Agnes Balint Bjørke1, Cecilie Gjessing Nome2, Ragnhild Sørum Falk3, Leif Gjerstad4, Erik Taubøll5, Kjell Heuser6. 1. Department of Neurology, Division of Clinical Neuroscience, Rikshospitalet, Oslo University Hospital, Oslo, Norway; Department of Neurology, Division of Neurology, Rheumatology and Habilitation, Drammen Hospital, Vestre Viken Hospital Trust, Drammen, Norway. Electronic address: a.b.bjorke@medisin.uio.no. 2. Institute of Clinical Medicine, Faculty of Medicine, University of Oslo, Oslo, Norway. Electronic address: cecilie.nome@medisin.uio.no. 3. Oslo Centre for Biostatistics and Epidemiology, Research Support Services, Oslo University Hospital, Oslo, Norway. Electronic address: r.s.falk@medisin.uio.no. 4. Department of Neurology, Division of Clinical Neuroscience, Rikshospitalet, Oslo University Hospital, Oslo, Norway; Institute of Clinical Medicine, Faculty of Medicine, University of Oslo, Oslo, Norway. Electronic address: leif.gjerstad@medisin.uio.no. 5. Department of Neurology, Division of Clinical Neuroscience, Rikshospitalet, Oslo University Hospital, Oslo, Norway; Institute of Clinical Medicine, Faculty of Medicine, University of Oslo, Oslo, Norway. Electronic address: erik.tauboll@medisin.uio.no. 6. Department of Neurology, Division of Clinical Neuroscience, Rikshospitalet, Oslo University Hospital, Oslo, Norway. Electronic address: kjell.heuser@ous-hf.no.
Abstract
PURPOSE: To evaluate risk factors for drug resistance and polypharmacy in patients with temporal lobe epilepsy. METHODS: Patients with temporal lobe epilepsy, treated for more than 5 years, completed questionnaires on antiepileptic drug use and effect. Logistic regression models were used for analysis of risk factors. RESULTS: Of 135 patients included in the study, 65% were classified as drug resistant and 41% identified as using polypharmacy. Poor effects associated with first-choice antiepileptic drug were reported by 59% of the patients, and 70% reported poor effects of second-line treatment. The most frequently used first-generation antiepileptic drugs had a similar mean effect to those of second-generation. Univariate regression analyses showed a significant association between drug resistance and mesial temporal sclerosis, seizure onset below 18 years, and lack of family history of epilepsy. However, multivariate regression analysis showed no association with any demographic or clinical features. Unsuccessful treatment with the first antiepileptic drug increased the risk of drug resistance by 18 times, and the risk of poor effect from the second antiepileptic drug by 9 times. Disease duration was associated with annual risk for drug resistance of 7% and for polypharmacy of 5%. CONCLUSIONS: A poor effect from initial pharmacotherapy is the only early risk factor for drug resistance found in this study. Long disease duration increases the risk of drug resistance and polypharmacy. Second-generation antiepileptic drugs provide no additional effect for poor responders to first-generation drugs.
PURPOSE: To evaluate risk factors for drug resistance and polypharmacy in patients with temporal lobe epilepsy. METHODS:Patients with temporal lobe epilepsy, treated for more than 5 years, completed questionnaires on antiepileptic drug use and effect. Logistic regression models were used for analysis of risk factors. RESULTS: Of 135 patients included in the study, 65% were classified as drug resistant and 41% identified as using polypharmacy. Poor effects associated with first-choice antiepileptic drug were reported by 59% of the patients, and 70% reported poor effects of second-line treatment. The most frequently used first-generation antiepileptic drugs had a similar mean effect to those of second-generation. Univariate regression analyses showed a significant association between drug resistance and mesial temporal sclerosis, seizure onset below 18 years, and lack of family history of epilepsy. However, multivariate regression analysis showed no association with any demographic or clinical features. Unsuccessful treatment with the first antiepileptic drug increased the risk of drug resistance by 18 times, and the risk of poor effect from the second antiepileptic drug by 9 times. Disease duration was associated with annual risk for drug resistance of 7% and for polypharmacy of 5%. CONCLUSIONS: A poor effect from initial pharmacotherapy is the only early risk factor for drug resistance found in this study. Long disease duration increases the risk of drug resistance and polypharmacy. Second-generation antiepileptic drugs provide no additional effect for poor responders to first-generation drugs.