Penicillin epileptogenic focus in the rat: requisites for transcortical reflex triggering

Epileptiform discharges elicited by natural or electrical stimulations, proprioceptive or cutaneous, were studied in the rat with an experimental acute focus induced by penicillin application in the motor area. EEG paroxystic spikes were easily triggered with restricted foci (0.5 to 1 mm2) located in the representation area of the stimulated region. However, despite the large overlap of sensory and motor cortical limb areas in the rat, EEG spikes, either spontaneous or triggered, were followed by muscular jerks only with much larger foci: at least 2 and 4 mm2, respectively, for anterior and posterior limb areas. Cutaneous stimulations were the most efficient in discharge production; however, discharges were triggered indifferently by muscular or cutaneous afferent fibers in about three-fourths of the cases. The temporal relation between EEG spike and myoclonic jerk were very close. A latency analysis (delay between triggered EEG spike and EMG response, parallel latency fluctuation of both phenomena, delay between spontaneous EEG spike and jerk) supported the hypothesis that a transcortical reflex mechanism, rather than a spinal excitability rebound, was involved in the jerk genesis. Iontophoretic ejection of penicillin within layers III-IV resulted in the development of electroclinical paroxysms. However, similar penicillin ejection within layer V, did not allow efferent discharge production. It is concluded that the involvement of a large surface or volume of cortical tissue is required to produce efferent discharges following EEG paroxysms. This observation is likely related to the unexpectedly wide representation of individual muscles at the motor cortical level.