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Relation of Supraspinal and Drug Modulation to Parkinsonism

JACK STERN, M.D.; ARTHUR A. WARD, JR., M.D.

Arch Neurol. 1962;6(5):404-413.

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

Introduction

In recent years, neurosurgeons have been empirically placing lesions in the globus pallidus and the ventrolateral nucleus of the thalamus (V.L.) in patients with parkinsonism, with resultant diminution of rigidity, hypokinesia, and tremor.^{10,13,18,42,44,52} The role of these structures in the physiology of movement and its distortions is incompletely understood and requires further elucidation. The adventitious appearance of "extrapyramidal" symptoms with the administration of psychotropic drugs has also raised the question of how drugs like chlorpromazine can reproduce the symptom complex of parkinsonism.^1,2,49,57

It has been demonstrated that stimulation of globus pallidus,^20,54 V.L.,^3,17,54 substantia nigra,³ and the cerebral cortex^13,16,57 all effect an inhibition of the -efferent system or of the myotatic reflex. The administration of chlorpromazine also produces -inhibition.^19,51 This inhibition has been recorded by monitoring ventral-root -efferent impulses, muscle spindle discharges, or the myotatic reflex in the variously anesthetized and unanesthetized preparation. . . . [Full Text PDF of this Article]

Author Affiliations
DALLAS, TEXAS; SEATTLE

Special Research Fellow, National Institutes of Health, U.S. Public Health Service (BT-652), and, presently, Department of Neurosurgery, University of Texas Southwestern Medical School, Dallas (Dr. Stern).

Footnotes
Received for publication Sept. 19, 1961.

Division of Neurosurgery, University of Washington School of Medicine, Seattle.

Supported in part by a research grant from Parkinson's Disease Foundation, Inc.

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