THE PATHOPHYSIOLOGY AND PHARMACOLOGY OF PHOTIC CORTICAL REFLEX MYOCLONUS

We studied 6 patients with myoclonus elicited by flash stimulation (1 - 15 Hz). Multichannel electromyographic recording showed a rostrocaudal recruitment order for the generalized myoclonic jerk. In all patients, each flash induced a large (36.9 +/- 5.7 muV) frontal biphasic wave with an onset latency of 42 msec that preceded the earliest muscle response in the face by at least 4 msec (range, 4-7 msec), the activity in the biceps by 11 to 14 msec, and the activity in tibialis anterior by 26 to 34 msec. Occipital potentials evoked by the same flash stimulation had a latency of 33.7 msec and were of normal amplitude (2.1 +/- 1.2 muV). Brain-mapping analysis indicated that the frontal activity correlated with the myoclonus originated in the premotor and motor cortices. These findings provide evidence for a cortical origin of this form of stimulus-sensitive myoclonus in humans. Administration of apomorphine and lisuride (intravenously) and levodopa-carbidopa (orally) abolished the photic myoclonus. Intravenous 5-hydroxytryptophan plus carbidopa (orally) and piracetam (orally) were also effective against photic myoclonus. The wide range of drugs active against photic cortical myoclonus suggests the participation of several biochemical mechanisms in its origin.