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Joseph H. Friedman, MD
Roger Williams General Hospital Brown University Providence, RI

Robert G. Feldman, MD
Boston University School of Medicine and University Hospital Boston Veterans Administration Hospital

JAMA. 1986;255(17):2291-2292.

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

In Reply.—

We thank Drs Sandyk and Iacono for their interest in our article and for their intriguing hypothesis. Testing any hypothesis concerning NMS is difficult given the rarity of the condition, the absence of an animal model, and the critical nature of the illness, necessitating immediate intervention.

Our criticisms of their hypothesis include the following: (1) The arguments advanced are logical but tenuous in that the cited animal work deals with rodents that were not parkinsonian models. Also they were given intracisternal¹ or intraventricular² injections of β-endorphin and were, therefore, clearly not physiological models. (2) We think it more reasonable to state that β-endorphin may modulate catecholamine systems rather than that they "control" them. (3) The use of nalaxone in septic shock is not universally accepted, as implied in the letter.³ (4) Nalaxone has been tried in the treatment of Parkinson's disease but was without benefit. . . . [Full Text PDF of this Article]

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