F151. Sensorimotor cortex plasticity correlates with effectiveness of pallidal stimulation in dystonia

Abstract

Introduction Deep brain stimulation (DBS) of the globus pallidus interna (GPi) is an effective symptomatic treatment of farmacoresistant dystonic syndromes. The sensorimotor cortex of dystonia patients exhibits an exaggerated responsiveness to the TMS (transcranial magnetic stimulation) in conditioning protocols. The aim of our study was to analyse the excitability of the primary motor cortex (MI) in relation to modulation of input from the primary somatosensory cortex (SI) in dystonia patients treated by GPi DBS. Methods We examined 21 patients (mean age 51 ± (SD)17 years) with dystonia treated by GPi DBS. The SI was modulated in DBS ON and OFF conditions by a 2-min series of paired associative stimulation (PAS) with 5 Hz frequency, consisting of electrical stimulation of the median nerve followed by 20 ms of subthreshold TMS pulse. The excitability of the MI was tested by motor evoked potentials (MEP) applied before and after the PAS. The clinical effect (CE) was expressed as a change in the dystonic score between DBS ON condition and the preoperative state. Results The SI PAS caused a decrease of the MEP amplitude in dystonia patients with the GPi DBS ON state in comparison with GPi DBS OFF state ( p p N = 8, p p N = 13, >25% CE) had the MEP amplitude unchanged after the SI PAS in both of the GPi DBS conditions. Conclusion The SI PAS intervention applied over SI cortex affected motor cortex excitability in dystonia patients but not in healthy controls. The GPi DBS reduced the sensorimotor cortex plasticity of dystonia patients under level seen in the GPi DBS off state and even under the level seen in healthy controls. Surprisingly, only poor responders to GPi DBS therapy showed a loss of an inhibitory effect of the SI on the MI immediately after switching stimulation off in comparison with good responders and healthy controls. This may suggest, that the GPi DBS normalizes the excitability of MI through strengthening of the sensorimotor interaction and causes long lasting cortical plasticity changes in good responders which may contribute to better suppression of the dystonic symptoms. Supported by the grants GACR 16-13323S, PROGRES Q27/LF1 and MJFF11362.