No abstract

To clarify the relationship between cognitive function and CBZ therapy, auditory event-related potentials (P300) were examined in 23 patients with Benign Childhood Epilepsy with Centrotemporal Spike (BCECT) compared with 54 normal controls. The results were 1) the mean P300 latency in BCECT (368 +/- 29 msec) was significantly prolonged compared with that in normal controls (349 +/- 30 msec), but most individual patients showed normal values. 2) The prolongation of P300 latency was greatest during the course of therapy. 3) On repeated examination of P300, P300 latency was found to gradually become shorter with age in spite of continuous CBZ therapy. At initiation of CBZ therapy, the P300 latency became shorter; on the other hand, P300 latency became shorter with the discontinuation of CBZ. 4) The age-corrected P300 latency showed a significant positive correlation with the serum concentration of CBZ. Our results suggest that CBZ therapy has both an undesirable effect (chronic impairment) and a desirable effect (improvement of underlying dysfunction caused by epileptogenesis) on cognitive function.

The clinical and epidemiological findings in children with epilepsy who experienced skin rashes induced by carbamazepine (CBZ) were prospectively evaluated. Thirty-three (9.9%) of 335 patients who received CBZ therapy experienced a skin rash. Seven had diffuse erythema, 13 miliary exanthema, 11 maculopapular or speckled reddish rash, 3 petechiae, and 2 mucocutaneous syndrome. A skin rash was more frequent in older children (over 6 years old). The skin rashes appeared soon after initiation of the therapy, i.e., from the 8th to 60th day (mean: 14.3 +/- 9.6 days) after the start of CBZ therapy and disappeared within a few days after discontinuation of the therapy. Haematological abnormalities (30.3%), such as leucocytopenia and thrombocytopenia, and hepatic dysfunction (27.3%) sometimes appeared concomitantly with the skin rash. CBZ is an effective and safe antiepileptic drug, but careful management is necessary on initiation of the therapy.

The effects of antiepileptic drugs (AED) on EEG background activity were evaluated in 37 newly treated children with epilepsy, compared with 46 age-matched healthy controls. Before AED therapy, the children with epilepsy, both partial (treated with carbamazepine, CBZ group) and generalized seizures (treated with valproic acid, VPA group), already exhibited significant slowing of EEG with increased delta and decreased alpha power. Following 3 to 6 months of AED therapy, this EEG slowing was enhanced in the CBZ group and reduced in the VPA group. Following 1 year of AED therapy, an increase in frequency was recognized in the CBZ group. These results suggest that 1) most children with epilepsy already exhibit slowing of the EEG at the onset of seizures, which may reflect CNS developmental deficit, 2) the short-term effects on EEG are different between CBZ and VPA, and 3) EEG development with age continues under continuous AED administration. The EEG background activity in children with epilepsy is affected by many factors, which include the underlying CNS dysfunction of the epilepsy itself and also AED therapy (type of AEDs, duration of therapy, etc).