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Selective motor control and focal dystonia
If you have a question about this talk, please contact Hannah Critchlow.
This talk is part of the Cambridge Clinical Neuroscience and Mental Health Symposium, 29th – 30th September 2009 at West Road Concert Hall. This event is free to attend for cambridge neuroscientists although registration is required. To register, and for further information, please visit: http://www.neuroscience.cam.ac.uk/cnmhs/
Abstract: The ability to make fine movements, such as control of individual digits, is an important skill. The physiology of the ability is not well known, and its dysfunction is a prominent component of several movement disorders such as focal dystonia. The properties of individual corticospinal neurons include innervation of many spinal alpha-motoneurons, making the task particularly difficult. Additionally, the motor system appears to have a wide spread activation with even a focal movement. Hence, whatever capability there is for fine control must include some inhibition as well as excitation. The hypothesis has been suggested and largely proven that the motor system has a center-surround organization; so that unwanted movements are inhibited as the desired movement is commanded (Sohn and Hallett, 2004). This appears to be a cortical process aided by the basal ganglia. The precise physiological mechanisms of the surround inhibition have been investigated, but are not yet completed established. Patients with focal hand dystonia have difficulties with fine motor control and there is a concomitant dysfunction of the surround inhibition mechanism. Several intracortical circuits have been identified that are malfunctioning and can contribute to the abnormality of surround inhibition (Beck et al., 2008). A feature of these circuits are that they are all inhibitory with short latencies. A correlative abnormality has been seen in sensory systems in patients with focal dystonia. Behaviorally, there is a mild abnormality of spatial and temporal discrimination. The physiology underlying the temporal discrimination abnormality is a failure of a short latency inhibitory mechanism (Tamura et al., 2008). Hence there might be a similar abnormality of short latency inhibition in both motor and sensory function, suggesting a malfunction of a class of inhibitory interneurons. Proof of principle studies have demonstrated that training to improve surround inhibition and sensory discrimination can ameliorate dystonia.
Biography: Dr. Hallett obtained his M.D. at Harvard University and trained in Neurology at Massachusetts General Hospital. He had fellowships in Neurophysiology at the National Institutes of Health and at the Institute of Psychiatry in London. From 1976 to 1984, Dr. Hallett was the Chief of the Clinical Neurophysiology Laboratory at the Brigham and Women’s Hospital and Associate Professor of Neurology at Harvard Medical School. From 1984, he has been at the National Institute of Neurological Disorders and Stroke where he serves as Chief of the Human Motor Control Section and pursues research on the Physiology of Human Movement Disorders and other problems of Motor Control. He also served as Clinical Director of NINDS until July 2000. He is past President of the American Association of Electrodiagnostic Medicine and the Movement Disorder Society. He also served as Vice-President of the American Academy of Neurology. He is an Associate Editor of Brain and has just taken over as the Editor in Chief of World Neurology. Currently he also serves on the editorial boards of Clinical Neurophysiology, Acta Neurologica Scandinavica, Journal of Clinical Neurophysiology, Medical Problems of Performing Artists, Annals of Neurology, The Cerebellum, NeuroTherapeutics, and European Neurology. The main work of his group focuses on the physiology and pathophysiology of movement. Dr. Hallett’s interests in Motor Control are wide-ranging, and include brain plasticity and its relevance to neurological disorders and the pathophysiology of dystonia, parkinsonism, and myoclonus. Recently he has become interested in disorders of volition, including tic and psychogenic movement disorders.
This talk is part of the Clinical Neuroscience and Mental Health Symposium series.
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