Cerebellar output to ocular muscles via motor neurons in the brainstem control saccadic and smooth pursuit eye movements (reviewed by Thier and Ilg 2005; Krauzlis 2004). Eye movement irregularities in individuals at heightened risk for AUD suggest that these pathways may also be susceptible. This is consistent with oculomotor deficits in ADHD, further suggesting that cerebellar dysfunction may be a common neurobiological substrate for AUD and ADHD. Taken together, static ataxia and deficient control of eye movements may be present prior to prolonged alcohol consumption in subjects with a family history of AUD or those with behavioral predispositions to AUD. Longitudinal data from high risk offspring with slower derailment of postural control suggest this may be so (Hill et al. 2000b). Recent evidence suggests that there is an eight-fold increase in risk for SUD in those above the median for sway and below the median for P300 amplitude (Hill et al. 2009b).
