The Effects of Somatosensory Afference on Corticospinal Excitability in Uninjured and Spinal Cord Injured Individuals

Abstract

Primary somatosensory cortex (SI) is an important cortical structure involved in receiving and relaying sensory inputs to condition primary motor cortex (M1). The functional interaction between SI and M1 is important for motor control by providing surround inhibition, which is the inhibition of muscles not involved in the movement and in learning new motor skills. This interconnection is known as short-latency afferent inhibition (SAI) and may be probed using Transcranial magnetic stimulation and peripheral nerve stimulation. SAI is dependent on the afferent volley as increasing the nerve stimulation intensity increases the depth of SAI. Individuals with spinal cord injury show reductions in SAI evoked in lower limb and this may be a contributing factor to the impairments in motor control seen within this population. SAI has yet to be investigated in the upper limb in individuals with chronic cervical SCI and this thesis examines these alterations. Two experiments were performed examining M1 excitability (motor evoked potentials), SI excitability (somatosensory evoked potentials) and the interconnection between SI and M1 (SAI). The first Experiment investigated alterations in these measures in individuals with SCI while the second Experiment investigated these measures as a function of the afferent volley. The collective results from Experiment 1 indicate that motor evoked potentials and SAI are reduced but somatosensory evoked potentials are similar to controls. Further data from Experiment 2 indicate that SAI and SEPs increase as a function of the afferent volley and indicate that alterations seen in individuals with SCI may be due to cortical plasticity in the synapses from SI to M1 or within M1. The novel findings of this thesis have indicated aberrant cortical circuits in individuals with SCI and have indicated potential synapses that may be targets for TMS plasticity protocols to alter and restore function to these circuits.