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I. M. Tarlov, MD

Arch Neurol. 1967;16(5):536-543.

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

OUR laboratory experiments¹ have clearly demonstrated that intense hind-limb rigidity in dogs may be caused by spinal interneuron destruction. Such severe hypertonus, unlike decerebrate rigidity, or spasticity, is abolished neither by spinal cord severance above the lesion nor by posterior root division. Penry et al² and Rushworth et al³ have provided evidence suggesting that our findings may also explain a certain type of rigidity in man.

The patient to be presented, previously briefly reported,⁴ afforded the opportunity of demonstrating unequivocally that spinal interneuronal destruction produces intense rigidity. (The term rigidity is used because the hyperactive reflexes and clonus, as well as the lengthening reaction ["clasp-knife" phenomenon] so characteristic of spasticity, were not present in this case.) It was unaffected by spinal cord transection or by deafferentation of the affected extremities but was abolished by severing the anterior roots.

Report of a Case

A 31-year-old woman entered the . . . [Full Text PDF of this Article]

Author Affiliations
New York

From the departments of neurosurgery of the Hospital for Joint Diseases and Medical Center, the New York Medical College and the Metropolitan Hospital of New York.

Footnotes
Submitted for publication Oct 12, 1966; accepted Dec 3.

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