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Part II. Evidence of Fusimotor Depression in Human Spinal Shock

RICHARD A. WEAVER, MD; WILLIAM M. LANDAU, MD; JUDITH F. HIGGINS; ST. LOUIS

Arch Neurol. 1963;9(2):127-132.

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

The depression of neural activity which takes place in the distal spinal cord abruptly separated from rostral control is the classical model for interpreting the transient disturbances of neural function that follow acute lesions of the nervous system. The behavior of isolated spinal cord has been relatively easy to analyze because its afferent and efferent pathways are so accessible.

Modern neurological thinking is firmly based upon the observations of spinal cord behavior made in animals by Sherrington and in man by many clinicians of his generation. The riddle of spinal shock and the even more puzzling recovery to a hyperactive state which evolves out of it are little nearer solution now than when originally described. The most widely accepted explanation of shock is that the cord's internuncial pool and final common path are depressed below normal levels of excitability by the sudden transection of descending, largely excitatory pathways.¹ Some . . . [Full Text PDF of this Article]

Author Affiliations
From the Division of Neurology and the Beaumont-May Institute of Neurology, Washington University School of Medicine.

Footnotes
Submitted for publication Jan 11, 1963; accepted April 30, 1963.

National Institute of Neurological Diseases and Blindness, Public Health Service, Special Traineeship No. BT-528 (C1) (Dr. Weaver). Present address: Section of Neurology, Department of Medicine, University of Florida, Gainesville, Fla. Washington University Medical School Student Research Fellow (Judith F. Higgins).

Supported in part by US Public Health Service Grants B-882 and NB-04513.

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