Abstracts

RATIONALE: Oxcarbazepine (OXC) has been used in Europe since the 1980 s and recently marketed in the US. The mechanism of action closely resembles carbamazepine (CBZ) but there are less interactions with other drugs and no autoinduction. CBZ has been reported to aggravate BECTS, Lennox-Gastaut and CSWS syndromes. As no such data exist on OXC, we describe 13 children with epilepsy whose condition was exacerbated while on OXC. METHODS: All patients were cared for by the authors in 1992-1999. Most children had overnight ambulatory EEG or video-EEG recordings. All had MRI and trough drug level measurements. RESULTS: Six children had congenital spastic hemiplegia, one spastic diplegia and two mental retardation due to pre/perinatal vascular accidents or cortical dysgenesia. Two children with normal early development had abnormal MRI and two had cryptogenic etiology. Seizures at onset of epilepsy (mean age 2.9 years, range 0.4-4.8 years) were partial or generalized tonic-clonic in 12 children and epileptic spasms in one. Three children had rare atypical absences (AA) before OXC. OXC was introduced at mean age of 5.1 years (range, 1.8-8.8 years); eight children had previous valproate, carbamazepine, phenytoin or phenobarbital treatment. Within weeks, all children experienced clinical worsening (behavioral, motor and/or cognitive problems) combined with exacerbation of previous seizure types in 11 ( AA in 3) and new seizure types in 5 (AA in 1). All EEG recordings done within 8 months before OXC (N=6) were markedly abnormal and abnormalities increased during OXC in every case. Mean OXC blood level was 76 umol/l (range, 40-115 umol/l).CONCLUSIONS: Oxcarbazepine may aggravate symptomatic and cryptogenic localization related epilepsy. In our experience, children with spastic hemiplegia and those with abundant epileptiform EEG changes seem to be at increased risk. Signs and symptoms of aggravation are easily recognized with careful follow-up.