Abstract
BackgroundPain-related interactions between primary motor (M1) and primary sensory (S1) cortex are poorly understood. In particular, the time-course over which S1 processing and corticomotor output are altered in association with muscle pain is unclear. We aimed to examine the temporal profile of altered processing in S1 and altered corticomotor output with finer temporal resolution than has been used previously.MethodsIn 10 healthy individuals we recorded somatosensory evoked potentials (SEPs) and motor evoked potentials (MEPs) in separate sessions at multiple time-points before, during and immediately after pain induced by hypertonic saline infusion in a hand muscle, and at 15 and 25 minutes follow-up.ResultsParticipants reported an average pain intensity that was less in the session where SEPs were recorded (SEPs: 4.0±1.6; MEPs: 4.9±2.3). In addition, the time taken for pain to return to zero once infusion of hypertonic saline ceased was less for participants in the SEP session (SEPs: 4.7±3.8 mins; MEPs 9.4±7.4 mins). Both SEPs and MEPs began to reduce almost immediately after pain reached 5/10 following hypertonic saline injection and were significantly reduced from baseline by the second (SEPs) and third (MEPs) recording blocks during pain. Both parameters remained suppressed immediately after pain had resolved and at 15 and 25 minutes after the resolution of pain.ConclusionsThese data suggest S1 processing and corticomotor output may be co-modulated in association with muscle pain. Interestingly, this is in contrast to previous observations. This discrepancy may best be explained by an effect of the SEP test stimulus on the corticomotor pathway. This novel finding is critical to consider in experimental design and may be potentially useful to consider as an intervention for the management of pain.
Highlights
We aimed to examine the temporal profile of altered processing in S1 and altered corticomotor output with finer temporal resolution than has been used previously
Participants reported an average pain intensity that was less in the session where somatosensory evoked potentials (SEPs) were recorded (SEPs: 4.0±1.6; motor evoked potentials (MEPs): 4.9±2.3)
The time taken for pain to return to zero once infusion of hypertonic saline ceased was less for participants in the SEP session (SEPs: 4.7±3.8 mins; MEPs 9.4±7.4 mins)
Summary
The time-course over which S1 processing and corticomotor output are altered, and the temporal relationship between them, is less clear This information is essential to understand the mechanisms that underpin altered sensorimotor function in pain. One study has examined the temporal relationship between altered activity in S1 and corticomotor output in response to acute muscle pain. That study demonstrated altered S1 processing (during pain) prior to reduced corticomotor output (present once pain had resolved) [5] This time-course suggests that either S1 and M1 excitability are modified by independent processes in the presence of pain, or that altered S1 processing during acute muscle pain mediates a latent reduction in motor output. We aimed to examine the temporal profile of altered processing in S1 and altered corticomotor output with finer temporal resolution than has been used previously
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