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

• Published in: Cerebral cortex (New York, N.Y. 1991) Vol. 11; no. 12; pp. 1136 - 1143
• Main Authors: Cools, Roshan, Barker, Roger A., Sahakian, Barbara J., Robbins, Trevor W.
• Format: Journal Article
• Language: English
• Published: United States Oxford University Press 01.12.2001; Oxford Publishing Limited (England)
• Subjects: Attention - drug effects; Attention - physiology; Caudate Nucleus - cytology; Caudate Nucleus - physiology; Cognition Disorders - drug therapy; Cognition Disorders - physiopathology; Dopamine Agents - administration & dosage; Humans; Neural Pathways; Parietal Lobe - cytology; Parietal Lobe - physiology; Parkinson Disease - drug therapy; Parkinson Disease - physiopathology; Reversal Learning - drug effects; Reversal Learning - physiology
• ISSN: 1047-3211; 1460-2199; 1460-2199
• DOI: 10.1093/cercor/11.12.1136

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.