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PAW36 Oculomotor deficits in presymptomatic and early Huntington's disease and their structural brain correlates
  1. S Hicks,
  2. H D Rosas,
  3. C Berna,
  4. R Scahill,
  5. E Durmas,
  6. R A Roos,
  7. B Levitt,
  8. S J Tabrizi,
  9. C Kennard,
  10. A Durr
  1. 1University of Oxford, National Hospital for Neurology and Neurosurgery, Oxford, UK
  2. 2Institute of Neurology, UCL, London, UK
  3. 2Track-HD Investigators, University College London, London, UK
  1. Correspondence to stephen.hicks{at}clneuro.ox.ac.uk

Abstract

Background Oculomotor deficits are potentially a preclinical predictor of Huntington's disease (HD). Saccadic abnormalities include delayed initiation, low velocity and disinhibition and can be partially explained by neurodegeneration of the caudate nucleus, a region vital to saccadic control.

Methods In the longitudinal multicentre Track-HD study, we tested 240 HD gene carriers, 120 of whom were presymptomatic, on a pro/anti saccade task using a saccadometer (Ober). 3-T structural MRI scans were made in the same session.

Results Overall HD subjects showed significantly increased antisaccade error rates and saccades that were longer and more variable in both latency and duration. Significant effects were seen in the presymptomatic group with a predicted time to clinical onset of up to 10 years. Interestingly, longitudinal changes in saccade latency variance were apparent after only 1 year. Antisaccade performance correlated with brain volume loss in the caudate and globus pallidus and with thinning of the occipital and parietal lobes. Longer saccade duration correlated with thinning of the parietal eye fields and the visual cortex. Diffusion tensor imaging revealed that antisaccade performance worsened as fibre integrity decreased in the sensorimotor and prefrontal cortices.

Conclusions Together these results show the validity of oculomotor testing in presymptomatic HD and the functional consequences of widespread neurodegeneration associated with HD.

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