Abstracts

Most seizures of patients with temporal lobe epilepsy (TLE) are characterized by manual and oral automatisms preceded by abdominal aura. Head version, hand dystonia and secondary generalization reflect spread of epileptic seizure activity. The aim of the present study was to evaluate whether different spread pattern in temporal lobe epilepsy are more likely to generalize secondarily than others., We searched the data base of the University of Munich Epilepsy Monitoring Unit for the terms dystonia, version and temporal lobe epilepsy (TLE). The first consecutive 62 TLE patients with seizure evolutions characterized by either dystonia (n=24) or head version (n=38) were included in the study. MRI and high quality EEG-videos recordings were available in all patients. 82 seizure evolutions with dystonia were intraindividually compared with 68 seizures of these patients without dystonia. In addition, 65 seizures with version were compared with 163 seizures of the same patients without version. All seizure evolutions were classified prospectively independent of the other clinical results based on a semiological seizure classification system. Head version was classfied independent of secondary generalization of a given seizure., The rate of secondary generalization was significantly higher in seizures with version (86%, 56 of 65) than seizures with dystonia (17%, 14 of 82) (p[lt] 0.001). The comparison of the rate of secondary generalization in seizures of the same patients with and without dystonia (and no version) revealed that the rate of secondary generalization was higher in seizures with dystonia (17% vs. 3%). However, the difference in rate of generalization was much higher in the seizures with version: 12% of the seizures generalized secondarily if no version was present as opposed to 86% in seizures with version., In TLE, epileptic spread to the frontal eye field, which is involved in generating head version is more likely to eventually lead to secondary generalization than spread to the basal ganglia, which is considered a generator of dystonia. These findings could support an inhibiting role of the basal ganglia for spread of epileptic activity.,