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)

In a double-blind crossover trial sodium valproate or placebo was added to the existing anticonvulsant treatment of 20 patients with chronic uncontrolled epilepsy. Sodium valproate 1200 mg/day significantly reduced the frequency of both tonic-clonic and minor seizures in these patients. Only mild and transient side effects occurred (drowsiness, ataxia, and nausea), and these may have been due to the effect of adding sodium valproate to existing phenobarbitone or phenytoin treatment. Further controlled trials are needed to assess more fully the efficacy of this drug in various types of epilepsy.
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PMID:Controlled trial of sodium valproate in severe epilepsy. 110 59

In children with congenital rubella infection the deficits remain stable; neurologic deterioration after the first few years of life is not believed to occur. We have encountered three patients with a definite or presumptive diagnosis of congenital rubella, in whom a progressive neurologic illness developed that began in the second decade and was characterized by spasticity, ataxia, intellectual deterioration, and seizures. High antibody titers to rubella virus in serum and spinal fluid were present in two, and all had increased cerebrospinal-fluid protein and gamma globulin. Extensive attempts to recover a virus from brain and body fluids were unsuccessful. The brains of two patients showed a widespread, progressive, subacute panencephalitis mainly affecting white matter. These data suggest that rubella virus may be a cause of progressive panencephalitis.
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PMID:Progressive rubella panencephalitis. Late onset after congenital rubella. 111 60

Twenty-two out of 235 patients with undoubted or suspected MS, treated at the Neurological Clinic, Uppsala, during the eight-year period, 1966-1973, had paroxysmal symptoms during the course of their disease. Paroxysmal dysarthria and ataxia (7 cases), and tonic seizures (5 cases) were the most common types of attacks. Some types of attacks (paroxysmal hemiataxia and crossed paraesthesiae, paroxysmal itching, diplopia as the single, paroxysmal symptom) do not seem to have been described previously. A patient with tonic seizures caused by a localized, traumatic lesion of the cervical spinal cord is also described. It is suggested that the paroxysmal phenomena in MS are caused by a transversely spreading ephaptic activation of axons within a partially demyelinated lesion in fibre tracts somewhere in the central nervous system. The different paroxysmal phenomena are discussed in the light of this hypothesis.
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PMID:Paroxysmal attacks in multiple sclerosis. 114 14

Nine cases of multiple sclerosis with paroxysmal disorders were treated with acetazolamide. In most cases a brain-stem origin of the seizures was suggested by their particular pattern: crossed syndromes (facial spasm associated with contralateral weakness of the arm and leg, paroxysmal paraesthesiae in one side of the face and weakness of the contralateral leg), paroxysmal dysarthria, and ataxia. One patient with a Brown-Sequard syndrome complained of paroxysmal paraesthesiae in the lower limbs, for which a spinal origin was admitted. In all patients the paroxysmal disorders were promptly suppressed or markedly reduced by acetazolamide.
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PMID:Treatment with acetazolamide of brain-stem and spinal paroxysmal disturbances in multiple sclerosis. 115

Intravenous infusions of three levels of 2-deoxy-D-glucose (2DG) were made through chronically implanted jugular and portal cannulas in rats. Food and water intakes were unaffected by 100 mg/kg 2DG, enhanced by 200 and 400 mg/kg 2DG, and unrelated to the route of administration. Drug-induced drinking occurred as readily when food was present as in its absence. Infusions of 2DG also produced stupor and ataxia whose severity was proportional, as was feeding and drinking, to the dose administered. Drinking induced by 2DG is inconsistent with the glucoprivic theory of feeding, and it was proposed that the consummatory and aberrant behaviors elicited by 2DG may result from hypoglycemia-induced seizures in limbic structures of the brain.
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PMID:Drinking and feeding induced by jugular and portal infusions of 2-deoxy-D-glucose. 119 Mar 12

Fifty-two patients (age-range four months to 17 years) with drug-resistant convulsive disorders were treated for up to four years (average 15 months) with clonazepam, a benzodiazepine derivative. The types of seizures suffered by these patients were atypical petit mal, akinetic, massive infantile spasms, mixed minor motor seizures, myoclonic jerks, psychomotor, classic petit mal and grand mal. Evaluation of seizure control by clonazepam showed that the large majority of patients had improved--complete control of seizures was achieved in 27 per cent, and a greater than 50 per cent control was achieved in 61 per cent of the patients. Ten per cent of the patients showed no change and one patient worsened. Eight patients were successfully managed on clonazepam alone. Lethargy and ataxia were common side-effects but usually they were transient. No serious organic toxicity was noted.
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PMID:Treatment of minor motor seizures with clonazepam. 120 84

A 48-year-old man, who took by mistake a sip of ointment containing dichloroethane, survived, and showed a course of two phases of toxic symptoms. After an initial narcosis and an interval with few pathological symptoms seizures, myoclonia and somnolence occurred. Irreversible final disturbances were lasting mental defects, cerebellar dysarthria, ataxia, and hydrocephalus. Concomitant diseases were acute liver dystrophy, nephropathy, and anemia. The clinical picture of dichoroethane posoning is outlines, the pathogenesis of this particular cerebral lesion described, and the therapy discussed.
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PMID:[Dichloroethane poisoning with myoclonic syndrome, seizures and irreversible cerebral defects (author's transl)]. 122 Jun 46

In nine cases of phencyclidine hydrochloride poisoning, early signs of overdose included drowsiness, nystagmus, miotic pupils, blood pressure elevation, increased deep tendon reflexes, ataxia, anxiety, and agitation. In more severe cases, seizures, spasticity, and opisthotonos were seen in addition to deep coma and respiratory depression. Treatment included removal by emetics or lavage, hydration, and a quiet, reassuring environment. Spasticity, agitation, and ocular manifestions responded to diazepam. Psychiatric intervention was instituted after the patients were stable and no longer agitated.
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PMID:Phencyclidine. Nine cases of poisoning. 124 71

The anticonvulsive properties of orally administered cinnarizine [(E)-1-(diphenylmethyl)-4-(3-phenyl-2-propenyl)-piperazine], its difluoro derivative flunarizine [(E)-1-(bis-(4-fluorophenyl)methyl)-4-(3-phenyl-2-propenyl)-piperazine], diphenylhydantoin and phenobarbital, were studied against maximal metrazol seizures (MMS) in rats and maximal electroshock seizures (MES) in mice. In rats (MMS), the lowest ED50 for protection against tonic extension of hindpaws was 4.10 mg/kg (1 h 35 min after treatment) with sodium phenobarbital, 6.04 mg/kg (5 h 45 min) with flunarizine dihydrochloride, 9.84 mg/kg (2 h 34 min) with cinnarizine and 19.30 mg/kg (3 h 38 min) with diphenylhydantoin. In mice (MES), protection against tonic extension of hindpaws was (2 h after treatment) 7.0 mg/kg with diphenylhydantoin, 13.2 mg/kg with sodium phenobarbital, 20.9 mg/kg with flunarizine kihydrochloride and 49.0 mg/kg with cinnarizine. Except at subtoxic doses no side effects were observed in rats and mice given cinnarizine, flunarizine kihydrochloride or kiphenylhydantoin. Phenobarbital induced ataxia in rats and mice at 22 mg/kg and 42.7 mg/kg, respectively, and loss of righting reflex at 112.8 mg/kg and 160 mg/kg, respectively. Flunarizine is the longest-acting drug and has the slowest onset. At a dose of twice the minimal ED50 flunarizine affords protection against tonic extension of hindpaws in rats (MMS) for 23 h 30 min dephenylhydantoin for 11 h 38 min, phenobarbital for 8 h 22 min and cinnarizine for 8 h 16 min. Peak effect was reached with flunarizine at 5 h 45 min, with diphenylhydantoin at 3 h 38 min, with cinnarizine at 2 h 34 min and with phenobarbital at 1 h 35 min. The anti-MMS profiles of cinnarizine and flunarizine resemble that of dephenylhydantoin as all three compounds are selective blockers of tonic extension of hindpaws. Phenobarbital antagonized the whole MMS-pattern, i.e., tremors, clonic convulsions and tonic extension of fore- and hindpaws. However, the effects of phenobarbital against tremors, clonic convulsions and tonic extension of forepaws may reflect more a general CNS-depressant effect than a specific anticonvulsive activity since neurotoxic effects (ataxia and loss of righting reflex) appear at the same doses.
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PMID:Anticonvulsive properties of cinnarizine and flunarizine in rats and mice. 124 63

Two cases of cerebral abscesses caused by Pseudomonas pseudomallei are reported. The first case, a 51-year-old women had a sudden onset of progressive right hemiparesis and right facial palsy and died within 7 days. Postmortem examination disclosed brain abscess in association with disseminated infection outside the central nervous system. The second case, a 9-year-old boy displayed cerebral abscesses as an isolated manifestation. Recovery occurred after treatment with ceftazidime. Review of the ten case reports of cerebral melioidosis revealed that the lesion occurred in patients of all ages and was more common in men than in women. The frontoparietal lobe was the most common location. Fever, headache, and hemiparesis were frequent clinical manifestations while seizures, ataxia were uncommon. CT scanning, serum antibody titer along with hemoculture were useful investigate tools. The importance of early diagnosis and prompt treatment is emphasized for this fatal but treatable disease.
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PMID:Cerebral abscesses due to Pseudomonas pseudomallei. 128 75


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