Abstract

Professor Peter Brown obtained his medical degree from Cambridge University in 1984 and thereafter joined the Medical Research Council Human Movement and Balance Unit before moving to the Institute of Neurology, London. He worked as a neurologist at the affiliated National Hospital for Neurology and Neurosurgery, London, and within the Sobell Department of Movement Disorders and Motor Neurophysiology at the Institute of Neurology. He moved to the University of Oxford as Professor of Experimental Neurology in 2010.

There is growing interest in how synchronised activity across populations of neurons might underlie impairment in some diseases and there is now a general consensus that exaggerated oscillatory synchrony occurs within and between the basal ganglia and cerebral cortex in patients with Parkinson's disease (PD). In particular, activity in the β frequency band (13–30 Hz) is prominent, and can be attenuated by treatment with dopaminergic drugs. The latter suggests that elevated β activity may be a key disturbance in PD. Here, I will consider both correlative evidence and tests of causality that support a mechanistic link between pathologically exaggerated β activity and stiffness and slowness of movement in PD. Questions, however, remain with regards to the quantitative importance of β and the role of this activity under physiological circumstances. In particular, recent studies suggest that the modulation of β activity may play a part in both motor and cognitive domains. Finally, I will suggest how our new understanding of circuit-level disturbances in PD may provide a basis for the development of more sophisticated forms of therapeutic stimulation for Parkinson's disease, such as those using closed loop feedback control and specific temporal patterning.