Abstract
Several important advances in the pathophysiology of Huntington's disease (HD) have been achieved by means of neurophysiological techniques designed to investigate the excitability and plasticity of brainstem and cortical circuits in patients with the condition. Studies designed to investigate brainstem reflexes, with paired-pulse and repetitive stimulation of the supraorbital nerve (blink reflex), have demonstrated abnormal excitability and plasticity of brainstem interneurons. In addition, several authors have tested the excitability of the primary motor cortex (M1) with the transcranial magnetic stimulation (TMS) technique and reported abnormal excitability of inhibitory intracortical circuits (cortical silent period, short afferent inhibition). Studies investigating plasticity processes by means of repetitive TMS (rTMS) protocols have demonstrated altered short-term as well as long-term M1 plasticity. Abnormal cortical excitability and plasticity can be present in the early phase of HD and in asymptomatic HD carriers. Evidence from a single study of small cohorts of patients with HD supports the therapeutic application of rTMS for symptomatic improvement of chorea in HD.
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