Altered corticomotor latencies but normal motor neuroplasticity in concussed athletes

Persistent cognitive, affective, and motor symptoms have been associated with sports-related concussions including several neurophysiological changes in the primary motor cortex. In particular, previous research has provided some evidence of altered latencies of the corticomotor pathway and altered motor neuroplasticity. However, to date, no studies have assessed these neurophysiological metrics in a common group of athletes across different phases of injury and recovery. In this study corticomotor latencies and neuroplasticity were assessed in collegiate athletes with or without a history of prior concussion across two different phases of injury: either in an acute state of concussion (within 2 wk of injury) or in a chronic state of concussion (more than 1 yr after injury). Corticomotor latencies were determined by measuring the motor evoked potential (MEP) onset time, and motor neuroplasticity was assessed by measuring MEP amplitudes following application of anodal transcranial direct current stimulation (tDCS) over the primary motor cortex (M1). We found that concussed athletes had slower corticomotor latencies than nonconcussed athletes, and corticomotor latency was also positively correlated with the number of prior concussions. In contrast, there was no evidence of altered motor neuroplasticity in athletes regardless of concussion history. These findings suggest concussions may lead to permanent changes in the corticospinal tract that are exacerbated by repeated injury. NEW & NOTEWORTHY We are the first to assess corticomotor latencies and motor neuroplasticity in a common group of collegiate athletes across different phases of injury and recovery. We found that the number of concussions an individual sustains negatively impacts corticomotor latencies with a higher number of prior concussions correlating positively with longer latencies. Our findings indicate that concussions may lead to permanent changes in the corticospinal tract that are exacerbated by repeated injury.