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Alhassani G1, Liston M2, Schabrun S3
1Western Sydney University, School of Science and Health, Sydney, Australia, 2Kings College London, Centre for Human and Applied Physiological Sciences, London, United Kingdom, 3Neuroscience Research Australia (NeuRA), Sydney, Australia
Background: Bilateral deficits in sensorimotor function have been observed in some chronic unilateral musculoskeletal pain conditions. For example, individuals with chronic lateral epicondylalgia display decreased pressure pain thresholds, decreased maximal wrist extensor force, and reduced grip force on both the affected and unaffected limb. This observation suggests involvement of the central nervous system in the development of bilateral sensorimotor dysfunction. Interhemispheric inhibition (IHI) is a neurophysiological mechanism that could underpin the development of bilateral sensorimotor symptoms in chronic musculoskeletal pain. However, whether IHI is also altered in the acute stages of pain (lasting minutes) is unknown.
Purpose: The purpose of the study was to examine IHI in response to acute, experimental muscle pain lasting ~ 10 minutes.
Methods: In 20 healthy individuals (8 males), paired-pulse transcranial magnetic stimulation (TMS) was used to assess short (10ms) and long (40ms) latency IHI at multiple time points: before, immediately after, and 30 minutes following pain induced by hypertonic saline injection in the right, first dorsal interosseous (FDI) muscle. Single pulse TMS was used to assess corticomotor excitability over the optimal cortical site for FDI in the left ('affected') and right ('unaffected') hemisphere at each time point. Pain intensity was recorded every 30 s from the time of injection until pain reached 0/10 on an 11-point numerical rating scale. Pressure pain thresholds (PPTs) were recorded over the right and left FDI muscles at baseline and at 30 minutes follow-up. IHI and corticomotor excitability were analysed using a one-way repeated measures ANOVA with factor 'time'. PPT data was compared between time (baseline and 30 minutes follow-up) and sides (right, left) using a two-way repeated measures ANOVA.
Results: An average pain intensity of 4.8(1.3) points was reported. Compared with baseline, the magnitude of IHI from the left (affected) to the right (unaffected) hemisphere was reduced immediately after and at 30 minutes following the resolution of pain at both short (p 0.001) and long (p 0.001) latencies. Corticomotor excitability was reduced in the left hemisphere over time (p=0.003) but was unaltered in the right hemisphere. Pressure pain thresholds were reduced in the right (injected) FDI (p 0.001) and in the left FDI muscle (p=0.005) at 30 minutes follow-up.
Conclusion(s): These findings suggest a reduction in IHI from the affected to the unaffected M1 that occurs rapidly following the onset of acute pain and could contribute to the development of bilateral symptoms. Future studies should consider longer-lasting pain models to further elucidate the temporal profile of altered IHI.
Implications: These findings may have relevance for the investigation of bilateral symptoms in unilateral pain conditions. This study may also facilitate the development of therapeutic protocols aiming to restore the inhibitory imbalance in musculoskeletal pain.
Keywords: Interhemispheric inhibition, musculoskeletal pain, neuroscience
Funding acknowledgements: S.M. Schabrun receives salary support from The NHMRC Australia (1105040). G. Alhassani is supported by an APA scholarship.
Purpose: The purpose of the study was to examine IHI in response to acute, experimental muscle pain lasting ~ 10 minutes.
Methods: In 20 healthy individuals (8 males), paired-pulse transcranial magnetic stimulation (TMS) was used to assess short (10ms) and long (40ms) latency IHI at multiple time points: before, immediately after, and 30 minutes following pain induced by hypertonic saline injection in the right, first dorsal interosseous (FDI) muscle. Single pulse TMS was used to assess corticomotor excitability over the optimal cortical site for FDI in the left ('affected') and right ('unaffected') hemisphere at each time point. Pain intensity was recorded every 30 s from the time of injection until pain reached 0/10 on an 11-point numerical rating scale. Pressure pain thresholds (PPTs) were recorded over the right and left FDI muscles at baseline and at 30 minutes follow-up. IHI and corticomotor excitability were analysed using a one-way repeated measures ANOVA with factor 'time'. PPT data was compared between time (baseline and 30 minutes follow-up) and sides (right, left) using a two-way repeated measures ANOVA.
Results: An average pain intensity of 4.8(1.3) points was reported. Compared with baseline, the magnitude of IHI from the left (affected) to the right (unaffected) hemisphere was reduced immediately after and at 30 minutes following the resolution of pain at both short (p 0.001) and long (p 0.001) latencies. Corticomotor excitability was reduced in the left hemisphere over time (p=0.003) but was unaltered in the right hemisphere. Pressure pain thresholds were reduced in the right (injected) FDI (p 0.001) and in the left FDI muscle (p=0.005) at 30 minutes follow-up.
Conclusion(s): These findings suggest a reduction in IHI from the affected to the unaffected M1 that occurs rapidly following the onset of acute pain and could contribute to the development of bilateral symptoms. Future studies should consider longer-lasting pain models to further elucidate the temporal profile of altered IHI.
Implications: These findings may have relevance for the investigation of bilateral symptoms in unilateral pain conditions. This study may also facilitate the development of therapeutic protocols aiming to restore the inhibitory imbalance in musculoskeletal pain.
Keywords: Interhemispheric inhibition, musculoskeletal pain, neuroscience
Funding acknowledgements: S.M. Schabrun receives salary support from The NHMRC Australia (1105040). G. Alhassani is supported by an APA scholarship.
Topic: Pain & pain management
Ethics approval required: Yes
Institution: Western Sydney University
Ethics committee: Western Sydney University Human Research Ethics Committee
Ethics number: H11873
All authors, affiliations and abstracts have been published as submitted.
