Parkinson’s disease (PD) is characterized by motor symptoms including resting tremor, rigidity, and bradykinesia. However, cognitive and behavioral problems in PD are common1 and can have a significant effect on quality of life.^2,3 The prevalence of dementia in patients with PD has conservatively been estimated to range between 24 and 31%.⁴ The cognitive profile observed in PD patients with dementia (PDD) is substantially different from that of the primarily cortical dementia of Alzheimer’s disease (AD). Patients with PDD typically exhibit difficulties with executive functions, the retrieval aspects of memory, and visuospatial skills.⁴ They do not exhibit clear aphasia, apraxia, or agnosia, which are common features of AD. The onset of dementia in PD is insidious, typically occurring years after the onset of motor symptoms. However, cognitive difficulties have been observed even in early PD.⁵ Although debated, the pattern of early cognitive dysfunction in PD is believed to be generally similar to that of PDD.^6,7

The pathophysiology of cognitive symptoms in PD is believed to be different from that of the motor symptoms.^8–10 Several theories exist regarding the origins of this particular clinical manifestation. It is possible that cognitive dysfunction in PD is related to the depletion of striatal dopamine and its effect on non-motor cortico–striato–pallidal– thalamocortical (CSPTC) circuits.⁶ Nevertheless, other dopaminergic systems may mediate these cognitive changes, including mesocortical dopamine projections to the prefrontal cortex.^11,12 Other pathological processes, such as regional cortical Lewy body formation, are also likely to contribute to PD cognitive decline,¹³ as well as abnormalities of other neurotransmitter systems.¹⁴

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