The putative involvement of the cerebellum in the pathogenesis of CM syndromes has been long hypothesized, as pathological changes in patients with CM have commonly been found in the cerebellum rather than in the suspected culprit, the sensorimotor cortex. The hypothesis is that the increased cortical excitability seen in CM is due to loss of the cerebellar inhibitory control via cerebello-thalamo-cortical connections. Here, we explore this hypothesis by modulating cerebellar excitability by means of transcranial Direct Current Stimulation (tDCS), and assessing its effect on sensorimotor cortex excitability in CM patients. 

according to our data, anodal cerebellar tDCS can facilitate, and not inhibit, sensorimotor cortex excitability in CM. Although the results might suggest a role of the cerebellum in the pathophysiology of CM, the paradoxical effect of cerebellar tDCS on cortical excitability in CM is not clear. One hypothesis is that CM patients might have abnormal homeostatic plasticity within the sensorimotor cortex.