Five healthy male volunteers received single oral doses of 10 mg diazepam, 20 mg temazepam and placebo, in a double‐blind, randomised fashion. Smooth pursuit eye movement velocity and serum benzodiazepine concentration were measured before and after at 0.5,1,1.5,2,3,4,6,9 and 12 h after administration of the treatments. Significant decrease in smooth pursuit eye movement velocity as compared to placebo was observed between 0.5‐2 h after temazepam, and between 1‐2 h after diazepam. Smooth pursuit eye movement velocity was log‐linearly correlated with serum temazepam and diazepam concentration. The results demonstrate the relationship between serum benzodiazepine concentration and its effect on an objective measure of oculomotor performance.
Antiepileptic drugs, especially carbamazepine and phenytoin, are potent liver enzyme inducers. Since praziquantel, the drug used to treat neurocysticercosis, undergoes extensive liver first-pass metabolism, we carried out a prospective study to verify whether there was a decrease in oral bioavailability induced by carbamazepine and phenytoin. Carbamazepine and phenytoin significantly decreased concentrations of praziquantel, due to increased clearance secondary to induction of first pass-liver metabolism. The magnitude of the decrease is surprisingly high and may be responsible for failures of treatment.
Summary: Very few studies of photosensitivity or visual sensitive epilepsy could be called epidemiologic in the strict sense, that is, giving well-based incidence and prevalence rates of a well-defined clinical and electroencephalographic syndrome or group of syndromes. The available data suggest that photosensitivity is rare in the population as a whole, with an annual incidence rate around one case per 100,000 population. The incidence goes up to almost six per 100,000 in the late adolescent period, the age group at the highest risk. Well-established concepts, such as statements that one in 4,000 of the general population or that 10% of all epilepsy patients would be photosensitive, should be reevaluated. The more likely figures are a lifetime prevalence of one in 10,000 in the general population, perhaps as low as 2%, of the epilepsy population. Further epidemiologic studies, sensu strictu, are warranted to settle the basic question of the real incidence and prevalence of photoparoxysmal responses (PPRs) and epilepsy with seizures provoked by visual stimuli in the community.
Standard therapeutic regimens of praziquantel for neurocysticercosis use daily doses of 50 mg/kg for 15–21 days, with prolonged remission being achieved in 60–80% patients. In this prospective study, 100 mg/kg daily was used for 10 days in 13 patients aged 32 ± 15 years (mean ± SD) with severe intra-, extraparenchymal or mixed forms of neurocysticercosis. Patients were monitored with computerized tomography and cerebrospinal fluid (CSF) examination on days 1, 5 and 10. Full blood count, sedimentation rate, blood sugar, urea, creatinine, bilirubin, liver transaminases, alkaline phosphatase, urine analysis and electrocardiogram were carried out before and after treatment. Doses of dexamethazone and of other drugs used concomitantly were controlled. There was no toxicity, clinical or detected by the methods employed in the study. After 22 ± 5 (mean ± SD) months follow-up, 6 patients needed ventriculoperitoneal shunting, 2 had died, 7 were improved and led useful lives and 4 were in prolonged remission. There was no correlation between serum or CSF praziquantel correlation and outcome of treatment. The proposed regimen is well tolerated, may be as efficient as previously advocated regimens, requires less hospitalization time and may be adopted routinely for therapy of neurocysticercosis.
A 22-year-old woman with the Lennox-Gastaut syndrome developed serial apnoeic-tonic seizures with concomitant bursts of repetitive spikes at 16-20/sec, after receiving therapeutic doses of chlormethiazole, clonazepam, and diazepam for the treatment of serial tonic-clonic generalized seizures. There was a direct relationship between dose of chlormethiazole and frequency of apnoeic-tonic seizures. Since these tonic seizures have been noted during natural sleep and after sleep induced by various sedative drugs in patients with slow spike-wave in EEG, it is likely that the reduction in level of consciousness induced by sedative drugs is the causative factor.
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