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)

Chronic intoxication of phenytoin (PHT) is a well known cause of cerebellar atrophy or irreversible cerebellar ataxia. Little attention, on the other hand, is paid for acute PHT intoxication because its clinical signs are believed to be reversible. We here report a patient with acute PHT intoxication, which resulted in irreversible cerebellar ataxia with radiologically definite cerebellar atrophy. A 39-year-old man admitted to our hospital because of cerebellar ataxia and confusional state. He had been treated with PHT for convulsive seizures after receiving craniotomy for left parietal brain abscess 9 years before. The concentration of his serum PHT had been 4 to 7 micrograms/ml because he had frequently omitted taking drug, and the dose of PHT had been increased to 600 mg/day one year before. He had admitted to another hospital 2 months before for left Bell's palsy and had been obliged to take drug regularly. Cerebellar signs and confusion had gradually developed for 7 weeks. On admission to our hospital, he was awake but in severe confusional state with slurred speech and nystagmus. His serum PHT was 86 micrograms/ml, which returned to therapeutic range 2 weeks after the discontinuation of PHT. His consciousness normalized and nystagmus disappeared. However, slurred speech continued and neurological examination revealed postural tremor and severe limb ataxia. During the subsequent 10 months, his cerebellar signs showed minimal improvement. Computed tomographies of his brain on 3rd and 5th month after the onset of his cerebellar dysfunction showed the definite cerebellar atrophy which had not been noted on the CTs 7 months before and 7 weeks after the onset.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Cerebellar atrophy and persistent cerebellar ataxia after acute intoxication of phenytoin]. 156 34

A four-month-old infant with severe impetigo who had prolonged daily applications of lindane presented with two seizure episodes. His blood lindane level was 1.27 ppm. Caution should be exercised when using lindane in infants and children. Proper instruction and close supervision are essential.
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PMID:Lindane toxicity in an infant. 171 77

A 39-year-old man developed paroxysmal cough, occasional vomiting after cough, and subconjunctival hemorrhage. His illness was complicated by episodes of seizure, with clonic movements of the arms and legs, brief loss of consciousness, and confusion. The episodes were triggered by mild, unremarkable coughing paroxysms. A diagnosis of pertussis was confirmed serologically by measurement of IgG, IgA, and IgM antibodies to pertussis toxin and filamentous hemagglutinin. Serologic studies confirmed the presence of Bordetella pertussis infection in the patient's 10-year-old daughter and suggested that his wife was infected as well. This case report illustrates the occurrence of typical pertussis with serious complications in an adult. Further research is required to determine the scope of this problem and the need for a program of adult immunization against pertussis.
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PMID:Pertussis encephalopathy in an adult: case report and review. 177 35

The influence of drugs affecting the turnover and levels of histamine in brain and histamine antagonists on pentetrazole (PTZ)-induced and electroconvulsive seizure threshold in mice was studied. A 1.5-2-fold rise in histamine brain concentration (induced by treatment with histidine or metoprine), led to a concomitant increase of PTZ-induced seizure threshold. A histidine decarboxylase inhibitor (brocresine) induced a depletion of brain histamine by about 75% for at least 8 h, the seizure threshold was, however, only reduced at 6 and 8 h after the injection. At shorter intervals, the seizure threshold was substantially increased. Treatment with centrally acting H1 antagonists (dimethindene and promethazine) in non-sedative dosage diminished the PTZ seizure threshold significantly; no changes were seen after treatment with H2 and H3 antagonists (oxmetidine, ranitidine, zolantidine or thioperamide) and a H3 agonist (R-alpha-methylhistamine). The electroconvulsive threshold was hardly influenced. It is concluded that histamine has a certain anticonvulsant effect which is mediated through H1 receptors.
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PMID:Histamine in brain--its role in regulation of seizure susceptibility. 181 52

The first report of the rare combination of myotonia congenita, Klinefelter syndrome and primary hypoparathyroidism was reported. The patient was a 21-year-old man who presented with stiffness of the muscles for 12 years and a history of generalised convulsion for 8 years. His school studies declined gradually and his secondary schooling was interrupted. Examination revealed a muscular young man with myotonic percussion over the muscles of the body as well as the myotonic lid lag. Chvostek's sign was positive and his serum calcium level was very low whereas the serum phosphate was high. Symmetrical and extensive calcification of the brain parenchyma was demonstrated in the CT scan. His secondary sexual characteristics were not well developed and his testes were very small. Chromosome study confirmed the diagnosis of Klinefelter syndrome by the identification of 47 XXY chromosome. He was prescribed calcium replacement and the anticonvulsant was withheld with no more episodes of seizure.
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PMID:Myotonia congenita, Klinefelter syndrome and primary hypoparathyroidism: the first report of the unusual combination of three rare diseases in the literature. 186 Nov 36

Effect of some histamine (HA) agonists and antagonists were assessed on electroshock (MES) convulsions in mice and rats. In mice, pretreatment with the HA precursor, l-histidine (100, 500 and 1000 mg/kg) precipitated seizures after a subthreshold (30 mA) stimulus. Both incidence (%) and tonic hind limb extensor phase (THE) were more than that in vehicle treated controls. The H1 blockers, pheniramine (25 mg/kg) and promethazine (25 mg/kg) both protected against (60 mA) MES and both incidence of convulsions and THE were reduced. A similar protective effect was not seen with either the H2 blocker, cimetidine (up to 200 mg/kg), or atropine (1 mg/kg). In rats, both the classical antihistamines blocked MES seizures, whereas, the H2-blocker, cimetidine, and atropine were, ineffective. Further, both H1 blockers were ineffective in antagonizing seizures induced by pentylenetetrazole, INH, caffeine or strychnine. These results are discussed in light of a possible HA-ergic regulation of experimental convulsions.
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PMID:Histaminergic mechanisms in experimental convulsions. 187 53

We report on a male with intestinal lymphangiectasia, mild mental retardation, seizures, and a typical face; the syndrome was first delineated by Hennekam et al., Am. J. Med. Genet. 34:593-600 [1989]. His parents are consanguineous. This case seems to confirm the existence of the Hennekam syndrome.
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PMID:Intestinal lymphangiectasia, lymphedema, mental retardation, and typical face: confirmation of the Hennekam syndrome. 189 80

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 9-month-old boy presented with rapid deterioration of psychomotor development. He developed seizures at 2 months, and shortly thereafter lost motor skills and developed feeding difficulties, increased startle response, red maculas, and decreased vision. His measurements, including head circumference, were greater than the 95th centile. No organomegaly was found. Serum determination of the hemoxsaminidases confirmed the diagnosis of Sandhoff disease.
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PMID:A 7-year old white-male boy with progressive neurological deterioration. 195 28

This is a report on diagnostic and therapeutic experience in 6 patients aged 3 weeks to 6.3 years suffering from herpes simplex encephalitis. In 2 patients, a 3-week-old newborn and a 1.3-year-old boy, acyclovir-therapy started at days 8 and 17 respectively, following the demonstration of hemorrhagic necrosis in the brain by cranial CT-scan and IgM-specific HSV-antibodies in the blood. A 6.3-year-old girl was treated with acyclovir at day 10 of her illness, when cCT showed hemorrhagic necrosis in the brain. It was not before the 21st day, that diagnosis of HSE could be confirmed serologically. She suffered a relapse of encephalitis 5 weeks later. In a 3-month-old boy, treated with acyclovir at day 4 of his illness, IgM-specific HSV-antibodies were found already at day 4. His clinical course was complicated by subdural effusion. These 4 children survived with severe neurologic sequelae. Another 2 patients, a 5- and 7.5-month-old boy respectively, survived without apparent defect. In both cases vesicles upon the tongue appeared in the beginning of illness. Acyclovir-therapy started at day 7, diagnosis being confirmed serologically later. In our experience HSE should be suspected in children suffering from fever, drowsiness and focal or secondarily generalizing seizures. In these cases antiviral therapy should not depend on serologic findings.
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PMID:[Herpes simplex encephalitis in childhood]. 196 Dec 15


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