Altered cortical integration of dual somatosensory input following the cessation of a 20 min period of repetitive muscle activity.
The adult human central nervous system (CNS) retains its ability to reorganize itself in response to altered afferent input. Intracortical inhibition is thought to play an important role in central motor reorganization. However, the mechanisms responsible for altered cortical sensory maps remain more elusive. The aim of the current study was to investigate changes in the intrinsic inhibitory interactions within the somatosensory system subsequent to a period of repetitive contractions. To achieve this, the dual peripheral nerve stimulation somatosensory evoked potential (SEP) ratio technique was utilized in 14 subjects. SEPs were recorded following median and ulnar nerve stimulation at the wrist (1 ms square wave pulse, 2.47 Hz, 1x motor threshold). SEP ratios were calculated for the N9, N11, N13, P14-18, N20-P25 and P22-N30 peak complexes from SEP amplitudes obtained from simultaneous median and ulnar (MU) stimulation divided by the arithmetic sum of SEPs obtained from individual stimulation of the median (M) and ulnar (U) nerves. There was a significant increase in the MU/M + U ratio for both cortical SEP components following the 20 min repetitive contraction task, i.e. the N20-P25 complex, and the P22-N30 SEP complex. These cortical ratio changes appear to be due to a reduced ability to suppress the dual input, as there was also a significant increase in the amplitude of the MU recordings for the same two cortical SEP peaks (N20-P25 and P22-N30) following the typing task. No changes were observed following a control intervention. The N20 (S1) changes may reflect the mechanism responsible for altering the boundaries of cortical sensory maps, changing the way the CNS perceives and processes information from adjacent body parts. The N30 changes may be related to the intracortical inhibitory changes shown previously with both single and paired pulse TMS. These findings may have implications for understanding the role of the cortex in the initiation of overuse injuries.
Haavik Taylor
Heidi
H
Human Neurophysiology and Rehabilitation Laboratory, Department of Sport and Exercise Science, Tamaki Campus, University of Auckland, Auckland, New Zealand. h.taylor@auckland.ac.nz
Murphy
B A
BA
D000328:Adult; D000344:Afferent Pathways / Q000502:physiology*; D000704:Analysis of Variance; D001931:Brain Mapping; D004558:Electric Stimulation / Q000379:methods; D004569:Electroencephalography / Q000379:methods; D004576:Electromyography / Q000379:methods; D005073:Evoked Potentials, Somatosensory / Q000502:physiology*; D005260:Female; D006801:Humans; D008297:Male; D008475:Median Nerve / Q000502:physiology / Q000528:radiation effects; D018482:Muscle, Skeletal / Q000294:innervation / Q000502:physiology* / Q000528:radiation effects; D009433:Neural Inhibition / Q000502:physiology*; D009473:Neuronal Plasticity; D011930:Reaction Time / Q000502:physiology; D013003:Somatosensory Cortex / Q000502:physiology*; D014459:Ulnar Nerve / Q000502:physiology / Q000528:radiation effects