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. 2014 Apr 29;82(17):1514-20.
doi: 10.1212/WNL.0000000000000356. Epub 2014 Mar 28.

Modifiable cardiovascular risk factors and axial motor impairments in Parkinson disease

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Modifiable cardiovascular risk factors and axial motor impairments in Parkinson disease

Vikas Kotagal et al. Neurology. .

Abstract

Objective: Cardiovascular comorbidities associate with neurodegeneration in the elderly and may contribute to extranigral pathologies and medically refractory axial motor features in Parkinson disease (PD).

Methods: We explored differences in the estimated rate of axial motor feature accrual between patients with PD with and without elevated cardiovascular risk factors as estimated by the Framingham General Cardiovascular Disease risk-scoring algorithm in a cross-sectional cohort study. All participants underwent motor evaluations with the Movement Disorders Society revised Unified Parkinson's Disease Rating Scale (MDS-UPDRS), [(11)C]dihydrotetrabenazine (DTBZ) monoaminergic brain PET imaging, and MRI.

Results: Participants with PD with elevated Framingham risk (FR) scores (n = 63, 74.1%) showed higher unadjusted rates of total MDS-UPDRS (t = 3.60, p = 0.0006) and axial motor scores (t = 3.98, p = 0.0001) per estimated year of motor symptoms compared to participants with normal-range risk scores (n = 22, 25.9%). After controlling for sex, Montreal Cognitive Assessment score, frontal leukoaraiosis severity, and striatal DTBZ activity, elevated risk factor status was associated with the rate of accrual of axial motor impairments (R(2) = 0.206; t = 2.62, p = 0.011) but not with total MDS-UPDRS motor score (R(2) = 0.198; t = 1.51, p = 0.135). Frontal leukoaraiosis was associated with the rate of axial and total MDS-UPDRS scores per year of symptoms and also with elevated systolic blood pressure (R(2) = 0.291; t = 2.30, p = 0.024) in a separate risk-factor model.

Conclusion: Cardiovascular risk factors may contribute to axial motor features in PD. Early modification of cardiovascular risk factors, including hypertension, deserves further study as a novel disease-modifying strategy in PD.

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