Carbamazepine (CBZ) is an effective anticonvulsant agent. Current literatur
e reports describe several cases of seizure exacerbation and/or EEG worseni
ng due to CBZ with a high prevalence in children and adolescents; we report
10 new cases, Nine patients had epilepsy; one showed delayed psychomotor d
evelopment and frequent EEG paroxysmal abnormalities. Four patients were on
monotherapy, six on polytherapy. All but one had therapeutic CBZ plasma co
ncentrations. Seizures increased in frequency in nine, and in eight patient
s new seizure types appeared, mostly absences. Cognitive functions/behaviou
r worsened in eight; EEG recordings showed slowing background activity and
increased paroxysmal abnormalities, in six cases diffuse/generalized spike
waves were seen and in two continuous spike wave discharges. The mean time
of clinical EEG worsening was 1-2 days after introduction of CBZ at therape
utic doses. After CBZ withdrawal clinical EEG improvement was evident in a
few days. The underlying pathogenetic mechanism is not yet understood. Howe
ver, the pathophysiology of seizure exacerbation might be related to the in
teraction between age-related alterations in the balance of excitation and
inhibition in the developing thalamocortical circuitry and the essential ac
tivity of CBZ that tends to induce interictal discharges.