Cases reported "Epilepsy, Complex Partial"

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1/6. Periodic lateralized epileptiform discharges after complex partial status epilepticus associated with increased focal cerebral blood flow.

    Periodic lateralized epileptiform discharges (PLEDs) are typically associated with encephalitis, cerebral abscess, cerebral infarct, and status epilepticus. There is considerable debate as to whether this pattern is ictal or interictal when seen in association with status epilepticus. We present a patient with complex partial status epilepticus who developed PLEDs and remained comatose despite optimal drug therapy. technetium 99m single-photon emission computed tomography (SPECT) showed hyperperfusion that resolved with further aggressive antiepileptic drug therapy, indicating that this pattern may indeed be ictal. Further studies are needed to define the significance of PLEDs in patients with status epilepticus. The role of SPECT in differentiating PLEDs as an interictal or ictal pattern also requires further study.
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keywords = coma
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2/6. Bilateral periodic lateralized epileptiform discharges in Mycoplasma encephalitis.

    status epilepticus and prolonged coma developed in two patients with respiratory tract infections caused by mycoplasma pneumoniae. Serial electroencephalography initially revealed bilateral, independent, periodic, lateralized epileptiform discharges. This pattern was replaced several days later by other electroencephalographic abnormalities.
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keywords = coma
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3/6. Neuropsychiatric manifestations of defect in mitochondrial beta oxidation response to riboflavin.

    A 29 year old woman is described with severe hyperemesis gravidarum, atypical migraine, numerous admissions to hospital for psychiatric illness, non-epileptic seizures, and valproate-induced coma. Metabolic studies and measurement of [9,10(n)-3H]palmitate oxidation by cultured fibroblasts suggested a multiple acyl-CoA dehydrogenation disorder. Treatment with riboflavin abolished headaches and abnormal behaviour and normalised the plasma free carnitine level. Subtle defects in mitochondrial beta oxidation may be a treatable cause of disordered behaviour in adults.
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keywords = coma
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4/6. Deliberate overdose with the novel anticonvulsant tiagabine.

    Tiagabine is a novel antiepileptic drug which acts by decreasing gamma aminobutyric acid uptake in astrocytes and neurones. Here the first case of deliberate overdose with this compound in a patient on concomitant phenytoin is reported. On admission to hospital his conscious level deteriorated to grade III coma. No changes in the electrocardiogram were noted. Recovery from the initial effects was rapid, and there were no sequelae. Plasma levels of tiagabine (3.1 micrograms/ml) 4 hours after ingestion were 30 times higher than at typical steady state during therapeutic dosing. The effects of poisoning with current first-line antiepileptic drugs are reviewed. The newer agents, particularly those with greater biochemical specificity, may be safer in overdose than the more established anticonvulsants.
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ranking = 1
keywords = coma
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5/6. Valproate-induced coma: case report and literature review.

    OBJECTIVE: To report a case of hyperammonemia without hepatic dysfunction as a possible cause of lethargy, stupor, and coma in a woman after valproic acid (VPA) administration, and discuss the possible different mechanisms of ammonia elevation and coma. CASE SUMMARY: A woman diagnosed with complex partial seizures that secondarily generalize was treated with phenytoin (PHT) 250 mg/d for 18 years. Three months before admission, this dosage was increased to 300 mg/d and phenobarbital (PB) 100 mg/d was added because the seizures were incompletely controlled. The patient developed a progressive inability to walk. She was diagnosed as having PHT intoxication. VPA therapy was begun while PHT was being tapered and progressive impairment of consciousness occurred. This evolved into a coma without focal neurologic signs, and was accompanied by isolated hyperammonemia without hepatic failure. DISCUSSION: Adverse effects attributable to VPA were reviewed in the literature. Occasionally, VPA may lead to severe secondary effects such as hepatic failure and coma. In these cases increased blood concentrations of transaminases, bilirubin, and ammonia have been found. Several reports have stressed the existence of hyperammonemic coma without biochemical evidence of hepatic failure, which is what occurred in our patient. This suggests that isolated hyperammonemia and hepatic failure after VPA treatment may have a different biochemical basis. CONCLUSIONS: VPA-induced coma with hyperammonemia and without evidence of hepatic failure should be considered in patients being treated with PHT or PB when VPA is administered concomitantly. This case report shows the importance of clinical monitoring and immediate drug discontinuation when drowsiness, gastrointestinal symptoms, or lethargy occur.
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ranking = 10
keywords = coma
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6/6. Valproate-associated carnitine deficiency and malignant cerebral edema in the absence of hepatic failure.

    We describe a 27-year-old woman who developed encephalopathy and cerebral edema during treatment of refractory complex partial seizures that included acute administration of valproate (VPA) at a dosage of 35 mg/kg per day. Multiple random VPA levels were within therapeutic range, and results of liver function studies did not show evidence of hepatic failure. Cerebral computerized tomography (CT) showed evidence of massive cerebral edema with central herniation. Just prior to death, plasma levels of free and acyl carnitines were markedly decreased. Analysis of urinary organic acids showed increased excretion of lactate, but a normal distribution of VPA metabolites. carnitine deficiency may predispose patients to the development of coma and life-threatening cerebral edema associated with acute administration of VPA, even in the absence of concomitant hepatic failure. We suggest specific guidelines for the evaluation and management of altered consciousness in patients with seizures receiving VPA.
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keywords = coma
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