Abstracts

RATIONALE: Focal clonic seizures are a frequent epileptic phenomenon. However, there is little data about the pathomechanism of this seizure type. METHODS: In 4 patients with intractable epilepsy and chronically inserted subdural electrodes, focal clonic muscle responses of hand and leg were elicited by cortical electrical stimulation and recorded by surface electrodes. Stimulus parameters were systematically changed. In addition, 3 patients who had a posterior rhizotomy for spastic cerebral palsy underwent intraoperatively epidural stimulation of the lumbar spine with EMG recordings. RESULTS: A stable rhythmic clonic muscle response (3.5-8 Hz) could be elicited by cortical stimulation at frequencies between 20 Hz - 50 Hz. During contractions, there was simultaneous EMG-activity of antagonistic muscles while a lack of muscle activity was seen during the periods of relaxation despite of continuing stimulation. The clonus frequency decreased from 4.0-8.0Hz at 50 Hz stimulation to 3.0-3.5 Hz at 20 Hz (correlation: P < 0.05) paralleled by a prolongation of the bursts of muscle activity and of the relaxations. The bursts consisted of trains of compound muscle action potentials following each other according to the stimulation frequency. Within the five seconds stimulation periods, the clonus frequency decreased over time due to a prolongation of bursts and relaxations (P<0.05). In contrast to cortical stimulation, there was always a 1:1 relationship between stimulus and muscle twitch during spinal stimulation with frequencies between 1 - 50 Hz. CONCLUSIONS: This study supports the view that a clonic muscle response is triggered by supraspinal, probably cortical mechanisms. As in epileptic seizures, cortical stimulation may cause a direct activation of many pyramidal tract (PT) neurons which then may result in specific excitation of mainly GABAergic interneurons by recurrent axon-collaterals. This simultaneous activation of inhibitory interneurons may have a temporal and spatial summation effect which finally leads to a temporary hyperpolarisation of PT neurons suppressing intermittently further output to the spinal motorneurons despite continuous stimulation.