Carbamazepine-10,11-Epoxide in Epilepsy A Pilot Study

• Published in: Archives of neurology (Chicago) Vol. 47; no. 8; pp. 888 - 892
• Main Authors: Tomson, Torbjörn, Almkvist, Ove, Nilsson, Bengt Y, Svensson, Jan-Olof, Bertilsson, Leif
• Format: Journal Article
• Language: English
• Published: Chicago, IL American Medical Association 01.08.1990
• Subjects: Adult; Anticonvulsants. Antiepileptics. Antiparkinson agents; Biological and medical sciences; Carbamazepine - analogs & derivatives; Carbamazepine - blood; Carbamazepine - therapeutic use; Dose-Response Relationship, Drug; Epilepsy - blood; Epilepsy - drug therapy; Female; Humans; Male; Medical sciences; Middle Aged; Neuropharmacology; Neuropsychological Tests; Pharmacology. Drug treatments; Pilot Projects; Single-Blind Method; Human; Chemotherapy; Nervous system diseases; Treatment; Convulsion; Metabolite; Epilepsy; HPLC chromatography; Anticonvulsant; Metabolism; Pharmacokinetics
• DOI: 10.1001/archneur.1990.00530080072013
• ISSN: 0003-9942

• The effects of carbamazepine-10,11-epoxide, an active metabolite of carbamazepine, were evaluated in seven outpatients with frequent epileptic seizures. The study included an initial 4-week period with the carbamazepine dose optimized for each patient. Patients were then crossed over, dose by dose, to carbamazepine-10,11-epoxide and followed up for another 4 weeks. Dosing was single blind. The evaluation of the anticonvulsant effect was hampered by marked fluctuations in plasma levels during treatment with carbamazepine-10,11-epoxide. There was, however, no significant change in seizure control. During epoxide treatment, no subjective side effects were reported despite epoxide plasma concentrations up to 57 μmol/L. Neuropsychological assessment revealed a significant improvement in finger motor speed and logical reasoning during the carbamazepine-10,11-epoxide period. Subnormal serum sodium levels in two patients were normalized after switching from carbamazepine to the epoxide. Continued investigations with this active metabolite of carbamazepine in epilepsy are therefore justified.