Abstract
Over the last three decades, measuring and modulating cerebellar activity and its connectivity with other brain regions has become an emerging research topic in clinical neuroscience. The most important connection is the cerebellothalamocortical pathway, which can be functionally interrogated using a paired‐pulse transcranial magnetic stimulation paradigm. Cerebellar brain inhibition reflects the magnitude of suppression of motor cortex excitability after stimulating the contralateral cerebellar hemisphere and therefore represents a neurophysiological marker of the integrity of the efferent cerebellar tract. Observations that cerebellar noninvasive stimulation techniques enhanced performance of certain motor and cognitive tasks in healthy individuals have inspired attempts to modulate cerebellar activity and connectivity in patients with cerebellar diseases in order to achieve clinical benefit. We here comprehensively explore the therapeutic potential of these techniques in two movement disorders characterized by prominent cerebellar involvement, namely the degenerative ataxias and essential tremor. The article aims to illustrate the (patho)physiological insights obtained from these studies and how these translate into clinical practice, where possible by addressing the association with cerebellar brain inhibition. Finally, possible explanations for some discordant interstudy findings, shortcomings in our current understanding, and recommendations for future research will be provided. © 2019 The Authors. Movement Disorders published by Wiley Periodicals, Inc. on behalf of International Parkinson and Movement Disorder Society.
Highlights
The anatomical connections between the cerebellum and contralateral motor cortex were described already in the 1960s in animal experiments, some time had elapsed before novel technological interventions allowed the functional exploitation of this tract in humans
Encouraging results of this stimulation technique have been reported in patients with degenerative cerebellar ataxias, the scarcity of adequately powered, randomized, double-blind, shamcontrolled trials and lack of etiological homogeneity in these studies are important shortcomings that need to be appreciated
cerebellar brain inhibition (CBI) seems to be reduced in degenerative cerebellar diseases, but can potentially return into the physiological range after multiple sessions of anodal cerebellar or cerebellospinal transcranial direct current stimulation (tDCS)
Summary
The following full text is a publisher's version. For additional information about this publication click this link. https://hdl.handle.net/2066/218922. (small errors), suggests that distinct neural mechanisms are engaged in response to errors of varying size and that the cerebellum is most implicated early on during the motor adaptation process.[9] A reduction of CBI magnitude was later confirmed to be specific to the early (rather than late) stage of skill learning.[10,11] Interestingly, CBI alterations correlated with the amount of skill acquisition and locomotor adaptation, which indicates a direct association between changes in the degree of cerebellar excitability and performance of these tasks.[10,12] Similar reductions in CBI have been reported during both the execution and observation of a visuomotor procedural learning task that is dependent on a proper cerebellar function, but only if the learning had not been acquired previously.[13] The mechanistic underpinning of reduced CBI during the process of motor learning possibly entails a temporarily diminished excitability of Purkinje cells due to a decrease in synaptic transmission efficacy between parallel fibers and Purkinje cells, emanating from simultaneous activation of climbing and parallel fibers This phenomenon has been established in vivo in animal studies and named longterm depression.[11,14,15,16,17]. Possible explanations for the sometimes discordant interstudy findings, shortcomings in our current understanding, and recommendations for future research will be discussed
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