ALTHOUGH myoclonus is a relatively common clinical phenomenon, substantial basic information regarding its neural mechanism is not available. That the thalamus may play a role has been recently suggested.1 The current communication expands upon these earlier observations and examines in somewhat greater detail the alterations in myoclonic threshold associated with lesions of the primate thalamus.
Myoclonus is an involuntary movement characterized by brief, jerky, shock-like contractions of a muscle or groups of muscles. It is encountered as a normal finding in the course of falling to sleep, as a nonspecific and transient finding in many diseases of the nervous system, and as a consistent finding in the disorders of familial myoclonus and myoclonic epilepsy (of Unverricht). No etiology has been determined. Myoclonic movements are characteristically arrhythmic; they occur at a rate of 10 to 50 per minute and may appear in short paroxysms at irregular intervals. Although any muscle
Milhorat TH. Experimental Myoclonus of Thalamic Origin. Arch Neurol. 1967;17(4):365–378. doi:10.1001/archneur.1967.00470280031004
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