Influence of hypertension on neurocognitive domains in nondemented Parkinson’s disease patients. 1Department of Clinical and Health Psychology, McKnight Brain Institute, University of Florida, 101 South Newell Drive, Gainesville, FL 32601, USA ; Center for Movement Disorders and Neurorestoration, McKnight Brain Institute, University of Florida, 3450 Hull Road Gainesville, FL 32607, USA. 2Center for Movement Disorders and Neurorestoration, McKnight Brain Institute, University of Florida, 3450 Hull Road Gainesville, FL 32607, USA. One may ask the question “why examine the influence of cardiovascular risk factors on cognition in Parkinson’s disease if the relationship has been shown to exist in normal elderly samples?” The answer relates Parkinson’s disease being associated with both protective and risk factors of cardiovascular disease (Nanhoe-Mahabier et al., 2009).
Findings from the current study showed a relationship between hypertension and lower scores of tests of executive functioning and verbal delayed recall. Findings were contrary to previous studies examining the influence of cardiovascular risk factors on dementia status in Parkinson’s disease, but consistent with a wealth of literature among normal elderly individuals showing cardiovascular risk factors to negatively impact specific neurocognitive domains. Overall, this study supports the view that cardiovascular risk factors are related to cognitive impairment in Parkinson’s disease, similar to what has been reported in normal aging. Health comorbidities, particularly cardiovascular risk factors, are well known to pose risks for cognitive decline in older adults.
Specifically, both levodopa medication and degeneration of the locus coeruleus secondary to Lewy body depositions may lead to decreased norepinephrine levels, which lead to blood vessel dilation, decreased cardiac output and ultimately lower blood pressure. This result was corroborated by the finding that higher pulse pressure values (a surrogate measure of cardiovascular risk) related to worse cognitive functioning in domains of executive function, verbal delayed recall and processing speed. The relationship between cardiovascular risk factors and cognitive impairment is likely due to small vessel disease associate chronic cerebral hypoperfusion (Libon, 2005).


Even though levodopa use may be associated with the fringe benefit of lowering blood pressure, hypertension is still common among individuals with Parkinson’s disease, and has a detrimental impact on cognition. To date, little attention has focused on the impact of these comorbidities on Parkinson’s disease (PD).
One mechanism contributing to cognitive impairment in Parkinson’s is disruption of frontal-subcortical circuits secondary to dopamine striatal dopamine depletion. On the other hand, Parkinson’s disease is associated with decreased mobility and increased homocysteine levels (secondary to levodopa) that may increase an individual’s vulnerability to cardiovascular disease. Furthermore, individuals with more severe Parkinson’s disease motor symptoms (measured by a clinician rated scoring system; Unified Parkinson’s Disease Rating Scale motor scores) showed a stronger relationship between pulse pressure and cognitive impairment (Figure 1). Figure depicts linear relationship between pulse pressure and executive function, delayed verbal memory and processing speed for each Unified Parkinson Disease Rating Scale Part III (UPDRS) quartile (higher quartile means more severe motor symptoms). Deep subcortical white matter is particularly vulnerable to chronic mild drops in blood perfusion, due to receiving a less direct supply of blood. Figure portrays frontal-subcortical circuits important for cognition (Alexander, Delong & Strick, 1986).
This study examined the prevalence and contribution of comorbidities on cognitive status in PD patients, above and beyond the effects of disease severity. The relationship between pulse pressure and cognition was strongest among individuals in the lowest UPDRS quartile (most severe motor symptoms). Damage to deep subcortical white matter may disrupt frontal-subcortical circuits important for cognitive functioning.


Disruption of these circuits may be due to: 1) substantia nigra degeneration in Parkinson’s disease (PD) leading to dopamine (DA) deficiency and 2) disruption of white matter tracts (internal capsule and thalamic projections) between grey matter structures. Limited studies have focused on the detrimental role of cardiovascular risk factors on cognition in Parkinson’s disease, despite the fact that over two decades of studies have shown cardiovascular risk factors to be related to slowed processing speed and frontal-executive dysfunction.
Specifically white matter tracts connecting the dorsal-lateral prefrontal cortex (a cortical area important for executive functioning), the striatum, and the thalamus may be damaged among individuals with chronic hypertension.
A cross sectional design was used, including neuropsychological data on 341 PD patients without severe cognitive decline.
The finding of an interaction between pulse pressure and Parkinson’s disease motor severity is particularly interesting and may suggest that the frontal-subcortical circuits may be receiving a double hit (dopamine deficiency and white matter disruption) among individuals with both Parkinson’s disease and hypertension (Figure 2). Data were analyzed using a series of multiple hierarchical regressions, controlling for PD-related disease variables. The presence of hypertension significantly contributed to domains of executive function and verbal memory. The cooccurrence of orthostatic hypotension moderated the relationship between hypertension and executive function.



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