Objective: To explore the effect of high-frequency repetitive sensory stimulation (HF-RSS) on the excitability of the sensorimotor cortex in acquired dystonia

Background: Dystonia is currently considered a network disorder that also involves the somatosensory system. At a behavioural level, the most consistent sensory abnormality is increased somatosensory temporal discrimination threshold (STDT), which has been recently associated with physiological measures of reduced inhibition within S1. HF-RSS is a patterned electric stimulation, applied to the skin through surface electrodes, that enhances intracortical inhibitory mechanisms within S1 in healthy subjects (HS). However, we have recently demonstrated that, when applied in patient with primary dystonia, it paradoxically further reduces excitability of several measures of inhibition in the somatosensory and motor cortex¹. HF-RSS aftereffects have been described as a form of short-lasting synaptic plasticity.

Method: Ten patients affected by acquired dystonia were included in the study. All participants underwent STDT testing, somatosensory evoked potential (SEP) recording, and transcranial magnetic stimulation (TMS) at baseline and after 45-minute session of HF-RSS. TMS measures consisted of motor evoked potentials (MEP) and short-interval intracortical inhibition (SICI). The results were compared to those obtained from HS.

Results: At baseline, patients showed reduced SICI compared to HS, while all the other measures were normal. HF-RSS induced the same aftereffects in the two groups, namely: significant reduction of STDT, increased amplitude of both N20-P25 and P14 SEP components, enhanced inhibition at SEP recovery cycle and sensory lateral inhibition, increased early and late high-frequency oscillations area, increased SICI.

Conclusion: Our data show that HF-RSS induces the same responses in patients with acquired dystonia and HS, differently from those of primary dystonia patients¹. Our results are in line with previous studies and demonstrate that, in acquired dystonia, cortical plasticity is normal and that the somatosensory system is not involved in its pathophysiology. This suggests that, while reduced SICI is required for the clinical expression of dystonia, sensorimotor cortical plasticity is not.

References: 1. Erro, R., Rocchi, L., Antelmi, E., Liguori, R., Tinazzi, M., Berardelli, A., Rothwell, J. and Bhatia, K.P. (2018), High frequency somatosensory stimulation in dystonia: Evidence fordefective inhibitory plasticity. Mov Disord., 33: 1902-1909. doi:10.1002/mds.27470

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MDS Abstracts - https://www.mdsabstracts.org/abstract/exploring-the-pathophysiology-of-acquired-dystonia-by-the-use-of-high-frequency-somatosensory-stimulation/