Abstract
Dystonia is a specific type of abnormal movement characterized by involuntary movement, abnormal posture, or both due to persistent or intermittent muscle contractions. At present, symptomatic treatment is mainly used including a combination of psychological and rehabilitation treatments, oral medications, botulinum toxin injections and deep brain stimulation surgery. Existing animal studies suggested that the cerebellum affects dystonia through at least three mechanisms: 1) abnormal cerebellar efferent signal patterns; 2) abnormal connections between the cerebellum and basal ganglia nuclei; 3) abnormalities in the shape or structure of cerebellar cells. The specific role of cerebellum in dystonia has been explored from clinical and pathological observations, neuroelectrophysiology and neuroimaging. In the past, the main function of cerebellum was to maintain body balance and coordinate movement, while dystonia was mainly a disorder of basal ganglia. In recent years, with the development of the "cerebellum-thalamus-cerebral cortex" circuit, the cerebellum has been considered as a new node related to dystonia. As the role of cerebellum in dystonia becomes more and more important and non-invasive brain stimulation techniques have been developed, repetitive transcranial magnetic stimulation (rTMS) for cerebellum is gradually being used. Transcranial magnetic stimulation (TMS) is one of the most widely used neurophysiological techniques in human research. A magnetic field of varying intensity is applied to the central nervous system to generate local currents in the cerebral cortex. rTMS is the traditional mode of stimulation for TMS. Low frequency magnetic stimulation (≤1 Hz) inhibits cortical excitability in the stimulating region, while high frequency stimulation (>1 Hz) increases the excitability of cortical area of stimulation. Theta rhythm burst stimulation (θ rhythm burst stimulation, TBS) is a new type of rTMS. Intermittent TBS (iTBS) can increase excitability of thecortical area, while continuous TBS (cTBS) can inhibit activation of the cerebral cortex. Based on the theory of cerebellar-brain inhibition, TMS can improve symptoms by modulating cerebellar-brain inhibition. Stimulation of the cerebellar cortex by iTBS can inhibit the development of subsequent associative plasticity in the motor cortex, whereas inhibition of the cerebellar cortex by cTBS can enhance subsequent plasticity in the motor cortex. Therefore, cerebellum has gradually become a new regulatory target of higher brain functional stimulation.
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