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Cerebrovascular responses to somatomotor stimulation in Parkinson's disease: A multivariate analysis.

Authors
  • Barnes, Sam C1
  • Panerai, Ronney B1, 2
  • Beishon, Lucy1, 2
  • Hanby, Martha1
  • Robinson, Thompson G1, 2
  • Haunton, Victoria J1, 2
  • 1 Department of Cardiovascular Sciences, University of Leicester, Robert Kilpatrick Clinical Sciences Building, Leicester, UK.
  • 2 NIHR Leicester Biomedical Research Centre, BHF Cardiovascular Research Centre, Glenfield Hospital, Leicester, UK.
Type
Published Article
Journal
Journal of Cerebral Blood Flow & Metabolism
Publisher
SAGE Publications
Publication Date
Aug 01, 2022
Volume
42
Issue
8
Pages
1547–1558
Identifiers
DOI: 10.1177/0271678X211065204
PMID: 35287495
Source
Medline
Keywords
Language
English
License
Unknown

Abstract

Parkinson's disease (PD) is a common neurodegenerative disorder, yet little is known about cerebral haemodynamics in this patient population. Previous studies assessing dynamic cerebral autoregulation (dCA), neurovascular coupling (NVC) and vasomotor reactivity (VMR) have yielded conflicting findings. By using multi-variate modelling, we aimed to determine whether cerebral blood flow (CBF) regulation is impaired in PD patients.55 healthy controls (HC) and 49 PD patients were recruited. PD subjects underwent a second recording following a period of abstinence from their anti-Parkinsonian medication. Continuous bilateral transcranial Doppler in the middle cerebral arteries, beat-to-beat mean arterial blood pressure (MAP; Finapres), heart rate (HR; electrocardiogram), and end-tidal CO2 (EtCO2; capnography) were measured. After a 5-min baseline period, a passive motor paradigm comprising 60 s of elbow flexion was performed. Multi-variate modelling quantified the contributions of MAP, ETCO2 and neural stimulation to changes in CBF velocity (CBFV). dCA, VMR and NVC were quantified to assess the integrity of CBF regulation.Neural stimulation was the dominant input. dCA, NVC and VMR were all found to be impaired in the PD population relative to HC (p < 0.01, p = 0.04, p < 0.01, respectively). Our data suggest PD may be associated with depressed CBF regulation. This warrants further assessment using different neural stimuli.

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