Elena Antelmi1,2,3, Roberto Erro1,4, Lorenzo Rocchi1,5, Rocco Liguori2,3, Michele Tinazzi4, Flavio Di Stasio5,6, Alfredo Berardelli5,6, John C Rothwell1, Kailash P Bhatia1. 1. Sobell Department of Motor Neuroscience and Movement Disorders, Institute of Neurology, University College London, London, UK. 2. Department of Biomedical and Neuromotor Sciences, Alma Mater Studiorum, University of Bologna, Bologna, Italy. 3. IRCSS, Istituto di Ricovero e Cura a Carattere Scientifico; Research Hospital, Institute of Neurological Sciences, Bologna, Italy. 4. Department of Neuroscience, Biomedicine and Movement Science, University of Verona, Verona, Italy. 5. Department of Neurology and Psychiatry, "Sapienza" University of Rome, Italy. 6. IRCCS Neuromed, Pozzilli (IS), Italy.
Abstract
BACKGROUND: Somatosensory temporal discrimination threshold is often prolonged in patients with dystonia. Previous evidence suggested that this might be caused by impaired somatosensory processing in the time domain. Here, we tested if other markers of reduced inhibition in the somatosensory system might also contribute to abnormal somatosensory temporal discrimination in dystonia. METHODS: Somatosensory temporal discrimination threshold was measured in 19 patients with isolated cervical dystonia and 19 age-matched healthy controls. We evaluated temporal somatosensory inhibition using paired-pulse somatosensory evoked potentials, spatial somatosensory inhibition by measuring the somatosensory evoked potentials interaction between simultaneous stimulation of the digital nerves in thumb and index finger, and Gamma-aminobutyric acid-ergic (GABAergic) sensory inhibition using the early and late components of high-frequency oscillations in digital nerves somatosensory evoked potentials. RESULTS: When compared with healthy controls, dystonic patients had longer somatosensory temporal discrimination thresholds, reduced suppression of cortical and subcortical paired-pulse somatosensory evoked potentials, less spatial inhibition of simultaneous somatosensory evoked potentials, and a smaller area of the early component of the high-frequency oscillations. A logistic regression analysis found that paired pulse suppression of the N20 component at an interstimulus interval of 5 milliseconds and the late component of the high-frequency oscillations were independently related to somatosensory temporal discrimination thresholds. "Dystonia group" was also a predictor of enhanced somatosensory temporal discrimination threshold, indicating a dystonia-specific effect that independently influences this threshold. CONCLUSIONS: Increased somatosensory temporal discrimination threshold in dystonia is related to reduced activity of inhibitory circuits within the primary somatosensory cortex.
BACKGROUND: Somatosensory temporal discrimination threshold is often prolonged in patients with dystonia. Previous evidence suggested that this might be caused by impaired somatosensory processing in the time domain. Here, we tested if other markers of reduced inhibition in the somatosensory system might also contribute to abnormal somatosensory temporal discrimination in dystonia. METHODS: Somatosensory temporal discrimination threshold was measured in 19 patients with isolated cervical dystonia and 19 age-matched healthy controls. We evaluated temporal somatosensory inhibition using paired-pulse somatosensory evoked potentials, spatial somatosensory inhibition by measuring the somatosensory evoked potentials interaction between simultaneous stimulation of the digital nerves in thumb and index finger, and Gamma-aminobutyric acid-ergic (GABAergic) sensory inhibition using the early and late components of high-frequency oscillations in digital nerves somatosensory evoked potentials. RESULTS: When compared with healthy controls, dystonicpatients had longer somatosensory temporal discrimination thresholds, reduced suppression of cortical and subcortical paired-pulse somatosensory evoked potentials, less spatial inhibition of simultaneous somatosensory evoked potentials, and a smaller area of the early component of the high-frequency oscillations. A logistic regression analysis found that paired pulse suppression of the N20 component at an interstimulus interval of 5 milliseconds and the late component of the high-frequency oscillations were independently related to somatosensory temporal discrimination thresholds. "Dystonia group" was also a predictor of enhanced somatosensory temporal discrimination threshold, indicating a dystonia-specific effect that independently influences this threshold. CONCLUSIONS: Increased somatosensory temporal discrimination threshold in dystonia is related to reduced activity of inhibitory circuits within the primary somatosensory cortex.
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