Oxcarbazepine in migraine headache: a double-blind, randomized, placebo-controlled study.

OBJECTIVE: To evaluate the efficacy, safety, and tolerability of oxcarbazepine (1,200 mg/day) vs placebo as prophylactic therapy for patients with migraine headaches. METHODS: This multicenter, double-blind, randomized, placebo-controlled, parallel-group trial consisted of a 4-week single-blind baseline phase and a 15-week double-blind phase consisting of a 6-week titration period, an 8-week maintenance period, and a 1-week down-titration period, after which patients could enter a 13-week open-label extension phase. During the 6-week titration period, oxcarbazepine was initiated at 150 mg/day and increased by 150 mg/day every 5 days to a maximum tolerated dose of 1,200 mg/day. The primary outcome measure was change from baseline in the number of migraine attacks during the last 28-day period of the double-blind phase. RESULTS: Eighty-five patients were randomized to receive oxcarbazepine and 85 to receive placebo. There was no difference between the oxcarbazepine (-1.30) and placebo groups in mean change in number of migraine attacks from baseline during the last 28 days of double-blind phase (-1.74; p = 0.2274). Adverse events were reported for 68 oxcarbazepine-treated patients (80%) and 55 placebo-treated patients (65%). The majority of adverse events were mild or moderate in severity. The most common adverse events (>or=15% of patients) in the oxcarbazepine-treated group were fatigue (20.0%), dizziness (17.6%), and nausea (16.5%); no adverse event occurred in more than 15% of the placebo-treated patients. CONCLUSIONS: Overall, oxcarbazepine was safe and well tolerated; however, oxcarbazepine did not show efficacy in the prophylactic treatment of migraine headaches.

Benign myoclonus of early infancy: an imitator of West's syndrome.

Benign myoclonus of early infancy is a rare condition characterized by nonepileptic spasms that may resemble the epileptic spasms seen in West's syndrome. The spells in benign myoclonus of early infancy begin before age 1 year and are self-limited. The electroencephalogram (EEG) is invariably normal, and neurologic development is not affected. West's syndrome is characterized by infantile spasms that appear before 1 year of age, an abnormal EEG with hypsarrhythmia, and a poor prognosis. We describe six infants who presented for evaluation of clusters of head, trunk or extremity spasms, eye blinking, brief jerking of upper extremities or trunk, and head nodding episodes. In most, a presumptive diagnosis of West's syndrome was made prior to the referral. One infant had been placed on valproate. Routine EEG recordings or prolonged video EEG monitoring were normal both during and between episodes. After the negative evaluations, the diagnosis of benign myoclonus of early infancy was made in each infant. Subsequently, no infant was treated with anticonvulsants. Follow-up revealed complete resolution of the episodes in all children within 2 weeks to 8 months of onset. All had normal neurologic development. Based on our cases and review of the literature, the prognosis for this disorder is excellent. Care should be taken to recognize this rare entity and avoid unnecessary and potentially harmful antiepileptic therapy.

Neuromuscular transmission defect caused by carbamazepine.

The clinical effect of carbamazepine (CBZ) on neuromuscular transmission is described in two children who presented in coma with diffuse hypotonia and areflexia following CBZ overdose. Repetitive nerve stimulation (RNS) showed a decremental response only at high-frequency stimulation. With supportive care, the patients made an uneventful recovery. Follow-up RNS was normal. This is the first report of a clinically evident neuromuscular transmission defect produced by CBZ. We postulate that CBZ's known effect on decreasing sodium channel depolarization produced a defect in neuromuscular transmission. The report emphasizes the contribution of RNS in the evaluation of coma of uncertain etiology, particularly in cases of possible intoxication, and the potential for CBZ to compromise neuromuscular transmission in normal individuals or in patients with a decreased neuromuscular transmission safety factor.