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  • Title: Cognitive impairment in Parkinson's disease is multifactorial: A neuropsychological study.
    Author: Smith CR, Cullen B, Sheridan MP, Cavanagh J, Grosset KA, Grosset DG.
    Journal: Acta Neurol Scand; 2020 Jun; 141(6):500-508. PubMed ID: 32002988.
    Abstract:
    BACKGROUND: In Parkinson's disease, mild cognitive impairment and dementia are associated with α-synuclein deposition and spread. However, coexistent Alzheimer's disease and cerebrovascular disease are common at autopsy, and may affect cognition. Our objective was to map cognitive impairment in Parkinson's disease to these different causes using clinical assessment. METHODS: Neuropsychological testing was performed in a cross-sectional sample of cognitively impaired patients with Parkinson's disease. The pattern of deficits in varying cognitive domains was mapped to the presentations that typify different diseases. Data were analysed by an expert multidisciplinary panel, referencing diagnostic criteria, to reach a consensus diagnosis for the cognitive dysfunction. RESULTS: There were 45 participants with Parkinson's disease and cognitive impairment, 73.3% male, mean age 69.1 years (SD 8.3). Twenty-seven (60.0%) had mild cognitive impairment, and 18 had dementia (40.0%). Cognitive impairment was primarily attributable to Lewy body disease alone in 19 of 45 patients (42.2%), to Lewy body disease plus Alzheimer's in 14 of 45 (31.1%), to Lewy body plus cerebrovascular disease in 6 of 45 (13.3%), and to Lewy body plus Alzheimer's and cerebrovascular disease in 1 of 45 (2.2%). The cognitive decline was not primarily Lewy-related in 5 of 45 patients (11.1%); in 4 of 45 (8.9%), it was primarily attributable to Alzheimer's disease, and 1 of 45 (2.2%) had behavioural-variant frontotemporal dementia. CONCLUSION: Neuropsychological testing identifies distinct patterns of cognitive impairment in Parkinson's disease that provide clear pointers to comorbid disease processes, the most common being Alzheimer's disease. This approach may prove useful in clinical practice and has implications for clinical trials that target α-synuclein.
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