Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0036572 (seizures)
 80,221 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Cat scratch disease is usually benign, self-limited and without sequelae. Margileth has established four clinical criteria, three of which must be satisfied to make the diagnosis: 1) a history of animal exposure, usually kitten, with primary skin or ocular lesions; 2) regional chronic adenopathy without other apparent cause; 3) a positive cat scratch disease antigen skin test; and 4) lymph node biopsy demonstrating noncaseating granulomas and germinal center hyperplasia. Central nervous system involvement in cat scratch disease has been previously reported, although it is extremely uncommon. In a several-month period, we encountered two cases of cat scratch disease complicated by encephalopathy. The intents of this paper are twofold: 1) to briefly review the current literature on cat scratch disease, 2) to demonstrate that cat scratch disease complicated by encephalopathy presents acutely with seizures, posturing and coma and resolves rapidly with supportive care.
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PMID:Cat scratch encephalopathy. 187 46

Of 40 patients with thrombotic thrombocytopenic purpura, 17 were treated with plasma exchange, 15 with exchange transfusions, and 6 with both types of therapy. One patient died before being treated and another patient was seen but not treated. Plasma exchange was performed daily for a mean of seven exchanges per patient. The replacement fluid during plasma exchange was fresh frozen plasma in all cases. The complete response rates for each type of treatment were as follows: 88% for plasma exchange (15 patients), 47% for exchange transfusions (7 patients), and 67% for exchange transfusions and plasma exchange (4 patients). Clinical and laboratory factors were examined for any statistically significant association with therapy response. Treatment with plasma exchange was statistically the initial factor most strongly associated with prognosis. Paresis, paresthesias, seizures, mental status change, and coma showed no association with response to treatment. Some of the laboratory factors that did not show significant association with treatment response were the initial creatinine, hemoglobin, platelet count, lactate dehydrogenase, and total bilirubin. This study supports the hypothesis that plasma exchange has significantly improved the prognosis of patients with thrombotic thrombocytopenic purpura. These patients should be treated aggressively regardless of the severity of their symptoms.
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PMID:Thrombotic thrombocytopenic purpura treated with plasma exchange or exchange transfusions. 187 81

Due to the increased indications of using carbamazepine, a higher number of intoxications is to be expected. A case report is given of a 42-year-old patient who took about 250 tablets (50 g) carbamazepine (Finlepsin) in a suicide attempt. The maximum serum level of carbamazepine was 118.74 mumol/l. After a gastric lavage and the use of activated charcoal the detoxication was carried out by forced diuresis and one-time haemodialysis. The unconscious patient was ventilated for 8 days after intubation. Two hours after admission three generalised seizures occurred. A long-term hypotension and electrolyte shifts were balanced and a bronchoscopy and lavage were necessary. Bronchopneumonia occurred as a complication. The patient became conscious on the 5th day of treatment, the extubation was accomplished on the 12th day and on the 15th day she was transferred to the psychiatric clinic for further treatment of the basic disease. Since a specific antidote does not exist, general intensive therapeutic measure after carbamazepine intoxication are discussed. After gastric lavage to eliminate the poison, the patient should receive hourly doses of activated charcoal plus vigorous cathartic-like solutions of mannitol and sorbitol and forced diuresis. In case of complicated coma haemoperfusion is recommended.
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PMID:[Carbamazepine poisoning]. 188 28

An outbreak of food poisoning resulting in 13 deaths in children occurred in Malaysia during the Chinese Festival of the Nine-Emperor Gods in 1988. The offending food was a Chinese noodle called 'Loh See Fun' (LSF). The source was traced to a factory where a banned food preservative was added to make the LSF. The food poisoning was attributable to aflatoxins and boric acid. The clinical features included vomiting, pyrexia, diarrhoea, abdominal pain, anorexia, giddiness, seizures, and eventual coma. Initially, many presented with a Reye-like syndrome. Eleven post-mortem examinations were performed. The pathological findings included extensive coagulative necrosis of the liver with proliferative 'ductal/ductular metaplasia of the hepatocytes'. Giant cell formation, central vein sclerosis, bile stasis, and steatosis were also noted. There was presence of acute tubular necrosis, superficial upper gastrointestinal erosions, and ensuing encephalopathy. The eventual cause of death is acute hepatic and renal failure.
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PMID:An outbreak of aflatoxicosis and boric acid poisoning in Malaysia: a clinicopathological study. 189 May 47

A 24-year-old man was admitted to our hospital, because two days before the admission he had abruptly lost consciousness following generalized convulsive seizures. He had a past history of transient amnesia and a favor for peanuts. His grandparents had a record of consanguinity. On admission, he was comatose and flaccid with his four extremities. Laboratory examination revealed the followings; mild degree of abnormal liver function, slight elevation of blood ammonia, irregular theta basic rhythm on EEG, marked brain edema on CT and a normal liver ultrasonography. From the second hospital day, in addition to antiepileptic drugs and adrenocorticosteroids, branched chain amino acid was administered to reactivate damaged brain functions. Thereafter, the concentration of blood ammonia increased to more than 3,000 micrograms/dl, and as a result he fell into status epilepticus. On the fourth hospital day, the levels of citrulline in the plasma and urine taken on the first hospital day were found to have increased by 20 and 100 times, respectively. Although the transfusion of branched chain amino acid was stopped, he died while in coma on the 12th hospital day. Enzymatic analyses of necropsied liver specimens revealed that the quantitative activity of argininosuccinate synthetase had decreased to less than 10% in his urea cycle. In this patient, it was noted that, after transfusion of branched chain amino acid, his brain activities turned worse and blood ammonia was markedly elevated. There is a possibility that intravenous administration of branched chain amino acid may interrupt the urea cycle balance in an adult patient of citrullinemia with dysfunction of the brain, kidney and muscle, especially with brain edema.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Adverse effects of branched chain amino acid transfusion on type-II citrullinemia--report of an adult case]. 191 26

A 32 year-old diabetic woman presented with an acute coma followed by epileptic seizures, aphasia and constructive apraxia. No ischemic lesion was demonstrated by CT scan and carotid angiograms. The other investigations showed sensorineural hearing loss, retinal degeneration, calcifications of the basal ganglia and lactic acidosis. The follow-up was marked by pseudo-dementia with personality disorders, memory deficits, behavioural changes, migrainous and epileptic features. Although there was no sign of muscular deficiency, a muscular biopsy showed characteristic ragged-red fibers and mitochondrial abnormalities at electron microscopy. The muscular biopsy enables us to classify this case as a mitochondrial encephalopathy similar to the MELAS syndrome. The stroke-like episodes are probably caused by a specific angiopathy involving the mitochondria of brain vessels.
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PMID:[Mitochondrial encephalopathy affecting only the central nervous system]. 196 61

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

In Canada in late 1987 there was an outbreak of an acute illness characterized by gastrointestinal symptoms and unusual neurologic abnormalities among persons who had eaten cultivated mussels. Health departments in Canada solicited reports of this newly recognized illness. A case was defined as the occurrence of gastrointestinal symptoms within 24 hours or of neurologic symptoms within 48 hours of the ingestion of mussels. From the more than 250 reports received, 107 patients met the case definition. The most common symptoms were vomiting (in 76 percent of the patients), abdominal cramps (50 percent), diarrhea (42 percent), headache, often described as incapacitating (43 percent), and loss of short-term memory (25 percent). Nineteen patients were hospitalized, of whom 12 required intensive care because of seizures, coma, profuse respiratory secretions, or unstable blood pressure. Male sex and increasing age were associated independently with the risks of hospitalization and memory loss. Three patients died. Mussels associated with this illness were traced to cultivation beds in three river estuaries on the eastern coast of Prince Edward Island. Domoic acid, which can act as an excitatory neurotransmitter, was identified in mussels left uneaten by the patients and in mussels sampled from these estuaries. The source of the domoic acid appears to have been a form of marine vegetation, Nitzschia pungens, also identified in these waters in late 1987. The contaminated mussels from Prince Edward Island were removed from the market, and no new cases have occurred since December 1987. We conclude that the cause of this outbreak of a novel and severe intoxication was the ingestion of mussels contaminated by domoic acid, a potent excitatory neurotransmitter.
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PMID:An outbreak of toxic encephalopathy caused by eating mussels contaminated with domoic acid. 207 68

In late 1987 there was an outbreak in Canada of gastrointestinal and neurologic symptoms after the consumption of mussels found to be contaminated with domoic acid, which is structurally related to the excitatory neurotransmitter glutamate. We studied the neurologic manifestations in 14 of the more severely affected patients and assessed the neuropathological findings in 4 others who died within four months of ingesting the mussels. In the acute phase of mussel-induced intoxication, the patients had headache, seizures, hemiparesis, ophthalmoplegia, and abnormalities of arousal ranging from agitation to coma. On neuropsychological testing several months later, 12 of the patients had severe anterograde-memory deficits, with relative preservation of other cognitive functions. Eleven patients had clinical and electromyographic evidence of pure motor or sensorimotor neuronopathy or axonopathy. Positron-emission tomography of four patients showed decreased glucose metabolism in the medial temporal lobes. Neuropathological studies in the four patients who died after mussel-induced intoxication demonstrated neuronal necrosis and loss, predominantly in the hippocampus and amygdala, in a pattern similar to that observed experimentally in animals after the administration of kainic acid, which is also structurally similar to glutamate and domoic acid. We conclude that intoxication with domoic acid causes a novel and distinct clinicopathologic syndrome characterized initially by widespread neurologic dysfunction and then by chronic residual memory deficits and motor neuronopathy or axonopathy.
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PMID:Neurologic sequelae of domoic acid intoxication due to the ingestion of contaminated mussels. 207 68

An 8-year-old boy developed seizures and coma 2 days after a trivial bicycle accident. Computed tomography failed to show pathology. Magnetic resonance imaging of the head showed infarction of the pons and right cerebellum. Angiography showed occlusion of the right vertebral and basilar arteries. Minor traumatic injuries to the cervical spine may result in vertebrobasilar occlusion. The neurologic manifestations of this disorder and emergency department diagnosis and management are discussed.
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PMID:Vertebrobasilar occlusion following minor trauma in an 8-year-old boy. 198 51


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