We studied risk factors of relapse after antiepileptic drug withdrawal in a retrospective analysis of 36 patients with idiopathic generalized epilepsy. These patients had been free of seizures for at least 2 years. Twelve patients (33%) experienced a recurrence <1 year after discontinuation or during antiepileptic drug withdrawal. Risk factors statistically related to seizure recurrence were as follows: onset in adolescence (13-18 years old) (p<0.005); >4 years duration of illness (p<0.05); >5 generalized tonic clonic seizures before control (p<0.05); juvenile myoclonic epilepsy or epilepsy with grand mal seizures on awakening (p<0.05). We conclude that these risk factors are decisive in judging whether antiepileptic drugs should be discontinued or not in patients with idiopathic generalized epilepsy.

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We investigated the effect of concurrent administration of lamotrigine (LTG) on the plasma concentrations of carbamazepine (CBZ) and its pharmacologically active metabolite carbamazepine-10, 11-epoxide (CBZ-E) in patients with symptomatic or cryptogenic localization-related epilepsies whose seizures were not controlled despite adequate therapy with other prevalent antiepileptic drugs. LTG is now in experimental use in Japan.
Eight study patients aged 12-22 (mean, 18 years 3 months) were first treated with CBZ, LTG was then added. Most of the patients were treated combined with other antiepileptic drugs, but they were not received those, such as phenytoin and valproic acid, which complicate the steady-state plasma concentrations of LTG as well CBZ and CBZ-E by the potential for pharmacokinetic interactions. The dosage of CBZ and other antiepileptic drugs concomitantly used was kept constant during the investigation.
When the daily dosage of 7.7±3.8 mg/kg of LTG was added to CBZ therapy (9.7±2.3 mg/kg/day) in 8 patients, both plasma level of CBZ-E and plasma CBZ-E/CBZ ratio increased significantly (p<0.05) from 1.29±0.30 to 1.45±0.40, ug/ml and 0.16±0.03 to 0.18±0.03, respectively. Plasma level of CBZ remained unchanged from 7.91±1.07 to 7.78±1.33μg/ml. Plasma level of LTG was 5.91±2.29 μg/ml.
It is evident that the concurrent administration of LTG affects plasma concentration of CBZ-E, while plasma CBZ level remains unaltered. Howevere, the effect of LTG on plasma concentration of CBZ-E is a little, and none of the patients showed toxic plasma concentration of CBZ-E or associated clinical toxicity.

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