Abstracts

RATIONALE: Focal clonic seizures are a frequent epileptic phenomenon. However, there are 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 high frequency cortical electrical stimulation and recorded by surface electrodes. In addition, 3 patients who had a lumbar posterior rhizotomy underwent intraoperatively epidural stimulation of the lumbar spine with EMG recordings. In both settings, the stimulus parameters were systematically changed and the effects on the EMG responses were analyzed.
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 agonistic and antagonistic muscles while a complete lack of muscle activity was seen during the periods of relaxation despite of continuing cortical stimulation. The contractions consisted of trains of compound muscle action potentials following each other according to the stimulation frequency. The clonus frequency decreased from 4.0-8.0 Hz at 50 Hz stimulation to 3.0-3.5 Hz at 20 Hz (correlation: P [lt] 0.05) paralleled by a prolongation of the bursts of muscle activity. When the stimulation frequency was cut in half, the number of stimuli blocked during the periods of relaxation decreased also of 50 %. Within most five seconds stimulation periods with stable stimulation frequencies, the clonus frequency decreased over time. Both the number of stimuli which formed an EMG burst and which were blocked during the following periods of relaxation increased towards the end of the stimulation periods. In contrast to cortical stimulation, there was always an 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 a great number of 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.