Prof. Peter Brown

Recording of the local field potential activity in the human subthalamic nucleus during voluntary movement

Recording of the local field potential activity in the human subthalamic nucleus during voluntary movement. The magnitude of different frequencies at any moment in time is colour coded from blue to yellow (high). The overlaid black traces show movements made by a joystick held in the opposite hand. There is a reduction in activity in the nucleus before and during each movement. X and Y axes are time (10 second tick marks) and frequency (Hz), respectively.

brown

Prof. Peter Brown

Director
MRC Programme Leader

Peter Brown is Professor of Experimental Neurology in the Nuffield Department of Clinical Neurosciences, University of Oxford, and Director of the MRC Brain Network Dynamics Unit at the University of Oxford.


Peter Brown graduated in Medicine at the University of Cambridge. He was appointed a Professor of Neurology at University College London in 2004, and in 2006 he became Head of the Sobell Department of Motor Neuroscience and Movement Disorders at the Institute of Neurology, University College London. He moved to the Nuffield Department of Clinical Neurosciences at the University of Oxford as Professor of Experimental Neurology in 2010. Professor Brown’s research group has been continuously funded by the Medical Research Council since 1995, and has received additional funding from the European Commission, Wellcome Trust, Rosetrees Trust and National Institute of Health Research Oxford Biomedical Research Centre.


Professor Brown began his research in disorders of Movement in the early 1990s, when he was instrumental in classifying and determining the underlying pathophysiology of myoclonus, and the stiff person and startle syndromes. He then developed an interest in the pathophysiology of Parkinson’s disease, which has since been sustained. Specifically, he has established the importance of exaggerated oscillatory synchronisation in the human disease and demonstrated that the most widely-used animal model of the disease, the 6-hydroxydopamine-lesioned rodent, shares the same pathophysiology. The latter has heightened the value of this model in the investigation of pathological circuit changes and novel treatment approaches. In 2008, he published the first objective demonstration that exaggerated oscillatory activity in the basal ganglia is causally linked to slowness of movement, and that therapeutic deep brain stimulation suppresses such activity.


This interest in Parkinson’s disease has also fuelled studies of healthy subjects where he has shown that more modest degrees of oscillatory synchrony in the motor system facilitate postural activity, whereas oscillations in the higher gamma-frequency band facilitate movement. In 2009, he provided the first demonstration that variations in physiological oscillatory activity in the human motor system are causally linked to changes in normal motor behaviour. In 2012, he demonstrated that larger behavioural effects could be had from induced oscillatory synchronisation in healthy humans provided that the behavioural context and hence underlying circuit resonances were appropriate.


More recently, Professor Brown’s interests have shifted more towards intervention and therapy. In 2013, he published two seminal proof-of-principle studies implementing adaptive brain-computer interface delivered control at the level of the cortex and of the basal ganglia to control tremor and Parkinsonism in patients. Therapeutic effects were sizeable, and in the case of stimulation of the basal ganglia, surpassed currently available treatment both in terms of efficacy and efficiency. In 2017, he showed that pathological oscillations could be efficiently suppressed by stimulating during certain oscillation phases, with attendant improvements in symptomatic manifestations in the form of tremor. In the same year, his group demonstrated that the pathological beta-band oscillations detected in Parkinson’s disease were markedly bursting in nature and that manipulation of the character of these bursts was a key determinant in the efficacy of levodopa and adaptive deep brain stimulation.
 

Selected Publications
Unit Publication
Herz DM
Little S
Pedrosa D
Tinkhauser G
Cheeran B
Foltynie T
Bogacz R
Brown P

2018.Curr. Biol., 28(8):1169-1178.e6.

Unit Publication
Tinkhauser G
Pogosyan A
Tan H
Herz DM
Kühn AA
Brown P
2017.Brain, 140(11):2968-2981.
Unit Publication
Tinkhauser G
Pogosyan A
Little S
Beudel M
Herz DM
Tan H
Brown P

2017.Brain, 140(4):1053-1067.

Unit Publication
Cagnan H
Pedrosa D
Little S
Pogosyan A
Cheeran B
Aziz TZ
Green AL
Fitzgerald J
Foltynie T
Limousin P
Zrinzo L
Hariz M
Friston KJ
Denison T
Brown P
2017.Brain, 140(1):132-145.
Unit Publication
Tan H
Pogosyan A
Ashkan K
Green AL
Aziz TZ
Foltynie T
Limousin P
Zrinzo L
Hariz M
Brown P
2016. eLife;5:e19089.