This thesis describes a series of experiments to investigate the effect of thermal stimulation on corticospinal excitability using transcranial magnetic stimulation (TMS). Experiment I showed that innocuous cooling or warming of a single digit, produced short-lasting and mixed patterns of modulation only during actual thermal stimulation, with the inhibition being the most common pattern observed. In line with this finding, cooling stimulation applied to a larger area (i.e. multi-digits) produced variable but more sustained modulation in motor evoked potential (MEP) amplitude in the post-cooling phase (Exp II). Notably, the responses to cooling in terms of either suppressed or enhanced corticospinal excitability tended to be fairly consistent in a given individual with repeated applications. When examining possible sources of the observed variable MEP modulation, we found that individual characteristics such as age, sex and changes in skin temperature had no major influences. We hypothesized that the variability of responses might be related to individual differences in the excitability of intra-cortical circuits involved in sensorimotor integration. To test this hypothesis, we performed Experiment III using conditioning TMS paradigms. This experiment revealed that TMS markers of sensorimotor integration (SAI and SAF levels) were good predictors of individual variations in cooling-induced modulation in corticospinal excitability. This provided evidence supporting the role of SAI and SAF as markers to predict individual’s response to focal thermal stimulation. The identification of such predictors could enhance the therapeutic applicability of this form of stimulation in neurorehabilitation. Collectively, these findings advance our understanding of the neurophysiological basis of thermal stimulation and shed light on the development of a more rational application of neurofacilitation techniques based on afferent stimulation in clinical populations, such as stroke survivors.

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. / Thesis / Master of Science (MSc)