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Thomas H. Milhorat, MD

Arch Neurol. 1967;17(4):365-378.

	Since this article does not have an abstract, we have provided the first 150 words of the full text PDF and any section headings.

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 . . . [Full Text PDF of this Article]

Author Affiliations
New York

From the Department of Neurosurgery, the New York Hospital-Cornell Medical Center, New York. This work was begun at the National Institute of Neurological Diseases and Blindness, Branch of Surgical Neurology, National Institutes of Health, Bethesda, Md.

Footnotes
Submitted for publication March 16, 1967; accepted May 20.

Read in part before the New York Academy of Medicine combined meeting; Section of Neurology and Psychiatry, New York Neurological Society, and the New York Society of Neurosurgery, May 10, 1966.

Reprint requests to Department of Neurosurgery, New York Hospital-Cornell Medical Center, 525 E 68th St, New York 10021 (Dr. Milhorat).

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