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Sympathoadrenal Hyperactivity and Neuroleptic Malignant Syndrome

To the Editor: We read with great interest the article by Ronald J. Gurrera, M.D. (1), a distinguished researcher, regarding the etiology of neuroleptic malignant syndrome. He correctly stated that the current theories of origin—hypothalamic hypodopaminergia and direct myotoxicity—do not explain the entire pathophysiological changes found in neuroleptic malignant syndrome. He further added that the treatment options based on these mechanisms are not reliable and are reported to be insufficiently effective in overall management of the symptoms of neuroleptic malignant syndrome. Similarly, when we reviewed and updated the relevant literature (2) and presented nine cases (3) of neuroleptic malignant syndrome, one of our main conclusions was that all the manifestations of neuroleptic malignant syndrome are not explained exclusively by dopaminergic antagonism in the central nervous system. Therefore, we recommended that other putative neurotransmitters and also peripheral factors should be explored in studying its pathophysiology.

The author partially bridged this gap by presenting an alternative hypothesis to that of sympathoadrenal hyperactivity, which, in a person genetically vulnerable to the development of neuroleptic malignant syndrome, is the interplay of the dysregulated and/or overactivated sympathetic nervous system in response to emotional or psychological stress. Although Dr. Gurrera did not highlight them, we feel that there are several future research implications in his article.

1. Despite a recent study’s negative results (4) regarding the genetic etiology of the features of neuroleptic malignant syndrome, further studies are needed to discover the phenotypes and genetic markers of this syndrome.

2. As the author claimed, this pathophysiological model explains most of the features of neuroleptic malignant syndrome; therefore, the unexplained manifestations should have been better elucidated. Their identification may in fact guide researchers to explore other possible alternative pathophysiological mechanisms underlying the development of neuroleptic malignant syndrome.

3. The author did not suggest any alternative treatments based on his hypothesis; hence, the hypothesis should be the avenue in future studies for developing suitable drugs for the treatment of both neuroleptic malignant syndrome and psychological disorders.

4. Finally, in the context of this new pathophysiological model, is it possible to prematurely rename neuroleptic malignant syndrome as "sympathoadrenal hyperactivity hyperpyrexia syndrome"?

REFERENCES

1. Gurrera RJ: Sympathoadrenal hyperactivity and the etiology of neuroleptic malignant syndrome. Am J Psychiatry 1999; 156:169–180[Abstract/Free Full Text]
2. Qureshi NA, Al-Amri AH, Al-Beyari TH, Abdelgadir MH, Al-Habeeb TA: Neuroleptic malignant syndrome: a comprehensive review and update. Saudi Pharmaceutical J 1996; 4:138–148
3. Qureshi NA, Al-Beyari TH, Al-Amri AH, Abdelgadir MH, Al-Habeeb TA: Neuroleptic malignant syndrome: a report of 9 suspected cases. Saudi Pharmaceutical J 1996; 4:179–189
4. Kawanishi C, Hanihara T, Shimoda Y, Suzuki K, Sugiyama N, Onishi H, Miyakawa T, Yamada Y, Kosaka K: Lack of association between neuroleptic malignant syndrome and polymorphisms in the 5-HT_1A and 5-HT_2A receptor genes. Am J Psychiatry 1998; 155:1275–1277

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