Abstract

Introduction: Motor output is modulated by somatosensory input and processing. To further understand the neurophysiological mechanisms underlying sensorimotor deficits in Parkinson's disease (PD), we examined the relationship between the primary sensory cortex (S1) and the motor cortex (M1). Non-invasive intermittent theta-burst stimulation (iTBS) was used to activate S1 and its influence on M1was probed. We hypothesized that [1] S1-iTBS will modulate M1 excitability, measured by motor evoked potentials (MEPs), and [2] these changes will be driven by intra-cortical (short-interval intra-cortical inhibition (SICI), long-interval intra-cortical facilitation (SICF)) and/or sensorimotor circuitry (short afferent inhibition (SAI), and long afferent inhibition (LAI)).

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