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 Clinical features of PDD vs. DLB and AD (Article) 
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Post Clinical features of PDD vs. DLB and AD (Article)
This Nov '06 article in the journal Neurology considers the clinical features of PDD (Parkinson's Disease Dementia) in comparison to AD and DLB.

I found the full article somewhat cumbersome to wade through as they are dealing with many different disorders, including "EPS" (extra-pyramidal symptoms, which I gather is a syndrome describing movement dysfunction). (Apparently EPS can occur with AD). I've copied the abstract below, which is probably enough for most folks. And below that are some additional excerpts. All the excerpts are about PDD and DLB.

The authors note that the clinical criteria for distinguishing PDD from DLB is the "temporal requirement that parkinsonism precedes dementia by more than 12 months." But, they ask, what clinical features are different between PDD and DLB? The authors found that: "These groups were nearly identical in all clinical features. Postural instability was more common in PDD, whereas spasticity was more common in DLB. Sexual disinhibition, alexia, and naming problems were more common in DLB compared with PDD."

For a "picture" of gait spasticity, see the video "The Physician's Guide to PSP" that I circulated the link to yesterday. A medical dictionary defines spasticity as: "of, relating to, or characterized by spasm," and "marked by spastic paralysis." Alexia is the "loss of ability to read."

If they found that "postural instability" was more common in PDD, then I don't understand how the authors can say that they were surprised the "prevalence of falls...was equally common in all three dementia groups." How can you have more postural instability (in PDD) without more falls?

In addition to prevalence of falls, the authors hypothesized that other clinical features would discriminate between the three forms of dementia they looked at. They were surprised by the results. "Other features that did not discriminate between groups included syncope, delusions, agitation, anxiety, myoclonus, and clock-drawing ability." This is surprising to me because I had heard on the online LBDcaregivers group that those with LBD couldn't draw the clock but those with AD could. (A Stanford neurologist I asked about this was more cautious and said he would be reluctant to make that claim.)

Despite this, the authors believe that clinicians should be able to distinguish between PDD and AD, and DLB and AD. The authors note that clinical criteria exists for diagnosing DLB, but not for PDD.

Beyond the preceding info, the most interesting conclusion was: male gender and visual hallucinations in PD predict dementia. Visual hallucinations was the strongest single predictor. This is somewhat surprising because a recent article I sent around indicated that visual hallucinations can be sleep disorder-related so someone with MSA could have hallucinations; yet, MSAers don't have dementia to the same degree that LBDers do (or those with PDD do).

Robin



Clinical phenotype of Parkinson disease dementia (I deleted some of the statistical figures)
James E. Galvin, MD, MPH; Jori Pollack; and John C. Morris, MD
NEUROLOGY 2006;67:1605­1611

Objective: To determine which clinical features best characterize Parkinson disease dementia (PDD), compared with Alzheimer disease (AD) and dementia with Lewy bodies (DLB), and to determine the pathologic basis for PDD.

Methods: We examined 103 participants enrolled in a longitudinal study (nondemented control 10, PD 42, DLB 20, AD 31) who were followed to autopsy using standardized protocols. We characterized the features of PDD using published criteria for AD and DLB as a framework. Statistical analysis was performed using Chi-squared and Fisher exact tests, Kaplan­Meier curves, and logistic regression models.

Results: The sample’s mean age was 74.0 years (range 53 to 91 years), and individuals were followed for a mean of 3.4 visits (range 1 to 12 visits). During longitudinal follow-up, 83% of subjects with PD developed dementia, defined as a Clinical Dementia Rating score of 0.5.

Features that distinguished PDD from AD included cognitive fluctuations, visual, and auditory hallucinations, depression, and sleep disturbance. These PDD features were identical to those observed for DLB.

The pathologic substrates for PDD included DLB (38%), AD (32%), and nigral LB alone (24%).

Clinical predictors of PDD were visual hallucinations and male gender.

Conclusions: Parkinson disease dementia (PDD) shares identical clinical features with dementia with Lewy bodies (DLB); both entities can be distinguished from Alzheimer disease. The presence of PDD/DLB features at any time during the course of PD is highly predictive of dementia and the presence of LB at autopsy; in particular, male gender and visual hallucinations in PD predict dementia.

PubMed ID #: 17101891


Some excerpts:

PDD is defined as "cognitive impairments that include cognitive and motor slowing, executive dysfunction, and impaired memory retrieval." (Diagnostic and Statistical Manual of Psychiatric Disorders)

"A distinctive clinical phenotype for PDD has yet to be identified... We hypothesize that...the clinical phenotype of PDD closely resembles that of DLB." I couldn't find a good definition of "phenotype" but it means something like "observable properties."

"Current clinical criteria for DLB distinguish PDD by the temporal requirement that parkinsonism precedes dementia by more than 12 months; these criteria, however do not otherwise indicate differences
between DLB and PDD. DLB increasingly is recognized since the introduction of ubiquitin and alpha-synuclein immunohistochemistry to aid clinicopathologic correlations."

"PDD vs AD. The PDD group had a greater male predominance and presence of EPS. The groups also differed in a number of clinical features. The PDD group had a greater frequency of cognitive fluctuation, visual hallucinations, auditory hallucinations, falls, depression, and sleep disturbances."

"DLB vs AD. The DLB group had a male predominanc and a higher frequency of EPS. Visual and auditory hallucinations, myoclonus, depression, and sleep disturbance were also more frequently present in DLB compared with AD."

This statement was in the article's Abstract: "The pathologic substrates for PDD included DLB (38%), AD (32%), and nigral LB alone (24%)." This is explained below: (note that 8 of 34 = 24%)

"Clinical­pathologic correlations. Autopsy reports were compared for all 103 participants. Three neuropathologic profiles composed PDD. Thirty-eight percent of PDD was caused by DLB, whereas 32% of PDD cases had AD with nigral LB. Interestingly, 8 of 34 PDD cases (all CDR 0.5) had only nigral LB at postmortem examination without sufficient amyloid or synuclein pathology to meet criteria for AD or DLB."


Sun Feb 04, 2007 4:32 pm
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