Cognitive impairment in Parkinson's disease: more than a frontostriatal dysfunction.

Cognitive deficit in Parkinson's disease has been traditionally considered as being mainly related to executive dysfunction secondary to frontostriatal affectation. However, this traditional consideration has recently been challenged. Forty-three nondemented PD patients (mean age = 59.19; SD = 9.64) and twenty control group subjects (mean age = 60.85; SD = 12.26) were studied. They were assessed on a wide range of cognitive functions. Patients showed motor slowing (p = .012), along with alterations in visuoperceptive (p = .001), visuospatial (p = .007) and visuoconstructive functions (p = .017), as well as in visual span (direct: p = .008; inverse: p = .037). Regarding executive functions, differences were not observed in classical measures for verbal fluency (phonetic: p = .28; semantic: p = .27) or in response inhibition (Stroop test: p = .30), while execution was altered in other prefrontal tasks (Wisconsin Test: p = .003; action fluency: p = .039). Patients showed altered performance in verbal learning processes (p = .005) and delayed memory (free: p = .032; cued: p = .006), visuospatial learning (p = .016) and linguistic functions (naming: p < .001; comprehension: p = .007). Poor performance in visuospatial memory is predicted by deficits in working memory and visuospatial perception. Taken together, the observed alterations not only suggest prefrontal affectation, but also temporal and parietal systems impairment. Thus, cognitive dysfunction in nondemented PD patients cannot be exclusively explained by frontostriatal circuit affectation and the resulting executive dysfunction.