Latorre, A;
Cocco, A;
Bhatia, KP;
Erro, R;
Antelmi, E;
Conte, A;
Rothwell, JC;
(2020)
Defective Somatosensory Inhibition and Plasticity Are Not Required to Develop Dystonia.
Movement Disorders
10.1002/mds.28427.
(In press).
![[thumbnail of Latorre et al, Mov Disord 2021.pdf]](https://discovery.ucl.ac.uk/style/images/fileicons/text.png) |
Text
Latorre et al, Mov Disord 2021.pdf - Accepted Version Access restricted to UCL open access staff Download (668kB) |
Abstract
BACKGROUND: Dystonia may have different neuroanatomical substrates and pathophysiology. This is supported by studies on the motor system showing, for instance, that plasticity is abnormal in idiopathic dystonia, but not in dystonia secondary to basal ganglia lesions. OBJECTIVE: The aim of this study was to test whether somatosensory inhibition and plasticity abnormalities reported in patients with idiopathic dystonia also occur in patients with dystonia caused by basal ganglia damage. METHODS: Ten patients with acquired dystonia as a result of basal ganglia lesions and 12 healthy control subjects were recruited. They underwent electrophysiological testing at baseline and after a single 45‐minute session of high‐frequency repetitive somatosensory stimulation. Electrophysiological testing consisted of somatosensory temporal discrimination, somatosensory‐evoked potentials (including measurement of early and late high‐frequency oscillations and the spatial inhibition ratio of N20/25 and P14 components), the recovery cycle of paired‐pulse somatosensory‐evoked potentials, and primary motor cortex short‐interval intracortical inhibition. RESULTS: Unlike previous reports of patients with idiopathic dystonia, patients with acquired dystonia did not differ from healthy control subjects in any of the electrophysiological measures either before or after high‐frequency repetitive somatosensory stimulation, except for short‐interval intracortical inhibition, which was reduced at baseline in patients compared to control subjects. CONCLUSIONS: The data show that reduced somatosensory inhibition and enhanced cortical plasticity are not required for the clinical expression of dystonia, and that the abnormalities reported in idiopathic dystonia are not necessarily linked to basal ganglia damage.
Archive Staff Only
 |
View Item |
