P172. Clinical and neurophysiological effects of cerebellar TMS in cervical dystonia

Abstract

Introduction Cervical Dystonia (CD) is a movement disorder causing involuntary neck muscle contractions which can lead to abnormal head movements and positions. Although the underlying pathophysiology of CD is poorly understood, there is a growing body of evidence suggesting that the cerebellum and its connections might play a key role in the development of focal dystonia. We therefore hypothesize that changes in cerebello-thalamocortical connections are a crucial part of CD pathophysiology. To test this hypothesis, we set out to study the impact of bilateral virtual lesions of the cerebellar hemispheres on selected clinical and neurophysiological parameters in patients with CD and matched controls. Methods An inhibitory protocol of repetitive transcranial magnetic stimulation (continuous thetaburst-stimulation, cTBS) was used to induce bilateral transient virtual lesions at the cerebellar hemispheres (CRB) in 10 patients with CD and in matched healthy controls. cTBS at the dorsal premotor cortex (PMd) and sham cTBS at the cerebellar hemispheres were used as control conditions. Clinical assessment included the subjective Clinical Global Impression (CGI) scale and the motor subcale of the Toronto Western Spasmodic Torticollis Rating Scale (TWSTRS-M) as rated by an experienced investigator in a blinded manner based on video sequences. Neurophysiological assessment comprised the resting motor threshold, mean motor evoked potential amplitude (at 130% RMT), and the duration of the cortical silent period (CSP), as obtained by transcranial magnetic stimulation at the motor hotspot of the contralateral first dorsal interosseus muscle. Results The protocol proved feasible and safe without any adverse effects. In CD patients (median TWSTRS-M 15.5 [range 14–22]) preliminary analysis points to an overall improvement of CD symptoms following cTBS at bilateral CRB (median CGI efficacy 3 [range 2–4]), but not in the control conditions, while the TWSTRS-M remained stable. cTBS at CRB or PMd may normalize the CSP duration, though a higher number of CD patients will be included prior to definite conclusions on the neurophysiological parameters of interest. Discussion Our preliminary results suggest that bilateral virtual lesions at the cerebellar hemispheres by cTBS may normalize neurophysiological parameters of cortical excitability in patients with CD, along with a subjective overall improvement of CD symptoms. Upon confirmation, our data may be in line with a pathogenetic – rather than compensatory – role of altered cerebello-thalamocortical connections in CD.