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H. P. H. Kremer, MD; R. A. C. Roos, MD
Department of Neurology Academic Hospital Rijnsburgerweg 10 2333 AA Leiden The Netherlands

Arch Neurol. 1992;49(4):349.

	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.

—The article by Myers and coworkers1 presented interesting observations on Huntington's disease progression and its relationship to several clinical variables. Specifically, the authors found significant associations between progression rate and age at onset and body weight (body mass index) at initial examination; fatter patients or late-onset patients deteriorated slower. The authors refrain from offering a biological explanation, but we think that the following might be considered. Recently, we² described selective neuronal loss in the hypothalamic lateral tuberal nucleus (NTL) of patients with Huntington's disease.² The log-transformed number of remaining NTL neurons was closely correlated with age at onset of the disease (n = 16; r= .78; P<.001).³ The function of this nucleus, situated in the tuberal part of the lateral hypothalamus, is unknown. In rodents, the lateral hypothalamic area (LHA) is involved in a large variety of behavioral and metabolic functions, eg, in the regulation . . . [Full Text PDF of this Article]

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