Melatonin Effect on Seizures in Children with Severe Neurologic Deficit Disorders

Nir Peled, Zamir Shorer, Eli Peled, Giora Pillar

From: Epilepsia, Volume 42, Issue 9, pp 1208–1210, September 2001

Summary: Purpose:  Recently, melatonin has been associated with antiepileptic activity, most probably because of its antioxidant activity as a free radical scavenger. This study aimed to expand the clinical experience with melatonin as an antiepileptic drug (AED) in humans.

Methods: Six children (aged 2–15 years), with severe intractable seizures, were treated with 3 mg of oral melatonin 30 min before bedtime, in addition to their previous AED treatment for 3 months. A diary of clinical seizure activity (time of day, duration, and type) was kept by parents for a month before and during treatment. Five patients underwent a baseline polysomnography, and three also were monitored during melatonin treatment.

Results: With the exception of the parents of one child, all reported a significant clinical improvement in seizure activity during treatment, particularly during the night. Sleep studies showed a decrease in epileptic activity in two of the three patients who were monitored during treatment, and a change of sleep efficiency from 84.2% to 89.7% (NS). Improvement in daytime behavior and in communication abilities was reported by parents, although it was not objectively measured.

Conclusions: This clinical observation adds to the growing data showing the antiepileptic effect of melatonin. However, owing to the paucity of well-controlled studies, using melatonin as an AED should be limited to this specific group of patients with intractable seizures.

The pineal hormone, melatonin, was identified during the late 1950s by Lerner et al. It is an indolamine that is synthesized from tryptophan in the pineal gland and released in a circadian pattern with a peak level at night (see recent review in ref. 2). Recently there have been preliminary reports indicating that melatonin may posses antiepileptic activity, attributed to its potent free-radical scavenging properties. These were supported by findings that an intraventricular injection of antimelatonin antibodies caused epileptic activity, and administration of the central-type benzodiazepine antagonist, Ro 15-1788, blunted the anticonvulsant response to melatonin. However, there is limited clinical experience with melatonin treatment in epilepsy patients. In the present study, we describe the effect of melatonin in six children with severe intractable epilepsy, which occurs particularly during the night.

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