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Anne B. Young, MD, PhD; John B. Penney, MD; Simon Starosta-Rubinstein, MD; Dorene Markel, MS; Stanley Berent, PhD; Jill Rothley; Annette Betley; Richard Hichwa, PhD

Arch Neurol. 1987;44(3):254-257.

Abstract
• Glucose metabolism was examined by positron emission tomographic scanning with¹⁸F-2-fluoro-2-deoxy-d-glucose in 29 persons at risk for Huntington's disease (HD), 28 age-matched controls, nine patients with stage I, and eight patients with stage II symptomatic HD. Absolute caudate metabolic rates and normalized indexes of caudate metabolism for at-risk persons were normal compared with controls. No at-risk person had caudate indexes outside two SDs of the controls' mean. Caudate metabolism in the earliest HD cases was significantly reduced compared with controls and atrisk persons, but within the 99% confidence levels of both groups. Stage II patients had caudate measures that were significantly depressed compared with those of stage I HD patients. Measurement of caudate glucose hypometabolism is unlikely to be sufficiently sensitive to serve as a presymptomatic marker of heterozygote status, although it will provide a sensitive marker for progressive caudate dysfunction in HD.

Author Affiliations
From the Departments of Internal Medicine (Mss Rothley and Betley and Dr Hichwa), Neurology (Drs Young, Penney, and Starosta-Rubinstein and Ms Markel), and Psychiatry (Dr Berent), University of Michigan, Ann Arbor.

Footnotes
Accepted for publication Oct 2, 1986.

Reprint requests to Neuroscience Building, 1103 E Huron St, Ann Arbor, MI 48104 (Dr Young).

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