Objective: By performing an extensive evaluation of neurophysiological measurements accounting for inhibitory mechanisms within the S1, we aim to find if a central nervous system node rather than another might explain abnormality in sensory gating in patients with isolated cervical dystonia.

Methods: Twenty-one consecutive patients with isolated idiopathic cervical dystonia (14 females, age 62.3 ± 8.8) and 21 age-matched healthy controls, all right handed were prospectively recruited. Both groups underwent tests for somatosensory temporal discrimination threshold (STDT) on the first and second fingers of both hands, neurophysiological investigations by measuring somatosensory evoked potentials (SEPs) recorded by stimulating the first and second fingers (on the dominant hand) and by recording N20 and P14 components. Paired SEPs at different interstimulus intervals (ISI at 5, 20 and 40 ms) and SEPs by simultaneous stimulation of the first and second fingers were recorded. Early (e)-High Frequency Oscillations (HFO) and late (l)-HFO areas were measured off-line.

Results: STDT values were slightly higher in dystonic patients, when compared to healthy controls and when evaluated on index finger and thumb of both hands. Mean latency and amplitude of of SEPs did not differ between the two groups. Simultaneous SEPs had larger amplitudes in the patients group. SEP recovery cycles had increased values in dystonic patients at every ISI. HFO area was decreased in the patients. Correlation between the neurophysiological and behavioral measurements disclosed a positive correlation between SDT and group (P = 0.028), STDT and recovery cycle at 5m (P = 0.000), STDT and l-HFO area (P = 0.001).

Conclusions: Both measurements reputedly related to mechanism acting locally and modulated by thalamic afferents were found to be impaired in dystonia. STDT values, instead, strongly correlated in both groups with measurements reputedly related only to inhibitory mechanisms acting locally. Basing on these findings and on the data pinpointing STDT as an endophenotypic trait of dystonia, loss of local inhibition may represent its neurophysiological substrate, which is necessary but not sufficient in order to manifest the disease. Therefore it might be hypothesize a possible double-hit model, with abnormities within the local inhibition being the remote landmark. Additional abnormalities of basal ganglia-thalamo afferents seem to be mandatory to develop the phenotype.

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MDS Abstracts - https://www.mdsabstracts.org/abstract/sensory-gating-and-inhibition-in-dystonia/