Cases reported "Epilepsy, Tonic-Clonic"

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1/76. Hypersensitivity reaction in a child due to lamotrigine.

    Lamotrigine is an anticonvulsant with a broad spectrum of activity that has been approved in the united states for use in adults with either partial or generalized seizures. This drug is being widely prescribed by pediatricians and neurologists because it is effective in children with idiopathic, resistant, generalized seizures and does not impair cognition. As with other anticonvulsants, a hypersensitivity syndrome has been described. Anticonvulsant hypersensitivity syndrome consists of the hallmark features of fever, rash, and lymphadenopathy. We report the first case of hypersensitivity syndrome in a child due to lamotrigine in which we believe the coadministration of valproic acid increased the duration of the reaction. Our patient had a high spiking fever, generalized morbilliform eruption, facial edema, lymphadenopathy, eosinophilia, atypical lymphocytosis, and an elevation in his liver function tests. The syndrome resolved with the discontinuation of the medication. Anticonvulsant hypersensitivity syndrome may occur with the administration of lamotrigine. Variable presentations may be seen, as hypersensitivity syndromes may be multisystem in nature. The prompt recognition of the signs and symptoms of this condition allows an accurate diagnosis so that the drug may be discontinued and other anticonvulsant treatment options instituted.
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2/76. Eighteen fractures in a man with profound mental retardation.

    A 39-year-old man with generalized tonic clonic epilepsy and profound mental retardation sustained 18 fractures (15 in appendicular and 3 in axial bones) during 19 years. Both femoral necks were fractured, requiring surgical repair. Although he had been on antiepileptic drugs for 35 years, he had no radiographic or biochemical sign of osteomalacia. He had a very low bone mineral density, suggesting osteoporosis. This case illustrates an important medical problem affecting people with developmental disability and a management challenge for their caretakers.
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3/76. cyclopentolate and grand mal seizure.

    The author describes a case of grand mal seizures that occurred on two occasions after ocular instillation of cyclopentolate 2% for refraction in a 11-year old epileptic girl. The first and the second crisis developed respectively 45 and 30 minutes after instillation of the drug. cyclopentolate should be contraindicated in known epileptic children.
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4/76. orphenadrine poisoning in a child: clinical and analytical data.

    orphenadrine is an anticholinergic drug used mainly in the treatment of Parkinson's disease. It has a peripheral and central effect and a known cardiotoxic effect when taken in large doses. We report the successful outcome of the treatment of a 2 1/2-year-old girl who accidentally ingested 400 mg of orphenadrine hydrochloride (Disipal). One hour after ingestion she presented neurological symptoms: confusion, ataxic walking, and periods of severe agitation. Generalized tonic-clonic seizures appeared resistant to the administration of multiple antiepileptics. They ceased after a supplementary dose of intravenous diazepam, endotracheal intubation, and mechanical ventilation. An episode of ventricular tachycardia responded well to i. v. lidocaine. physostigmine was administered in three successive doses. The initial orphenadrine plasma level (3,55 microg/ml) was in the toxic range, associated with high mortality. The calculated elimination half-life was 10.2 h and the molecule and/or its metabolites were found up to 90 h after ingestion.
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5/76. Lack of response to vitamin d therapy in a patient with hypoparathyroidism under anticonvulsant drugs.

    Case report of a 16-year-old boy suffering from idiopathic hypoparathyroidism with severe seizures who erroneously and unsuccessfully had received anticonvulsive therapy for 12 years. When the correct diagnosis was made, treatment with massive doses of vitamin D2 was started. However, this treatment became effective only after the anticonvulsive therapy was discontinued; the serum calcium, phosphorus and the plasma 25-hydroxycholecalciferol returned to normal values, and the seizures stopped.
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6/76. fetal heart rate during a maternal grand mal epileptic seizure.

    Although maternal ingestion of antiepileptic drugs is strongly suspected of causing congenital defects, particularly oral clefts, the effect of epilepsy itself or a combined effect of drug intake and epilepsy have not been excluded as etiological factors. Very little is known about fetal oxygenation during a maternal grand mal epileptic seizure. We describe two cases in which fetal heart rate was recorded during a maternal epileptic seizure during labor. The first fetus became clearly asphyctic as judged from the fetal heart rate recording: immediately after the epileptic seizure there was a 13-minute continuous bradycardia wave with decreased short-term variability. After the bradycardia a phase of tachycardia with decreased short-term and long-term variability occurred. In the other fetus there was only a short period of bradycardia, which was followed by a phase of tachycardia and decreased short-term and long-term variability. Both fetuses were vigorous at birth 43 and 87 minutes, respectively, after the epileptic seizures of their mothers. We conclude that a maternal grand mal epileptic seizure can be ominous to the fetus. It is therefore important that epileptic seizures are controlled by optimal medication throughout pregnancy.
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7/76. colitis may be part of the antiepileptic drug hypersensitivity syndrome.

    PURPOSE: To show that colitis may be part of the antiepileptic hypersensitivity syndrome. methods: Description of two case histories. RESULTS: The first patient was a 47-year-old man who developed fever, lymphadenopathy, influenza-like symptoms, facial edema, skin rash and diarrhea after 3 weeks of carbamazepine (CBZ) treatment. laparotomy because of severe abdominal pain 2 weeks later showed severe colitis with perforations. The second patient was a 41-year-old woman who developed fever, diarrhea, and skin rash 4 weeks after start of CBZ treatment. A colon biopsy confirmed colitis. Stool examinations did not show pathogenic microorganisms, and there was no evidence of Crohn's disease or ulcerative colitis. Both patients had elevated liver enzymes, peripheral eosinophilia, and eosinophils in the infiltrate of the colon. CONCLUSIONS: In view of the close temporal relation between start of CBZ intake and development of colitis, the presence of fever, lymphadenopathy, and rash, and improvement after discontinuation of CBZ, we conclude that the two patients developed an AED hypersensitivity syndrome. Our case histories demonstrate that severe colitis may be part of this syndrome.
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8/76. Temporary pure red-cell aplasia during valproate monotherapy: clinical observations and spectral electroencephalographic aspects.

    We report the case of a 4-year-old boy with pure red-cell aplasia associated with sodium valproate monotherapy. Treatment with valproate was initiated because of idiopathic tonic-clonic seizures; he became free of seizures. During the introduction of and ongoing antiepileptic drug treatment, clinical and laboratory controls using electroencephalographic (EEG) spectral analysis were performed at regular intervals and disclosed normal values. Ten months after the introduction of valproate, clinical examination was normal except for marked pallor. Peripheral blood showed macrocytic anemia and the bone marrow finding was isolated absolute erythroblastopenia. At the same time, significant changes in EEG background activity were present as well-defined slowing. There was an increase in the relative power of theta activity and a decrease in alpha 2 activity in the occipital regions. Valproate was discontinued and phenobarbital therapy introduced. A complete resolution of the hematologic damage was observed after valproate withdrawal. Recovery of the hematologic parameters started 14 days after discontinuation of valproate therapy, while normalization of EEG background activity was observed earlier. The patient maintained stable hematologic values and seizure control without disturbances of the spectral EEG. After 6 months of phenobarbital therapy, re-administration of sodium valproate was not followed by recurrence of any clinical or electrophysiologic symptoms or abnormalities.
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9/76. Autosomal dominant partial epilepsy with auditory features: description of a new family.

    PURPOSE: To report the clinical and genetic study of a new family with autosomal dominant partial epilepsy with auditory features (ADPEAF). methods: All the living affected members underwent a full clinical, neurophysiological, and magnetic resonance imaging (MRI) study. Genetic analysis was performed by typing their dna with seven microsatellite markers previously found to cosegregate with ADPEAF on chromosome 10q24. RESULTS: The three living affected members had a childhood onset of rare and drug-responsive tonic-clonic seizures constantly preceded by a humming sensation. Routine and sleep electroencephalograms revealed rare and inconstant focal abnormalities over both temporal regions. MRI detected atrophy with increased T2 signal in the subcortical lateral portion of the right temporal lobe in one case. Analysis of 10q24 polymorphic alleles showed the same haplotype in all three affected members but different alleles in unaffected individuals. CONCLUSIONS: ADPEAF is a distinct condition with homogeneous clinical features. Genetic findings are consistent with linkage of ADPEAF to chromosome 10q24.
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10/76. seizures during lithium-amitriptyline therapy.

    Epileptiform seizures occurred in a 34-year-old woman who was receiving amitriptyline and lithium carbonate therapy for treatment of endogenous depression. While receiving amitriptyline maintenance therapy, she was given lithium on two separate occasions, and despite serum levels of lithium in the therapeutic range, grand mal seizures developed. The seizures may represent a toxic reaction either to lithium or to combined drug therapy. Controlled studies are needed to evaluate both the efficacy and toxicity of combined drug therapy in affective disorders.
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