Sarah Pirio Richardson1. 1. Department of Neurology, University of New Mexico Health Sciences Center, Albuquerque, NM, USA. Electronic address: spiriorichardson@salud.unm.edu.
Abstract
OBJECTIVE: This study aims to understand whether the enhanced dPMI, seen in writer's cramp patients previously, extends to other populations of focal dystonia patients (e.g. cervical dystonia) as an endophenotypic marker. METHODS: We studied 9 healthy subjects and 9 patients with CD. dPMI was tested by applying conditioning transcranial magnetic stimulation to the left dorsal premotor cortex and then a test pulse to the ipsilateral motor cortex at an interval of 6ms. We also looked at the duration of the cortical silent period (CSP)-a measure of cortical excitability. RESULTS: CD patients had enhanced dPMI at rest (mean 57.0%, SD 16.2) in contrast to healthy volunteers (mean 124.1%, SD 35.7) (p<0.001). CSP latencies (in ms) in CD patients (mean 108.0, SD 33.1) were significantly shorter than in healthy volunteers (mean 159.1, SD 55.2) (p<0.05). CONCLUSIONS: CD patients showed enhanced dPMI in a hand muscle-distant from their affected body part-similar to writer's cramp patients. This enhanced inhibition was independent of disease severity and neck posture. This suggests that enhanced dPMI may be an endophenotypic marker of dystonia. SIGNIFICANCE: The abnormal dorsal premotor-motor connection in cervical dystonia is a potential novel and important avenue for therapeutic targeting.
OBJECTIVE: This study aims to understand whether the enhanced dPMI, seen in writer's cramppatients previously, extends to other populations of focal dystoniapatients (e.g. cervical dystonia) as an endophenotypic marker. METHODS: We studied 9 healthy subjects and 9 patients with CD. dPMI was tested by applying conditioning transcranial magnetic stimulation to the left dorsal premotor cortex and then a test pulse to the ipsilateral motor cortex at an interval of 6ms. We also looked at the duration of the cortical silent period (CSP)-a measure of cortical excitability. RESULTS:CDpatients had enhanced dPMI at rest (mean 57.0%, SD 16.2) in contrast to healthy volunteers (mean 124.1%, SD 35.7) (p<0.001). CSP latencies (in ms) in CDpatients (mean 108.0, SD 33.1) were significantly shorter than in healthy volunteers (mean 159.1, SD 55.2) (p<0.05). CONCLUSIONS:CDpatients showed enhanced dPMI in a hand muscle-distant from their affected body part-similar to writer's cramppatients. This enhanced inhibition was independent of disease severity and neck posture. This suggests that enhanced dPMI may be an endophenotypic marker of dystonia. SIGNIFICANCE: The abnormal dorsal premotor-motor connection in cervical dystonia is a potential novel and important avenue for therapeutic targeting.
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