[Pathophysiology of dystonia]

Dystonia is a diverse movement disorder characterized by involuntary muscle co-contraction of the agonist and antagonist, which may cause twisting and repetitive movements or abnormal posture. Dystonia is the least understood movement disorder associated with the basal ganglia dysfunction. While dysfunction of cortico-striatal-thalamo-cortical motor circuits is likely to play a fundamental role in the pathophysiology of dystonia, the disorder does not easily fit into the hypokinetic or the hyperkinetic category of basal ganglion diseases. There was evidence of widespread impairment of the inhibition involving multiple levels of the nervous system. There was also significant data to support the notion that the sensory function and sensorymotor integration were debit in patients with dystonia. The reciprocal inhibition curves between the forearm muscles were abnormal at the spinal cord level, as well as the blink reflex recovery curves at the brain stem level. The motor cortex excitability was enhanced while the transcranial magnetic stimulation. The dystonia showed decreased inhibition of the intracortical inhibition and facilitation and short cortical silent period. The pre-movement gating of the somatosensory evoked potentials and the somatosensory homunculus were abnormal in dystonia. This review provides an overview of the recent studies of the pathophysiology of dystonia, with an emphasis on the cortical plasticity. The possible beneficial effects of the transcranial magnetic stimulation (TMS) and repetitive transcranial magnetic stimulation (rTMS) with new paradigm are also discussed.