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Biomedical subjects

D J Beintema

Publications and source records attributed to D J Beintema.

3 recordsLinked to original sources

Seven day administration of lamotrigine in epilepsy: placebo-controlled add-on trial.

A double-blind placebo-controlled trial of 7 days administration of lamotrigine as add-on therapy was performed in 10 patients with frequent therapy-resistant, chiefly partial, seizures. Dosage was adjusted on the basis of estimated half-life. Six patients showed a 50% seizure reduction on lamotrigine and two an increase. Side effects (ataxia, dizziness and apathy) occurred in 3 patients, but only at blood levels above 3 micrograms/ml, and were rapidly relieved when the dose was reduced in two. EEG spike counts were significantly reduced on lamotrigine. There was no evidence of interactions with co-medication.

Adolescent↗

Epileptic nystagmus.

"Epileptic nystagmus" unaccompanied by other ictal phenomena is rare. We report four new cases confirmed by ictal EEG and video or cine recording in which nystagmus was a prominent and sometimes the only clinical manifestation of the seizures. The ictal EEG showed a parietal focus in three instances and generalized spike-wave activity in one.

Adolescent↗

The effect of sleep deprivation on the EEG in epilepsy.

Many published studies report an increased incidence of epileptiform EEG activity following sleep deprivation in persons with epilepsy in whom a previous routine EEG was normal or inconclusive. Few such studies, however, permit a clear distinction to be made between the effects of sleep deprivation per se, sleep induction following deprivation, or simply repeated EEG recording. Sixty-nine patients have been investigated in whom a routine waking record, a secobarbital-induced sleep recording and an EEG following 24 h sleep deprivation were obtained in random order irrespective of whether or not the initial EEG contained epileptiform activity. For each record the incidence of epileptiform activity if any, was quantified in terms of discharges per minute for wake, drowsiness and each sleep stage. The findings confirmed the marked activating effect of light sleep on the EEG but there was no evidence of an overall increase in discharge rate after sleep deprivation either in the waking state or in the various sleep stages when these were compared with secobarbital-induced or spontaneous sleep. There was a significant increase of generalized discharges in the waking state only, after sleep deprivation, but a decrease in incidence of focal epileptiform activity. It is concluded that although specific indications may exist for the use of sleep deprivation, as a general method of EEG activation in epilepsy it has no advantages over barbiturate-induced sleep to offset the greater inconvenience to patients.

Adult↗