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Cerebral Cortex, Vol. 11, No. 12, 1136-1143, December 2001
© 2001 Oxford University Press

Enhanced or Impaired Cognitive Function in Parkinson's Disease as a Function of Dopaminergic Medication and Task Demands

Roshan Cools, Roger A. Barker1, Barbara J. Sahakian2 and Trevor W. Robbins

Department of Experimental Psychology, University of Cambridge, Downing Street,, 1 Cambridge Centre for Brain Repair and Department of Neurology, University of Cambridge, Robinson Way and, 2 Department of Psychiatry, University of Cambridge, Addenbrooke's Hospital, Cambridge, UK

Trevor W. Robbins, University of Cambridge, Department of Experimental Psychology, Downing Street, Cambridge CB2 3EB, UK. Email: twr2{at}cam.ac.uk.

We investigated how dopamine (DA) systems contribute to cognitive performance in the domain of learning and attentional flexibility by examining effects of withdrawing DA-ergic medication in patients with Parkinson's disease (PD). Medication remediated impairments in switching between two tasks, thought to depend on circuitry connecting the dorsolateral prefrontal cortex and the posterior parietal cortex to the dorsal caudate nucleus, which is profoundly DA-depleted in PD. By contrast, the same medication impaired probabilistic reversal learning that implicates orbitofrontal cortex– ventral striatal circuitry, which is relatively spared of DA loss in PD. Hence, DA-ergic medication improves or impairs cognitive performance depending on the nature of the task and the basal level of DA function in underlying cortico-striatal circuitry.


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