Assessment of cardiac structure and function in a murine model of temporal lobe epilepsy.

Sudden unexpected death in epilepsy (SUDEP) is a significant cause of premature seizure-related death. An association between SUDEP and cardiac remodeling has been suggested. However, whether SUDEP is a direct consequence of acute or recurrent seizures is unsettled. The purpose of this study was to evaluate the impact of status epilepticus (SE) and chronic seizures on myocardial structure and function. We used the intracortical kainate injection model of temporal lobe epilepsy to elicit SE and chronic epilepsy in mice. In total, 24 C57/BL6 mice (13 kainate, 11 sham) were studied 2 and 30 days post-injection. Cardiac structure and function were investigated in-vivo with a 9.4 T MRI, electrocardiography (ECG), echocardiography, and histology [Haematoxylin/Eosin (HE) and Martius Scarlet Blue (MSB)] for staining of collagen proliferation and fibrin accumulation. In conclusion, we did not detect any significant changes in cardiac structure and function neither in mice 2 days nor 30 days post-injection.

Evaluation of long-term antiepileptic drug use in patients with temporal lobe epilepsy: Assessment of risk factors for drug resistance and polypharmacy.

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.