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THOMAS W. LANGFITT, MD; KOICHIRO KAMEI, MD; GILBERT Y. KOFF, PhD; SAMUEL M. PEACOCK, JR., MD

Arch Neurol. 1963;9(6):593-606.

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Introduction

In the search for the pathophysiological basis of rigidity in parkinsonism the suggestion has been made that abnormalities in the supranuclear control of the -motoneuron may be contributory. Since it has been demonstrated that a lesion in the globus pallidus may ameliorate rigidity and a lesion in the ventral nucleus of the thalamus may completely abolish it, efforts have been directed toward obtaining a better understanding of the anatomy and physiology of these structures. Hassler¹⁷ has postulated that a function of the substantia nigra might be supranuclear control of the -motoneurons. Destruction of the substantia nigra, seen frequently in parkinsonism with rigidity as the predominant sign, would then lead to insufficient excitation of the -motoneurons and in turn the muscle spindles. Thus, he believes rigidity is due, at least in part, to insufficient motoneuron excitation. In keeping with this theory, Stern and Ward³⁹ have demonstrated inhibition . . . [Full Text PDF of this Article]

Author Affiliations
PHILADELPHIA

From the Department of Neurosurgery, Pennnsylvania Hospital.

Footnotes
Submitted for publication July 3, 1963; accepted Aug 23.

Presented in part at the Federation Meetings, Atlantic City, NJ, April 17, 1963.

Head, Department of Neurosurgery, Pennsylvania Hospital (Dr. Langfitt); Research Fellow, Department of Neurosurgery, Pennsylvania Hospital (Dr. Kamei); Neuropharmacologist, Department of Neurosurgery, Pennsylvania Hospital (Dr. Koff); Senior Neurophysiologist, Department of Neurosurgery, Pennsylvania Hospital (Dr. Peacock).

Aided by the John A. Hartford Foundation, Inc., and US Army Chemical Corps contract DA18-108-CML-6652 (A).

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