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Cognitive impairment is common in PD, especially in the domain of executive function (28). Such deficits are usually the earliest cognitive signs in PD (117). Patients or caregivers often report difficulties with decision making, planning, and completion of goal-directed behaviors. When these cognitive deficits worsen, and patients have impairment of occupational or social functioning, a diagnosis of dementia is made (13). At this point, it is unclear whether the presence of early cognitive deficits leads to dementia. The rate of cognitive decline in PD can be variable depending upon the population subset. A recent community-based study estimated that the mean overall annual rate of cognitive decline in PD patients was one point on the Mini-Mental State Examination (MMSE) (118). However, patients with PD and dementia declined faster, at a rate of 2.3 points, whereas PD patients who did not develop dementia progressed at the same rate as age-matched controls.

Complicating the picture of dementia in PD is the clinical entity of DLB, a dementing illness characterized by parkinsonism, visual hallucinations, and fluctuating cognition (119). There are multiple clinical (parkinsonism, visual hallucinations, attention deficits, executive dysfunction) and pathological similarities (Lewy bodies in the limbic and neocortex) between the two disorders, leading to the hypothesis that the two conditions could be considered as opposite ends of the spectrum of one illness (120,121).

The clinical criteria for making a diagnosis of DLB and PD dementia have been updated (120). Patients whose disease begins with cognitive impairment are diagnosed with DLB, whereas patients who first develop parkinsonism and meet the criteria for a diagnosis of idiopathic PD are diagnosed with PD dementia when dementia occurs. Previously, a clinical diagnosis of DLB was made only if the dementia developed before or within a year of the onset of parkinsonian symptoms (122). However, long-term studies with neuropathological follow-up will be essential in determining whether this clinical distinction correlates with the underlying pathological substrate.

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