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Query: UMLS:C0036572 (seizures)
 80,221 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Evidence compatible with increased GABAergic tone contributing to the manifestations of hepatic encephalopathy (HE) in animal models of fulminant hepatic failure (FHF) includes: (i) increased resistance to drugs which induce seizures by reducing GABAergic tone; (ii) abnormalities of visual evoked responses (VERs) which resemble those induced by drugs which augment GABAergic tone; (iii) increased sensitivity of CNS neurons to a GABA agonist; and (iv) ameliorations of the encephalopathy induced by a GABA receptor antagonist. Evidence compatible with a benzodiazepine (BZ) receptor ligand with agonist properties contributing to increased GABAergic tone in animal models of FHF includes: (i) abnormalities of VERs which resemble those in BZ agonist-induced coma; (ii) increased sensitivity of CNS neurons to a BZ receptor agonist; (iii) excitation of CNS neurons induced by BZ receptor antagonists; (iv) reversal of the increased sensitivity of CNS neurons to a GABA agonist by a BZ receptor antagonist; (v) presence of a ligand(s) in brain which displaces a radiolabeled ligand from BZ receptors; and (vi) increased affinity of this ligand(s) for BZ receptors in the presence of GABA ("positive GABA shift").
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PMID:Hepatic encephalopathy, GABA-ergic neurotransmission and benzodiazepine receptor ligands. 196 4

A multidisciplinary workshop held from September 29 to October 1, 1989, at Airlie House, Warrenton, Virginia, considered the neurologic complications of whooping cough and pertussis vaccine. Pertussis mortality in the U.S. in 2-3/1000 cases. Seizures occur in 1.9% of cases, and encephalopathy in 0.3%. Reviewing all data, it appears likely that a combination of one or more bacterial toxins, asphyxia, CO2 retention and loss of cerebral vascular autoregulation is responsible for neurologic symptoms. The timing of the encephalopathy suggests that it results from increased lysis of bacteria, and release of endotoxin. The encephalopathy is not confined to the paroxysmal phase. In evaluating side-reactions to the vaccine, the following must be kept in mind: 1. Vaccines are not standardized between manufacturers. 2. For a given manufacturer, vaccines are not standard from one batch to the next. 3. Unless the vaccine is properly prepared and refrigerated, its potency and reactivity varies with shelf life. In fact, the whole question of vaccine detoxification has never been systematically investigated. Listed in order of increasing severity, observed adverse reactions include irritability, persistent, unusually high pitched crying, somnolence, seizures, a shock-like "hypotensive, hyporesponsive" state, and an encephalopathy. Since the neurologic picture is not specific for pertussis vaccination, its temporal relationship to the vaccination is the critical variable for determining causation. Although the majority of seizures following pertussis vaccination are associated with fever, it was the consensus of the neurologists attending the workshop, that these do not represent febrile convulsions, but are non-benign convulsions. The incidence of post-vaccine encephalopathy is difficult to ascertain.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Workshop on neurologic complications of pertussis and pertussis vaccination. 198 Dec 51

Environmental and occupational exposure to lead still generates concern, and recent studies have focused such concern on the role of body burden of lead during the fetal/neonatal period, especially in the genesis of disturbed central nervous system development. This discussion provides some comparative observations on the neurotoxicity of inorganic and organic lead species. The characteristics acute, predominantly cerebellar encephalopathy associated with neonatal high lead exposure contrasts to the subtle, axo-dendritic disorganization shown to be associated with low-level neonatal inorganic Pb2+ exposure. There is a preferential involvement of the hippocampus in both low-level inorganic Pb2+ and organolead exposure, and the clinical syndromes of irritability, hyperactivity, aggression, and seizures are common features of disturbed hippocampal function. Neurotransmitter system abnormalities have been described with inorganic Pb2+, but recent attention has focused on the abnormalities in glutamate, dopamine and/or gamma-aminobutyric acid (GABA) uptake, efflux, and metabolism. Abnormalities of GABA and glutamate metabolism are also found with the organolead species. While the pathogenesis is still unclear, the interactive role of Pb2+ on mitochondrial energy metabolism, Ca2+ uptake, intracellular Ca2+ homeostasis, and neurotransmitter influx/efflux is considered. Consideration is given to low-dose inorganic Pb2+ and organolead effects on mitochondrial and/or plasmalemmal membranes inducing either Cl-/OH- antiport-linked depolarization, inhibition of intracellular ATP biosynthesis and transduction. and/or abnormalities induced due to the preferential affinity of Pb2+ for intracellular Ca2(+)-cytoplasmic protein, e.g. calmodulin. Testable hypotheses are presented that may provide an understanding of the pathogenesis underlying dystrophic neuronal development under the influence of inorganic or organolead intoxication.
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PMID:Comparative observations on inorganic and organic lead neurotoxicity. 198 34

We describe 5 patients with a relapsing encephalopathy in association with Hashimoto's disease and high titers of anti-thyroid antibodies. The presentation is usually with a subacute onset of confusion, alteration in conscious level, and focal or generalized seizures. The relapsing course, association with myoclonus or tremulousness, and episodes of stroke-like deterioration are characteristic features. The long-term prognosis is favorable with steroid therapy, though additional immunosuppressive therapy may be required. Neurologic investigation typically shows a diffusely abnormal EEG, high CSF protein level without pleocytosis, and normal brain CT and cerebral angiogram. Isotope brain scan may show patchy abnormal uptake. Hashimoto's encephalopathy should be recognized as a definite neurologic entity and added to the list of CNS complications of thyroid disease.
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PMID:Hashimoto's encephalopathy: a steroid-responsive disorder associated with high anti-thyroid antibody titers--report of 5 cases. 199 66

One hundred neonates determined prospectively to be at risk for neurologic handicap underwent magnetic resonance imaging with a high-field (1.5 T) imager. Thirty-three demonstrated a total of 37 lesions consistent with hypoxic-ischemic encephalopathy, including periventricular leukomalacia (n = 12), basal ganglia hemorrhage (n = 5), multicystic encephalomalacia (n = 5), and focal parenchymal hemorrhage (n = 15). Diagnoses by ultrasonography and computed tomography were compared with those by magnetic resonance imaging in 29 and 17 infants, respectively. Ultrasonography agreed more frequently with magnetic resonance imaging than did computed tomography. Ultrasonography detected 79% of lesions demonstrated by magnetic resonance imaging whereas computed tomography detected only 41%. Periventricular leukomalacia was seen most often in preterm infants, basal ganglia hemorrhage and multicystic encephalomalacia primarily occurred in term infants, and focal parenchymal hemorrhage occurred at all gestational ages. Basal ganglia hemorrhage and multicystic encephalomalacia were strongly associated with histories of perinatal asphyxia, seizures, and early abnormal neurological status. All infants with basal ganglia hemorrhage (5/5) and multicystic encephalomalacia (5/5) and the majority with periventricular leukomalacia (9/12) and focal parenchymal hemorrhages (9/15) had developmental abnormalities at discharge.
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PMID:Prospective observations of 100 high-risk neonates by high-field (1.5 Tesla) magnetic resonance imaging of the central nervous system. II. Lesions associated with hypoxic-ischemic encephalopathy. 201 18

After a few days of prodromal illness with diarrhea and fever there was an abrupt onset of coma, seizures, severe shock, and hyperpyrexia in two infants; they than developed bleeding, pancytopenia, and impairment of liver and renal function. Both infants survived with major neurologic sequelae. The clinical symptoms and laboratory parameters were compatible with hemorrhagic shock and encephalopathy syndrome which was first described in 1983. The clinical course and biochemical features of this disease and its differential diagnoses are described, and etiology and pathogenesis are discussed. Furthermore it will be discussed, whether the hemorrhagic shock and encephalopathy syndrome is actually a "new" disease or just a new label for a known disorder.
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PMID:[Hemorrhagic shock and encephalopathy syndrome in infancy and childhood]. 203 47

An 8-month-old boy and a 7-month-old girl presented with an acute, Coombs-positive auto-immune haemolytic anaemia and severe hepatitis. The clinical manifestations were pallor, jaundice and hepatomegaly. The liver histology revealed diffuse giant cell transformation and extensive necrosis with central-portal bridging. Combined immunosuppressive regimen with steroids and azathioprine led to prolonged clinical and biological remission with a respective 2 years and 7 months follow up. The girl, however, after 7 months developed a progressive encephalopathy of unknown aetiology, while liver and haematological disease were still under control. She died subsequently from severe recurrent seizures. We conclude that acute Coombs-positive giant cell hepatitis of infancy can be improved by sustained immunosuppressive therapy.
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PMID:Coombs-positive giant cell hepatitis of infancy: effect of steroids and azathioprine therapy. 204

Complications that can lead to death during shigellosis include intestinal as well as systemic manifestations. The former include intestinal perforation, toxic megacolon, and dehydration, and the latter include sepsis, hyponatremia, hypoglycemia, seizures and encephalopathy, hemolyticuremic syndrome, pneumonia, and malnutrition. Data on the frequency of these complications come primarily from hospital-based studies, in which sepsis-either with Shigella or with other Enterobacteriaceae-and hypoglycemia are the most common causes of death. Management of these two complications requires broad-spectrum empiric antibiotic treatment of all severely ill, malnourished patients with shigellosis as well as frequent feedings to prevent hypoglycemia. Unfortunately, in developing countries, access to parenteral broad-spectrum antimicrobial agents is often limited, and frequent feedings are often precluded by the severe anorexia that is characteristic of shigellosis. Realistic approaches to the reduction of mortality from shigellosis must continue to focus on prevention and early antimicrobial therapy rather than on treatment of established complications.
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PMID:Potentially lethal complications of shigellosis. 204 57

Ifosfamide-associated central nervous system toxicity has been reported in 5% to 30% of patients treated with ifosfamide. Its pattern is characterized by metabolic encephalopathy with confusion, blurred vision, mutism, auditory or visual paranoid hallucinations, seizures, and rarely coma. The biochemical cause of the neurotoxicity is not understood completely, but it is thought to result from an accumulation of drug metabolites with direct central nervous system effects. A case of ifosfamide neurotoxicity is reported that had unusual extrapyramidal features in a patient treated with a 5-day course of infused ifosfamide. Although usually spontaneously reversible with cessation of drug administration, ifosfamide neurotoxicity occasionally has been associated with prolonged psychopathologic sequelae. Death from irreversible encephalopathy has also been reported rarely. The authors believe that classic extrapyramidal symptoms should be considered to be a part of the neurotoxic profile of ifosfamide.
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PMID:Ifosfamide extrapyramidal neurotoxicity. 142 8

We report a girl with the Rett syndrome who had acute encephalopathy probably induced by calcium hopantenate (HOPA). This 4-year-6-month-old girl had a history of moderate developmental delay and had received HOPA administration when first admitted at 2 years 6 months of age with hypoglycemia, hyperammonemia, lactic and pyruvic acidemia, and non-ketotic dicarboxylic aciduria. After this episode, she showed the rapid destructive stage of the Rett syndrome, i.e., severe psychomotor retardation with loss of speech, peculiar stereotypic hand movements, autistic behavior and seizures. Despite subsequent investigations, including analysis of urinary metabolites of organic and amino acids, measurement of serum carnitine and a muscle biopsy, we could not clarify the primary metabolic abnormalities in this girl.
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PMID:A case of the Rett syndrome with acute encephalopathy induced during calcium hopantenate treatment. 206 99


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