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There you go again: Th steadfast fad of fixing spasticity. To the Editor: Presentation of the problem. The Role of tizanidine in the treatment of spasticity, the recent 80-page supplement to Neurology [1] subsidized by the manufacturer of tizanidine, sets me up front [2] as the stalking horse entree of the symposium. Of course, I was flattered to gain the editor's attention to my ancient essay [3]: ``he [Landau] considered destruction of parts of the segmental stretch reflex arc to be the most reasonable therapeutic approach to the treatment of spasticity.'' Not so. (Later in his own review, [4] Young more accurately indicates that I was referring only to the disabling positive symptom of flexor spasms in patients who are already paraplegic.) But whether my old ``hypothesis [actually current data, argument, and inference] was inaccurate'' is a trivial issue. What is the evidence that tizanidine pills are indeed a great remedy for the concrete disabilities of afflicted patients? ### Comment. Let's look at the record. This pamphlet includes Young's introduction, [2] his review [4] concerning definitions, pathophysiology, assessment, and therapy, and eight papers about the subject at issue. Coward's paper on neuropharmacology [5] concerns only animal models such as the ability of a particular compound to reduce the perpendicular elevation of the mouse tail caused by high doses of morphine. Tizanidine also depresses flexor and extensor reflexes in animals. Delwaide and Pennisi [6] describe electrophysiologic measures in spastic patients. Four …
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William M. Landau (1995) studied this question.
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