Cerebellar dysfunction may play an important role in vascular dementia.

The cerebellum has traditionally been seen as a brain area limited to the coordination of voluntary movement, gait, posture, speech, and motor functions. There are increasing evidence, however, proving that the cerebellum is implicated in processes associated with the control of cognition, behavior, and psychiatric illness. Furthermore, the fact that the cerebellum is reciprocally connected to a broad range of limbic structures including the amygdale and hippocampus, as well as the cerebral cortex including the prefrontal areas, provides a strong neuroanatomical argument in favor of cerebellar involvement in cognition regulation. Studies have already found the fact that after stroke, the cerebellum suffered from reduction in metabolism and blood flow in the cerebellar hemisphere contralateral to a destructive cerebral lesion. The notion of crossed cerebellar diaschisis (CCD) may contribute to the explanation of the phenomenon. Consequently, theoretically, stroke in any part of the brain including frontal lobe and hippocampus, will affect cerebellar function and the later then results in vascular dementia (VD). More recently, a few clinical trials found that electrical stimulation of fastigial nucleus (FNS) in cerebellum could improve symptom of VD, though the relationship between cerebellum and VD is unclear. Taken together, there seems to be sufficient empirical ground to assume that the cerebellum plays a role in the regulation of VD. The hypotheses of cerebellar role in VD, which will be discussed in this paper, if confirmed, may lead to the formulation of new pathogenesis and new therapeutic approaches to VD.