Motor signs during the course of Alzheimer disease. [Electronic version]

Cognitive Neuroscience Division, Taub Institute for Research in Alzheimer's Disease and the Aging Brain, Gertrude H. Sergievsky Center, and Department of Neurology, New York, NY 10032, USA.
Neurology (Impact Factor: 8.29). 10/2004; 63(6):975-82. DOI: 10.1212/01.WNL.0000138440.39918.0C
Source: PubMed


Motor signs (MOSIs) are common in Alzheimer disease (AD) and may be associated with rates of cognitive decline, mortality, and cost of care.
To describe the progression and identify predictors of individual MOSIs in AD.
A cohort of 474 patients with AD at early stages was followed semiannually for up to 13.1 years (mean 3.6 years) in five centers in Europe and the United States. MOSIs were rated using a standardized portion of the Unified Parkinson's Disease Rating Scale. Overall, 3,030 visits/assessments of MOSIs (average 6.4/patient) were performed. Prevalence and incidence rates were calculated, and cumulative risk graphs were plotted for individual non-drug-induced MOSI domains. Rates of change over time taking into account potential covariates were also estimated. With use of each MOSI domain as outcome in Cox models, predictors of MOSI incidence were identified.
At least one MOSI was detected in 13% of patients at first examination and in 36% for the last evaluation. Total MOSI score increased at an annual rate of 3% of total possible score. Rates of annual change for speech/facial expression (4%), rigidity (2.45%), posture/gait (3.9%), and bradykinesia (3.75%) were of similar magnitude, and their occurrence increased from first (3 to 6%) to last (22 to 29%) evaluation. Tremor was less frequent throughout the course of the disease (4% at first and 7% at last evaluation) and worsened less (0.75% increase/year).
Most motor signs occur frequently and progress rapidly in Alzheimer disease. Tremor is an exception in that it occurs less frequently and advances at slower rates.

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Available from: Jason Brandt, Jan 08, 2014
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    • "Clinical presentation of Alzheimer's disease (AD) is complex and extends well beyond the cognitive impairments that characterize this disorder (Duker et al., 2012). Alterations in facial expression, gait and posture, and manifestations of rigidity, bradykinesia, and tremor are found in late AD stages although mounting evidence suggests that motor problems emerge long before any recognizable sign of AD (Wilson et al., 2000; Scarmeas et al., 2004; Buchman & Bennett, 2011 ). Tau abnormal hyperphosphorylation and subsequent malfunction are postulated as crucial mechanisms in AD neuronal dysfunction where hyperphosphorylated and/or aggregated (insoluble) forms of Tau exhibit neurodegenerative action(s) that also interfere with normal Tau, sequestering and reducing soluble Tau forms (Ksiezak-Reding et al., 1988; Zhukareva et al., 2003). "
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