Dementia in Parkinson disease

Martin R Farlow MD (Dr. Farlow of Indiana University received research grant support from Accera, Biogen, Eisai,  Eli Lilly, Genentech, Roche, Lundbeck, Chase Pharmaceuticals, Novartis, Suven Life Sciences Ltd, and Boehringer Ingelheim; honorariums from Eisai, Forest Laboratories, Pfizer, Eli Lilly and Company and Novartis for speaking engagements; and fees from Accera, Alltech, Avanir, Axovant, Biogen, Eisai Med Res, Inc., Eli Lilly and Company, FORUM Pharmaceuticals, Genentech, Inc., Grifols, Helicon, INC Research, Lundbeck, Medavante, Medivation, Merck, Neurotrope Biosciences, Novartis, Pfizer, Prana, QR Pharm., Riovant Sciences Inc., Roche, Sanofi-Aventis, Schering-Plough, Toyama Pharm, Stemedica Cell Technologies Inc., vTv Therapeutics and UCB Pharma for consultancy. His spouse was employed by Eli Lilly.)
Originally released January 25, 1995; last updated May 31, 2016; expires May 31, 2019

This article includes discussion of dementia in Parkinson disease, dementia associated with Parkinson disease, dementia in Parkinson disease, and dementia with parkinsonism. The foregoing terms may include synonyms, similar disorders, variations in usage, and abbreviations.

Overview

Parkinson disease dementia is clinically distinct from other forms of dementia, including Alzheimer dementia and vascular dementia. Although it shares many of the pathologic features of dementia with Lewy bodies, it remains a separate and distinct entity. Understanding the distinguishing features of Parkinson disease dementia is helpful for screening patients, offering evidence-based treatments, and providing valuable information to patients and their caregivers.

Key points

 

• Parkinson disease dementia is a clinically distinct entity, separate from dementia with Lewy bodies, Alzheimer disease, vascular dementia, and other forms of neurodegenerative disease.

 

• Longitudinal studies have shown that the risk of Parkinson disease dementia increases with age, akinetic/postural instability forms of Parkinson disease, early hallucinations, early executive dysfunction, and duration of disease (63% after 12 years and 83% after 20 years).

 

• Attention (particularly fluctuations), visuospatial construction, and executive function are more impaired in Parkinson disease dementia compared with Alzheimer disease. In general, short-term memory and language are less impaired compared to Alzheimer disease.

 

• Patients with Parkinson disease dementia have a cholinergic deficit thought to be greater than that in Alzheimer disease patients. Cholinesterase inhibitors are approved as a treatment for Parkinson disease dementia and have shown benefit in terms of both cognitive function and behavioral function (including reduction in visual hallucinations).

Historical note and terminology

James Parkinson first described the shaking palsy, emphasizing the classic motor symptoms of Parkinson disease. Friedreich Lewy has commented on the mental impairment in many patients with parkinsonism, but cognitive performance and dementia in Parkinson disease have only received systematic study since the 1970s. In the late 1980s, clinicopathological studies identified a dementia syndrome with a substrate comprising widely distributed cortical and subcortical Lewy bodies, then referred to as dementia with Lewy bodies (McKeith et al 1996). Clinically, physicians began to separate dementia with Lewy bodies from dementia associated with Parkinson disease (also known as Parkinson disease dementia) based on different historical presentations and manifestations. The original hypothesis, which still holds true to today, is that dementia with Lewy bodies and Parkinson disease dementia are likely in the same spectrum of Lewy body disorders (McKeith and Burn 2000; Lippa et al 2007). This article primarily discusses Parkinson disease dementia, but references dementia with Lewy bodies in places when needed to better clarify the distinction between these 2 entities.

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