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Pavel Klein, MB, Bchir
Department of Neurology Box 394 University of Virginia Medical Center Charlottesville, VA 22908

Arch Neurol. 1989;46(11):1166.

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

To the Editor.

—I read with interest the article by Trouillas et al¹ in the November 1988 issue of the ARCHIVES. Their findings, akin to the ones they had previously published,² are interesting and potentially of great significance for patients with Friedreich's ataxia, olivopontocerebellar degeneration, and other degenerative diseases affecting the cerebellum.

Trouillas and coworkers' findings are at variance with a study that we performed.³ Inspired by Trouillas and coworkers' previously reported findings, we sought to corroborate them. Eight patients, four with Friedreich's ataxia, one with sporadic adult-onset cerebellar degeneration of the parenchymal (Holmes) type, and one each with posttraumatic, postinfectious, and multiple sclerosis—related cerebellar deficits, were administered the levorotatory form of 5-hydroxytryptophan, together with the peripheral decarboxylase inhibitor, benserazide, in dosages identical to those used by Trouillas et al.² In one case, half that dose was used as the higher dose-induced psychosis.

Our findings . . . [Full Text PDF of this Article]

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