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  Vol. 9 No. 2, August 1963 TABLE OF CONTENTS
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Fusimotor Function

Part III. The Spastic Monkey

GERALD E. MELTZER, MD; ROBERT S. HUNT, MD; WILLIAM M. LANDAU, MD

Arch Neurol. 1963;9(2):133-136.

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

Increased excitability of segmental reflex pathways is the traditional paradigm of positive symptoms resulting from loss of control by higher neural mechanisms. As yet no satisfactory explanation of this commonplace phenomenon has been given. It has been suggested that motoneurons deprived of a significant portion of presynaptic neural excitation become hyperexcitable in response to stimulation by surviving connections in accordance with Cannon's Law of Denervation.1 More recently it has been suggested that hyper-reflexia results from the sprouting of new excitatory synaptic connections from dorsal root neurons to the motoneuron pool.2 Either of these theories may be held to account for hyper-reflexia developing days or weeks after an acute lesion, but neither can account for the much earlier changes seen both clinically and in experimental studies. Thus the stretch reflex in the cat is sometimes increased in less than a minute following spinal cord transection,3 and in the . . . [Full Text PDF of this Article]


Author Affiliations

ST. LOUIS

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.

Washington University Medical School Student Research Fellows (Drs. Meltzer and Hunt).

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



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