F64. High frequency somatosensory stimulation in cervical dystonia: Evidence for defective homeostatic plasticity in sensorimotor inhibitory circuits

Abstract

Apart from motor symptoms, multiple deficits of sensory processing have been demonstrated in dystonia. The most consistent behavioural measure of this is abnormal somatosensory temporal discrimination threshold (STDT), which has recently been associated with physiological measures of reduced inhibition within the primary somatosensory area, namely paired-pulse somatosensory evoked potentials (pp-SEP) and high-frequency oscillations (HFO). High-frequency repetitive sensory stimulation (HF-RSS) is a patterned electric stimulation that, when applied to the skin through surface electrodes, has been recently reported to shorten STDT in healthy subjects and to increase the resting level of excitability in several different types of inhibitory interactions in the primary somatosensory cortex (S1) and even the primary motor cortex (M1). We asked here whether HF-RSS was able to increase inhibition also in dystonia, where a lack of inhibitory interactions has been previously described. We tested whether HF-RSS could augment cortical inhibition and, in parallel, ameliorate STDT in 12 patients with cervical dystonia. To this aim, STDT and a number of electrophysiological measures of S1 (pp-SEP, HFO, lateral inhibition) and M1 (short intracortical inhibition (SICI)) were measured before and after 45 min of HF-RSS. The results were also compared with those of 12 age-matched healthy controls. Compared with healthy controls, in whom HF-RSS, as expected, shortened STDT and increased S1 and M1 inhibition assessed with the mentioned tests, patients with cervical dystonia showed a consistent, paradoxical response: they had reduced suppression in pp-SEP, a reduced area of HFO, a smaller amount of lateral inhibition and less SICI. STDT deteriorated after HF-RSS, and the change was correlated with those in pp-SEP and HFO. We suggest that patients with dystonia have abnormal homeostatic plasticity in the inhibitory circuitry within S1, and possibly M1, and that this is responsible for their paradoxical response to HF-RSS.