, 2008, 2009c). Conversely, the methodological issue of primary importance in interpreting the implications selleck monoclonal antibody of the CSP duration for a given task is the TMS intensity, because the CSP does not depend on background EMG activity. In the present study, a stimulation intensity of 130% of RMT was utilised for four reasons. First, preliminary work determined that lower stimulation intensities of 115% of RMT and below, which result in short CSP durations, made it difficult for algorithms or visual inspection to quantify the CSP duration of the ADM at the low activation level of 5% of MVC. Second,

short CSP durations (< 75 ms) are due to spinal mechanisms, whereas longer silent periods (75–300 ms) are due exclusively to cortical mechanisms (Fuhr et al., 1991; Inghilleri et al., 1996; Chen et al., 1999). Because surround inhibition arises primarily from cortical mechanisms (Sohn & Hallett, 2004a; Beck et al., 2008; Beck & Hallett, 2011), the relatively

high stimulus intensity assured that the CSP durations elicited by TMS reflected intracortical inhibition. Third, stimulation intensities higher than 130% could have led to ceiling effects in the CSP duration, which could have precluded the ability to observe significant lengthening of the CSP in some experimental conditions. Fourth, stimulation intensities from 130 to 150% of RMT are the most common in the literature (Orth & Rothwell, 2004). Collectively, BTK phosphorylation these methodological considerations should have optimised the ability to determine the contribution of mechanisms underlying the CSP to surround inhibition. It has been proposed that surround inhibition is an important mechanism that acts to focus excitatory neural drive to muscles responsible for a given movement (agonists) while actively inhibiting activity in muscles not relevant to the movement (surround muscles) (Sohn & Hallett, 2004a; Beck et al., 2008; Beck & Hallett, 2011).

Strong support for these contentions comes from observations in movement disorders that are characterised by excessive activation of muscles not required Org 27569 in a given movement (Shin et al., 2010), especially FHD (Hallett, 2011). In contrast to healthy subjects, patients with FHD consistently exhibit facilitation as opposed to inhibition of the MEP of the surround muscle during agonist muscle activation, which indicates a loss of surround inhibition (Sohn & Hallett, 2004a; Beck et al., 2008). Based on these findings, extensive research has focused on the identification of the mechanisms underlying the generation of surround inhibition in healthy subjects and its impairment in motor disorders.