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Published online before print April 19, 2006, doi:10.1212/01.wnl.0000218215.43328.88)
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 Volume 67, Number 3, August 8, 2006
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NEUROLOGY 2006;67:485-487
© 2006 American Academy of Neurology
Brief Communications

Identification of an oculomotor biomarker of preclinical Huntington disease

C.V.P. Golding, PhD, C. Danchaivijitr, MRCP, T. L. Hodgson, PhD, S. J. Tabrizi, PhD, MRCP and C. Kennard, PhD, FRCP

From the Department of Clinical Neuroscience (C.V.P.G., C.D., C.K.), Faculty of Medicine, Imperial College; School of Psychology (T.L.H.), Exeter University; and Department of Neurodegenerative Disease (S.J.T.), Institute of Neurology and National Hospital for Neurology and Neurosurgery, London, UK.

Address correspondence and reprint requests to DrP. Golding, Room 10L18, Imperial College, Charing Cross Campus, St. Dunstan's Road, London, UK, W6 8RP; e-mail: c.golding{at}imperial.ac.uk

The authors examined oculomotor function to identify a biomarker of disease progression in genetically confirmed preclinical and early clinical Huntington disease (HD). Initiation deficits of voluntary-guided, but not reflexive, saccades were characteristic of preclinical HD. Saccadic slowing and delayed reflexive saccades were demonstrated in clinical but not preclinical HD. Saccadic measures provide biomarkers of disease progression in both preclinical and early clinical stages of HD.

This article was previously published in electronic format as an Expedited E-Pub on April 19, 2006, at www.neurology.org.

Editorial, see page 376

See also page 394

Supported by grants from the Hereditary Disease Foundation and Wellcome Trust.

Disclosure: The authors report no conflicts of interest.

Received July 6, 2005. Accepted in final form March 6, 2006.


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