Parkinson (20) contended that patients with shaking palsy did not exhibit significant intellectual changes; however, by the late 1800s, investigators had begun to recognize the presence of cognitive deficits in patients with PD (21). Mild neuropsychological changes are widely accepted to occur in early PD. Increasingly, it is recognized that cognitive alterations, especially in executive functions and/or memory, may already be present at the time of disease diagnosis. Recent studies estimate that one-quarter to one-third of patients may have deficits detectable on careful neuropsychological testing at the time of disease diagnosis (22,23). Cognitive declines early in the disease most often include deficient information processing speed, visuospatial abilities, verbal fluency, recall, and executive functions (24,25). The neuropsychological dysfunction associated with early PD is hypothesized to reflect nigrostriatal dopamine depletion and disruption of mesocortical and mesolimbic pathways. More pronounced cognitive dysfunction is evident only later in the disease, and is probably attributable to neurochemical changes extending beyond the dopaminergic system (26-28), in addition to structural neuropathology. The dementia (prevalence of about 30%), or perhaps more accurately dementias, observed in PD probably reflect diverse neuropathological entities. At autopsy, dementia in clinically diagnosed PD most often reveals AD or Lewy body dementia (LBD) pathology, or some combination of pathologies associated with these two conditions. Consequently, although dementia in PD generally conforms neurobehaviorally to a "subcortical dementia" profile early in its course, it is neuropsychologically heterogeneous across individuals and, almost invariably, later in its course has both cortical and subcortical features. Nonetheless, many cognitive features of early dementia in PD represent a more severe form of the cognitive changes observable in PD without dementia.
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