Related Experiment Video
Updated: Dec 8, 2025
Measuring and Manipulating Functionally Specific Neural Pathways in the Human Motor System with Transcranial Magnetic Stimulation
Published on: February 23, 2020
Interhemispheric Connectivity in Idiopathic Cervical Dystonia and Spinocerebellar Ataxias: A Transcranial Magnetic
Tommaso Bocci1, Davide Baloscio2, Roberta Ferrucci1
1"Aldo Ravelli" Center for Neurotechnology and Experiental Brain Therapeutics, Department of Health Sciences, University of Milan & ASST Santi Paolo e Carlo, Milan, Italy.
Background And Rationale:
Hyperkinetic movement disorders represent a heterogeneous group of diseases, different from a genetic and clinical perspective. In the past, neurophysiological approaches provided different, sometimes contradictory findings, pointing to an impaired cortical inhibition as a common electrophysiological marker. Our aim was to evaluate changes in interhemispheric communication in patients with idiopathic cervical dystonia (ICD) and spinocerebellar ataxias (SCAs).
Materials And Methods:
Eleven patients with ICD, 7 with genetically confirmed SCA2 or SCA3, and 10 healthy volunteers were enrolled. The onset latency and duration of the ipsilateral silent period (iSPOL and iSPD, respectively), as well as the so-called transcallosal conduction time (TCT), were then recorded from the abductor pollicis brevis of the right side using an 8-shaped focal coil with wing diameters of 70 mm; all these parameters were evaluated and compared among groups. In SCAs, changes in neurophysiological measures were also correlated to the mutational load.
Results:
iSPD was significantly shorter in patients with SCA2 and SCA3, when compared both to control and ICD (P < .0001); iSPOL and TCT were prolonged in SCAs patients (P < .001). Changes in iSPD, iSPOL, and TCT in SCAs are significantly correlated with the mutational load (P = .01, P = .02, and P = .002, respectively).
Discussion:
This is the first study to assess changes in interhemispheric communication in patients with SCAs and ICD, using a transcranial magnetic stimulation protocol. Together with previous data in Huntington's disease, we suggest that these changes may underlie, at least in part, a common disease mechanism of polyglutamine disorders.
