[Pathophysiology of involuntary movements--dystonia and myoclonus from viewpoint of brain activities].

Cortical myoclonus (CM) and focal dystonia (FD) are commonly characterized by co-contraction of agonist and antagonist muscles, enhancement by intentional movement, strong influence by sensory input, and spread to adjacent muscles. On the other hand, they are different in the nature of movements, speed of muscle contraction, speed of spread, and drug effects. There are abundant data indicating that CM is due to pathological hyperexcitability of the sensorimotor cortex (S1-M1), while, in FD, no definitive evidence to suggest cortical hyperexcitability has been found. Changes in regional cerebral blood flow (rCBF) studied by positron emission tomography (PET) during movements in patients with dystonia were inconsistent with regard to S1-M1, but the frontal cortex including the rostral SMA was shown to be overactivated, suggesting the thalamocortical disinhibition based on the basal ganglia disorders.