Brain, Vol. 124, No. 11, 2131-2146,
November 2001
© 2001 Oxford University Press
Review article |
Pathophysiology of bradykinesia in Parkinson's disease
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1 Dipartimento di Scienze Neurologiche, Istituto Neurologico Neuromed IRCCS, Università di Roma `La Sapienza', Rome, Italy, 2 MRC Human Movement and Balance Unit, The Institute of Neurology, London, UK, 3 The Royal Adelaide Hospital, The University Department of Medicine, Adelaide, Australia and 4 Human Motor Control Section, NINDS, NIH, Bethesda, Maryland, USA
Correspondence to:
Professor Alfredo Berardelli, Dipartimento di Scienze Neurologiche, Viale Università 30, 00185 Roma, Italy
Bradykinesia means slowness of movement and is one of the cardinal manifestations of Parkinson's disease. Weakness, tremor and rigidity may contribute to but do not fully explain bradykinesia. We argue that bradykinesia results from a failure of basal ganglia output to reinforce the cortical mechanisms that prepare and execute the commands to move. The cortical deficit is most apparent in midline motor areas. This leads to particular difficulty with self-paced movements, prolonged reaction times and abnormal pre-movement EEG activity. Movements are often performed with normally timed EMG bursts but the amount of EMG activity is underscaled relative to the desired movement parameters. There are also abnormalities in sensory scaling and sensorimotor integration. The brain appears to be able to compensate to some degree for the basal ganglia deficit. There is overactivity in the lateral premotor areas during task performance and movements can be speeded by giving sensory cues. Attention to movement is also beneficial. However, we propose that the engagement of compensatory processes may also lead to reduced performance in other tasks. For example, patients' problems in performing more than one task at the same time could result from lack of sufficient resources both to compensate for their basal ganglia deficit and to run two tasks simultaneously. Surgical therapies are unlikely to work solely by normalizing basal ganglia output to that seen in healthy individuals. It seems more plausible that surgery removes an interfering signal that allows more efficient compensation by other structures.
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