The Conover test indicated that there was no significant difference between those two sub-groups of patients (P = 1.00). Correlation analyses did not show
any signification association between the amount of SI and the PMv–M1 interactions, suggesting an independence of the two phenomena (Table 4). Our results showed that the PMv exerted a modulatory influence on the M1 at rest and during movement preparation, and that this influence was absent in patients. We confirmed that the PMv inhibited the M1 at rest Endocrinology antagonist in controls and that this inhibition was muscle specific. Moreover, contrary to our hypothesis, we showed that this inhibition was not enhanced during movement initiation, indicating that the ipsilateral ventral premotor–motor inhibition does not play a key role in SI in normal subjects. In accordance with the literature, we showed that healthy volunteers presented with SI (regarding the APB muscle) before and at movement onset and that this SI was absent in patients (Sohn & Hallett, 2004a,b; Beck et al., 2008, 2009a,b,c). In parallel with this inhibition, the excitability of the synergist muscle cortical representation was increased before and at movement onset in controls
as well as in patients with FHD without significant differences between the two groups, as previously reported (Beck et al., 2008). Indeed, we showed that MEPFDI was significantly enhanced at T50 and Tpeak. This preserved central excitation, in line with the literature, shows that the cortico-spinal Obeticholic Acid excitability of the synergist muscle is not impaired in patients with FHD. Together with this finding, we did not observe any differences in RTs between patients and controls (Stinear & Byblow, 2005; Beck et al., 2008, 2009a,b). Although RTs as well as the central excitation were not impaired in patients, it is noteworthy that some EEG studies have demonstrated an abnormal motor preparation in patients with FHD. Abnormally reduced isometheptene event-related
desynchronization or Bereitschaftspotential has been reported in patients with FHD, preceding voluntary, self-paced movements (Deuschl et al., 1995; Ikeda et al., 1996; Yazawa et al., 1999; Toro et al., 2000). Event-related desynchronization and Bereitschaftspotential reflect the activation of premotor and motor areas involved in movement preparation and execution. Abnormal event-related desynchronization or Bereitschaftspotential suggests an impairment of premotor and/or motor cortex activation during self-paced movement preparation. These complementary EEG–TMS data suggest that, although the excitability of the synergist muscle representation over the M1 is preserved in patients with FHD, the premotor–motor interactions preceding voluntary movement are impaired. Our results showed a lack of RT, RMT and rest MEP differences between patients and controls.