Within this theory, the cerebellum forms

an internal model through repeated performance and feedback. As a movement is repeated, selleck kinase inhibitor the cerebellum allows the movement to be executed skillfully without dynamic feedback. Analogous processes are postulated to support the skillful execution of mental acts. Prefrontal control of cognitive objects—the mental models that represent imagined scenes and constructed thoughts—are operated upon by feedback mechanisms and internal models supported by the cerebellum. A similar evolution of ideas is present in the proposal of Thach, 1998 and Thach, 2007), who suggested that a postulated role of the cerebellum in coordinating and temporally synchronizing multimuscled movements might find a parallel whereby the cerebellum links cognitive units of thought. Motivated by behavioral

disturbances in patients with cerebellar abnormalities, Jeremy Schmahmann was among the earliest modern proponents for a role of the cerebellum in nonmotor functions including neuropsychiatric illness (e.g., Schmahmann, 1991). He hypothesized, “It may also transpire that HIF-1 pathway in the same way as the cerebellum regulates the rate, force, rhythm, and accuracy of movements, so may it regulate the speed, capacity, consistency, and appropriateness of mental or cognitive processes,” further noting “the overshoot and inability in the motor system to check parameters of movement may thus be equated, in the cognitive realm, with a mismatch between reality and perceived reality, and the erratic attempts to correct the errors of thought or behavior. Hence, perhaps, a dysmetria of thought.” The concept of dysmetria of thought has been expanded considerably in recent years with observations of patients with cerebellar abnormalities (e.g., Schmahmann and Sherman, 1998, Tavano et al., 2007 and Schmahmann, 2010)

next and psychosis (e.g., Andreasen et al., 1998). Despite these ideas and other examples of cognitive impairments in patients with cerebellar lesions (e.g., Fiez et al., 1992, Grafman et al., 1992, Courchesne et al., 1994 and Stoodley and Schmahmann, 2009b; see also Tomlinson et al., 2013), there remains a general belief among neurologists that cerebellar lesions do not typically produce marked cognitive impairment, at least as contrasted to the severe motor disturbances that are obvious. It is difficult to know where the gap lies between clinical impressions and the impairments that have now been documented in several studies. One possibility is that clinicians are not testing appropriately for cognitive and affective disturbances in patients with cerebellar damage. Another possibility is that, in the end, the cognitive deficits are relatively subtle even in many cases of large cerebellar lesions. Several explorations of deficits in patients with cerebellar lesions have found minimal cognitive impairment (e.g., Helmuth et al., 1997).