, 1984). In cats, lesions of the flocculus abolish Vestibuloocular reflex adaptation (Luebke and Robinson, 1994). The rate of rotation adaptation in humans is increased by anodal transcranial direct current stimulation over the ipsilateral cerebellum but not over primary motor cortex (Galea et al., 2011). Visuomotor adaptation is not disrupted by lesions

in the corticospinal tract caused by ischemic stroke in humans (Reisman et al., 2007, Scheidt and Stoeckmann, 2007 and Scheidt et al., 2000) and is largely unaffected in Parkinson’s disease (PD) (Bédard and Sanes, 2011 and Marinelli et al., 2009) and Huntington’s disease (Smith Pexidartinib supplier and Shadmehr, 2005). Thus, motor cortex, the corticospinal tract, and

the basal ganglia do not seem to be necessary structures for visuomotor adaptation. Subtleties and controversies arise, however, because abnormalities in adaptation paradigms have been seen in patients who do not have known cerebellar impairment and patients with cerebellar disease can reduce errors under certain experimental conditions. We shall discuss these in turn and provide potential explanations that show why these exceptions do not disprove the cerebellar hypothesis for adaptation. In two recent studies, patients with PD were able to adapt to a rotation as well Selleck CP690550 as age-matched controls but did not show savings in re-exposure (Bédard and Sanes, 2011 and Marinelli et al., 2009). We have recently argued that savings in adaptation paradigms is not due to forward model-based error reduction but is instead Oxalosuccinic acid attributable to an addition operant process (Huang et al., 2011). Using this new framework, we can explain the result in PD because it is known that operant learning is disrupted in these patients (Knowlton et al., 1996). Patients with stroke in the left superior parietal lobule showed markedly impaired ability to adapt to a visuomotor rotation (Mutha et al., 2011), which would appear to contradict the idea that the cerebellum is the (sole) locus for adaptation. We have recently argued, however, that the parietal cortex receives the output of a

cerebellar forward model, which is then integrated with peripheral sensory feedback (Tanaka et al., 2009). Thus, the parietal cortex may be the downstream target of the cerebellum and thus disruption of this target can impair adaptation. A recent study reported that patients with spinocerebellar ataxia type 6 were able to adapt to an incremental introduced forcefield but not if the forcefield was introduced as a large step (Criscimagna-Hemminger et al., 2010). There are two ways to interpret these data. One is that adaptation to small errors is carried out in a noncerebellar structure. Alternatively, these patients brought down error using a non-adaptation-based mechanism. There is direct and indirect support for the second interpretation.