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

Methods The Track-HD study tested 240 genetically confirmed HD gene carriers and 120 controls longitudinally over 4 years. 120 of the participants were presymptomatic with a predicted time to onset of between 5–15 years. All participants completed a range of tasks including a mixed pro/anti saccade task and a 3T MRI.

Results Oculomotor

In cross-sectional analyses, patients, premanifest subjects and controls were significantly different in a range or variables including antisaccade error rate, latency, prosaccade duration, and amplitude variability. Longitudinally premanifest gene carriers showed no systematic change, while HD patients exhibited annual systematic increases in antisaccade latency and prosaccade amplitude variability. Some premanifest gene carriers showed a small annual lengthening of prosaccade duration and an increase in antisaccade latency that may be indicative of their nearness to symptomatic onset.

Neural Correlates

Antisaccade performance correlated negatively with grey matter volume in the caudate and globus pallidus, white matter volume in the internal capsule, and thickness of the occipital and parietal cortices. Longer saccade duration correlated with isolated thinning of the parietal eye-fields and visual cortex. Diffusion tensor imaging revealed that reduced performance on the antisaccade task correlated with lower integrity of fibres in the prefrontal cortices.

Conclusions These results show that while this oculomotor test may be insensitive to premanifest HD progression, it may reveal the many interrelated functional consequences of neurodegeneration associated with HD.