The functional role of sensory attenuation in movement

Abstract

Our ability to move in a controlled, precise manner is central to our successful interaction with the world. Conversely, disorders of movement control are amongst the most devastating of human illnesses. The work in my PhD aims to make a meaningful contribution to understanding motor control in humans, work which has a direct link to pathophysiology of movement disorders and which I plan to test in patients with Parkinson’s disease. Parkinson’s disease is the second most common neurodegenerative disorder in the world, affecting ~7 million people, with ~130,000 patients in the UK. The primary motor symptom of Parkinson’s disease is bradykinesia, a slowing and reduction in amplitude of voluntary movement. Though the major anatomical site of neurodegeneration – the basal ganglia - and the main neurotransmitter involved – dopamine – have been known for many years, it has been surprisingly difficult to provide a clear neurobiological mechanism for this fundamental movement deficit in Parkinson’s disease. The key to understand motor control in humans is to investigate how sensory information is related to movement. Previous research has demonstrated that the amplitude of somatosensory sensory evoked potentials elicited by median nerve stimulation are attenuated at prior to and during rest, motor preparation and movement in healthy subjects. My PhD will focus on this neurophysiological sensory attenuation and relate these phenomena to theories of motor control in both healthy subjects and PD patients

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