemistry in the brains of patients who may or may not have a history of trauma. The presence of betaAPP-IR(+) has been variously interpreted as either that diffuse traumatic axonal injury (TAI) is indeed a universal finding in cases of fatal traumatic brain injury (TBI) or there are other causes of betaAPP-IR(+) axons which under certain circumstances may be sufficient to mimic TBI and therefore make the medico-legal interpretation of certain cases very difficult. To address some of the uncertainties we have undertaken a detailed analysis of the amount and distribution of betaAPP immunohistochemistry in 63 cases of fatal TBI, 17 cases of patients dying after cardiac arrest, 12 cases dying in association with status epilepticus, 3 cases of carbon monoxide (CO) poisoning, 13 cases of hypoglycaemia and in 60 controls. Three patterns of betaAPP-IR(+) were identified. First, diffuse multi-focal, second, corresponding to the outline of an infarct or haematoma, and thirdly a mixture of the two. The first pattern was seen in cases of the lesser grades of TAI, CO poisoning, and hypoglycaemia, the second pattern in cases in which there was evidence of raised intracranial pressure and the third in cases of severe TAI. It is concluded that the proper interpretation of cases requires the examination of a sufficient number of blocks ( [Formula: see text] ), processing using standardised protocols including betaAPP immunohistochemistry and in some cases the mapping of any IR(+) on anatomical line diagrams. betaAPP carried out on a small number of randomly taken blocks is likely to lead to misinterpretation of the clinico-pathological correlations and possibly to a miscarriage of justice.
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PMID:Trials and tribulations of using beta-amyloid precursor protein immunohistochemistry to evaluate traumatic brain injury in adults. 1554 68

The child who presents with acute coma runs a high risk of cardiopulmonary insufficiency, direct brain injury or even cerebral herniation. The case-management of such child requires a coma-specific emergent evaluation, immediate treatment of any hypoxicischemic insults and of the underlying cause. The coma-specific examination includes performance of child-adapted Glasgow Coma Score, the evaluation of brain stem functions such as pupillary response to light, cough- and gag reflex, and determination of all vital signs including body temperature. Treatment of hypoxicischemic insults includes control of airways and ventilation in patient with coma defined as GCS <8; liberal treatment of impaired cardiovascular states with isotonic fluids such as 0.9% sodium chloride; and treatment of cerebral herniation with head elevation, mannitol, hypertonic sodium chlorid fluids, steroids and hyperventilation. Immediately treatable causes are hypoglycemia, meningitis/encephalitis, opioid overdose and status epilepticus. Exclusion of rapidly progressive intracranial lesions almost always requires referral to the tertiary centre with head CT-scan facilities. Finally, an extensive etiology search of the stable coma is performed by looking for disease or trauma of the brain, for metabolic causes, for intoxications and for cardiopulmonary problems.
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PMID:[The comatose child]. 1613 15


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