title: Electrophysiology of focal clonic seizures in humans: a study using subdural and depth electrodes.
abstract: Focal clonic seizures are a frequent epileptic phenomenon. However, there are few data about their pathogenesis. Eleven patients with focal epilepsy who experienced focal clonic seizures during prolonged video-EEG monitoring were included in this study. Nine patients had subdural electrodes on the precentral gyrus and one patient had additional bilateral subthalamic nucleus (STN) depth electrodes. In five patients, the EEG was co-registered with the EMG of muscles which were involved in the clonic seizures. The frequency, pattern and evolution of the ictal EEG were analysed and their relationship to STN and EMG activity was studied. Focal clonic seizures were always associated with a polyspike-wave pattern in the EEG of the primary motor area (frequency range 1.6-3.4 Hz), while neighbouring electrodes not overlying the precentral gyrus showed different EEG patterns. At seizure onset, the ictal EEG derived from the precentral gyrus consisted of repetitive spiking for 8-28 s (median 19.5 s), accompanied by a continuous increase in muscle tone. This evolved to a pattern of polyspike-wave complexes which were associated with clinical clonus and lasted for 14-202 s (median 30.5 s). The clonic muscle contractions consisted of bursts of compound muscle action potentials (CMAPs) which occurred synchronously in agonistic and antagonistic muscles and were separated by periods of complete muscle relaxation. Each series of CMAPs followed the polyspikes in the EEG with a latency of 17-50 ms. The periods of muscle relaxation occurred during the EEG slow waves. Only some of the cortical spikes were followed by ipsilateral STN spikes. CMAPs followed the cortical polyspikes independently of whether or not STN spikes were seen. The study suggests that focal clonic seizures are focal tonic-clonic seizures. The epileptic clonus consisted of simultaneous contractions of agonistic and antagonistic muscles at regular intervals and was generated by localized polyspike-wave activity in cortical primary motor areas. Activation of the STN did not appear to be an essential component of clonic seizures.
authors.affiliation: Department of Neurology, University of Marburg, Germany. hamer@mailer.uni-marburg.de
authors.forename: H M
authors.initials: HM
authors.lastname: Hamer
authors.forename: H O
authors.initials: HO
authors.lastname: Lüders
authors.forename: S
authors.initials: S
authors.lastname: Knake
authors.forename: B
authors.initials: B
authors.lastname: Fritsch
authors.forename: W H
authors.initials: WH
authors.lastname: Oertel
authors.forename: F
authors.initials: F
authors.lastname: Rosenow
mesh_terms: D000200:Action Potentials; D000293:Adolescent; D000328:Adult; D001921:Brain / Q000503:physiopathology*; D004558:Electric Stimulation; D004566:Electrodes; D004569:Electroencephalography; D004576:Electromyography; D004594:Electrophysiology; D004828:Epilepsies, Partial / Q000503:physiopathology*; D005260:Female; D006801:Humans; D008297:Male; D008875:Middle Aged; D018482:Muscle, Skeletal / Q000503:physiopathology; D012189:Retrospective Studies; D020531:Subthalamic Nucleus / Q000503:physiopathology