F Pillmann1, K Schlote, K Broich, A Marneros. 1. Klinik und Poliklinik für Psychiatrie und Psychotherapie, Martin-Luther-Universität Halle-Wittenberg, Halle, Germany.
Abstract
RATIONALE: Olanzapine is similar in structure and pharmacology to clozapine. An increased incidence of electroencephalogram (EEG) abnormalities and seizures has been associated with clozapine but not with olanzapine, although isolated cases of seizures under olanzapine have been observed in high-risk patients. OBJECTIVE: To evaluate the frequency of epileptic and non-epileptiform EEG abnormalities during treatment with olanzapine. METHODS: Using a rating scale of demonstrated reliability, 43 EEGs of patients receiving 10-25 mg/day olanzapine in routine treatment were blindly rated and compared with EEG registrations from the same 43 patients with a different medication. RESULTS: There was no difference in epileptiform activity between the conditions with and without olanzapine. However, EEG slowing was significantly more frequent with olanzapine than under the other condition. This difference could not be attributed to concomitant medication. CONCLUSIONS: Although epileptiform activity did not increase under olanzapine, unspecific EEG abnormalities may be more frequent than with use of other neuroleptics. Careful surveillance of patients with risk factors for seizures is advisable. Further studies addressing the frequency and clinical relevance of EEG changes under olanzapine are necessary.
RATIONALE: Olanzapine is similar in structure and pharmacology to clozapine. An increased incidence of electroencephalogram (EEG) abnormalities and seizures has been associated with clozapine but not with olanzapine, although isolated cases of seizures under olanzapine have been observed in high-risk patients. OBJECTIVE: To evaluate the frequency of epileptic and non-epileptiform EEG abnormalities during treatment with olanzapine. METHODS: Using a rating scale of demonstrated reliability, 43 EEGs of patients receiving 10-25 mg/day olanzapine in routine treatment were blindly rated and compared with EEG registrations from the same 43 patients with a different medication. RESULTS: There was no difference in epileptiform activity between the conditions with and without olanzapine. However, EEG slowing was significantly more frequent with olanzapine than under the other condition. This difference could not be attributed to concomitant medication. CONCLUSIONS: Although epileptiform activity did not increase under olanzapine, unspecific EEG abnormalities may be more frequent than with use of other neuroleptics. Careful surveillance of patients with risk factors for seizures is advisable. Further studies addressing the frequency and clinical relevance of EEG changes under olanzapine are necessary.