Long-lasting somatosensory cortex dysfunction in some, but not all, individuals after sport-related concussion

Abstract

Systems-level neurophysiologic dysfunction has been documented after acute sport-related concussion in multiple studies over the past quarter century. However, little is known about focal intracortical function post-concussion. We aimed to leverage the high sensitivity of magnetoencephalography (MEG) for the detection of neural activity in specific cytoarchitectonic areas of somatosensory cortex to determine whether focal intracortical changes in function could be identified after sport-related concussion.

In a prospective case-control study short-latency and middle-latency sensory evoked fields (SEFs) evoked by median nerve stimulation at the wrist were compared in patients after acute sport-related concussion (n=21; 9 female, age 29.0±8.1 years) and non-injured controls (n=26; 10 female, age 31.5±11.3 years). The primary outcome measure was mean peak latency of the M60 (60ms) middle-latency SEF. Secondary outcomes included M20, M30, M100 SEF latencies and correlation with clinical symptom scores. Follow-up MEG recordings were acquired 1, 2, and 4 months post-injury.

At the group level, mean M60 latency was significantly delayed in patients compared with controls (77.07±17.4ms vs. 60.86±7.5ms; p = 0.0001). Delays in M30 and M100 latencies (padj = 0.027 and 0.068, respectively) were also identified in the patient group. There was no difference in mean M20 latency between patients and controls (padj = 0.96). SEF latencies and clinical symptom scores were not correlated acutely or in follow-up. Symptoms improved significantly by 1-month follow-up with no significant improvements in SEF latencies. At the individual level a minority of patients (9/21) had a peak M60 latency delay >3 standard deviations above the control mean. Some affected patients demonstrated an unusual temporal dispersion of the M60 topographic field; follow-up recordings suggested that a very slow “reassembly” of the M60 waveform can occur over time.

Delays in SEF latencies were identified in a subset of patients in this study that affected all evoked responses after the initial M20 SEF, localizing the post-concussion deficit to intracortical grey matter and U-fibres, with functional sparing of thalamocortical white matter tracts. The altered SEFs represent focal dysfunction at the earliest stages of cortical processing in primary (Brodmann area 3b) and then secondary (Brodmann area 43) somatosensory cortex. The focal cortical dysfunction showed no correlation with clinical symptom scores, mirroring the systems-level dissociation between post-concussion clinical and neurophysiologic findings. At the individual level, only some patients exhibited abnormalities in early somatosensory processing, suggesting substantial inter-individual differences in susceptibility to neurophysiologic dysfunction post-concussion that will need to be accounted for in future studies.