title: Impaired problem solving in Parkinson's disease: impact of a set-shifting deficit.
abstract: Parkinson's disease (PD) is associated with specific cognitive deficits in the absence of dementia, including the inability to suppress previously learned responses in a changed context. Our goal was to determine whether this set-shifting deficit is sufficient to account for impaired performance on a problem-solving task, or, instead, whether it is necessary to postulate deficits in one or more other cognitive capacities, such as logical deduction. Deductive reasoning and other conceptual abilities were assessed in 15 nondemented subjects with PD who had never been medicated, 15 nondemented subjects with PD who were currently receiving medication, and 15 healthy elderly control subjects. On a deductive reasoning task, Poisoned Food Problems, the PD groups made more errors than the control group. The PD groups' error pattern was characterized by intrusions of information from previous problems. By contrast, the PD groups made appropriate assessments of redundant and irrelevant information that appeared in these problems, and performed normally on other tests of concept formation and problem solving that did not require set shifting, indicating that the capacities for logical deduction and concept formation were intact. The set-shifting deficit, conceptualized as a difficulty in suppressing a prepotent response, appears to be a primary cognitive impairment in PD and presumably arises from dysfunction of the nigrostriatal-dorsolateral prefrontal cortex complex loop.
authors.affiliation: Department of Psychology, Boston University, MA 02215.
authors.forename: A
authors.initials: A
authors.lastname: Cronin-Golomb
authors.forename: S
authors.initials: S
authors.lastname: Corkin
authors.forename: J H
authors.initials: JH
authors.lastname: Growdon
mesh_terms: D000368:Aged; D000978:Antiparkinson Agents / Q000627:therapeutic use; D001288:Attention / Q000187:drug effects / Q000502:physiology*; D003210:Concept Formation / Q000187:drug effects / Q000502:physiology; D003342:Corpus Striatum / Q000187:drug effects / Q000503:physiopathology; D003704:Dementia / Q000188:drug therapy / Q000503:physiopathology* / Q000523:psychology; D004292:Dominance, Cerebral / Q000187:drug effects / Q000502:physiology; D005260:Female; D006801:Humans; D008297:Male; D008875:Middle Aged; D009434:Neural Pathways / Q000187:drug effects / Q000503:physiopathology; D009483:Neuropsychological Tests; D010300:Parkinson Disease / Q000188:drug therapy / Q000503:physiopathology* / Q000523:psychology; D010364:Pattern Recognition, Visual / Q000187:drug effects / Q000502:physiology; D017397:Prefrontal Cortex / Q000187:drug effects / Q000503:physiopathology; D011340:Problem Solving / Q000187:drug effects / Q000502:physiology*; D012718:Set, Psychology; D013378:Substantia Nigra / Q000187:drug effects / Q000503:physiopathology; D013850:Thinking / Q000187:drug effects / Q000502:physiology
chemical_list: D000978:Antiparkinson Agents