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Cognitive and MRI correlates of orthostatic hypotension in Parkinson’s disease

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Abstract

Orthostatic hypotension (OH) is a frequent nonmotor feature of Parkinson’s disease (PD), and its occurrence has been associated with cognitive impairment. The underlying mechanism could be mediated by development of cerebrovascular disease induced by chronic or episodic hypoperfusion, but the extent of brain vascular load in PD patients with OH has never been investigated. This study aimed to assess the relationship between OH and cognitive function in PD patients and to investigate the contribution of brain vascular lesions. Forty-eight PD patients underwent a tilt table test (TT) to assess supine and orthostatic blood pressure as well as an extensive neuropsychological evaluation to evaluate cognitive function. Brain magnetic resonance imaging was acquired in 44/48 patients and analyzed by a visual semiquantitative scale. Twenty-three patients presented OH at TT (13/23 were symptomatic), and 25 did not. There were no differences in motor severity or disease duration between patients with and without OH. In patients with OH we found significantly worse cognitive performance in specific tasks, such as sustained attention, visuospatial and verbal memory, compared with patients without OH. However, there were no differences in vascular burden between the two groups. Our study confirms that there is an association between OH and selective cognitive deficits in PD, but rebuts the hypothesis that this is underlined by the development of cerebrovascular disease.

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Conflicts of interest

All authors have no financial or other conflicts of interest that might bias their work.

Ethical standard

This study has been approved by local ethic committee of IRCCS San Camillo and has been performed in agreement with the ethical standards laid down in the 1964 declaration of Helsinki.

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Correspondence to Manuela Pilleri.

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Pilleri, M., Facchini, S., Gasparoli, E. et al. Cognitive and MRI correlates of orthostatic hypotension in Parkinson’s disease. J Neurol 260, 253–259 (2013). https://doi.org/10.1007/s00415-012-6627-y

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  • DOI: https://doi.org/10.1007/s00415-012-6627-y

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