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The Longitudinal Evolution of Cerebral Blood Flow Regulation after Acute Ischaemic Stroke

BACKGROUND: Acute stroke is known to impair cerebral blood flow (CBF) regulation, but the longitudinal changes of these effects have been poorly reported. The main CBF regulatory mechanisms [cerebral autoregulation (CA) and neurovascular coupling (NVC)] were assessed over 3 months after acute ischae...

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Autores principales: Salinet, Angela S.M., Panerai, Ronney B., Robinson, Thompson G.
Formato: Online Artículo Texto
Lenguaje:English
Publicado: S. Karger AG 2014
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4176407/
https://www.ncbi.nlm.nih.gov/pubmed/25298773
http://dx.doi.org/10.1159/000366017
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author Salinet, Angela S.M.
Panerai, Ronney B.
Robinson, Thompson G.
author_facet Salinet, Angela S.M.
Panerai, Ronney B.
Robinson, Thompson G.
author_sort Salinet, Angela S.M.
collection PubMed
description BACKGROUND: Acute stroke is known to impair cerebral blood flow (CBF) regulation, but the longitudinal changes of these effects have been poorly reported. The main CBF regulatory mechanisms [cerebral autoregulation (CA) and neurovascular coupling (NVC)] were assessed over 3 months after acute ischaemic stroke. METHODS: Recordings of CBF velocity (CBFv), blood pressure (BP), and end-tidal CO(2) were performed during 5 min baseline and 1 min passive movement of the elbow. Stroke patients were assessed <72 h of stroke onset, and at 2 weeks, 1 and 3 months after stroke. RESULTS: Fifteen acute stroke subjects underwent all 4 sessions and were compared to 22 control subjects. Baseline recordings revealed a significantly lower CBFv in the affected hemisphere within 72 h after stroke compared to controls (p = 0.02) and a reduction in CA index most marked at 2 weeks (p = 0.009). CBFv rise in response to passive arm movement was decreased bilaterally after stroke, particularly in the affected hemisphere (p < 0.01). Both alterations in CA and NVC returned to control levels during recovery. CONCLUSION: The major novel finding of this study was that both CA and NVC regulatory mechanisms deteriorated initially following stroke onset, but returned to control levels during the recovery period. These findings are relevant to guide the timing of interventions to manipulate BP and potentially for the impact of intensive rehabilitation strategies that may precipitate acute physiological perturbations but require further exploration in a larger population that better reflects the heterogeneity of stroke. Further, they will also enable the potential influence of stroke subtype to be investigated.
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spelling pubmed-41764072014-10-08 The Longitudinal Evolution of Cerebral Blood Flow Regulation after Acute Ischaemic Stroke Salinet, Angela S.M. Panerai, Ronney B. Robinson, Thompson G. Cerebrovasc Dis Extra Original Paper BACKGROUND: Acute stroke is known to impair cerebral blood flow (CBF) regulation, but the longitudinal changes of these effects have been poorly reported. The main CBF regulatory mechanisms [cerebral autoregulation (CA) and neurovascular coupling (NVC)] were assessed over 3 months after acute ischaemic stroke. METHODS: Recordings of CBF velocity (CBFv), blood pressure (BP), and end-tidal CO(2) were performed during 5 min baseline and 1 min passive movement of the elbow. Stroke patients were assessed <72 h of stroke onset, and at 2 weeks, 1 and 3 months after stroke. RESULTS: Fifteen acute stroke subjects underwent all 4 sessions and were compared to 22 control subjects. Baseline recordings revealed a significantly lower CBFv in the affected hemisphere within 72 h after stroke compared to controls (p = 0.02) and a reduction in CA index most marked at 2 weeks (p = 0.009). CBFv rise in response to passive arm movement was decreased bilaterally after stroke, particularly in the affected hemisphere (p < 0.01). Both alterations in CA and NVC returned to control levels during recovery. CONCLUSION: The major novel finding of this study was that both CA and NVC regulatory mechanisms deteriorated initially following stroke onset, but returned to control levels during the recovery period. These findings are relevant to guide the timing of interventions to manipulate BP and potentially for the impact of intensive rehabilitation strategies that may precipitate acute physiological perturbations but require further exploration in a larger population that better reflects the heterogeneity of stroke. Further, they will also enable the potential influence of stroke subtype to be investigated. S. Karger AG 2014-08-26 /pmc/articles/PMC4176407/ /pubmed/25298773 http://dx.doi.org/10.1159/000366017 Text en Copyright © 2014 by S. Karger AG, Basel http://creativecommons.org/licenses/by-nc/3.0/ This is an Open Access article licensed under the terms of the Creative Commons Attribution-NonCommercial 3.0 Unported license (CC BY-NC) (www.karger.com/OA-license), applicable to the online version of the article only. Users may download, print and share this work on the Internet for noncommercial purposes only, provided the original work is properly cited, and a link to the original work on http://www.karger.com and the terms of this license are included in any shared versions.
spellingShingle Original Paper
Salinet, Angela S.M.
Panerai, Ronney B.
Robinson, Thompson G.
The Longitudinal Evolution of Cerebral Blood Flow Regulation after Acute Ischaemic Stroke
title The Longitudinal Evolution of Cerebral Blood Flow Regulation after Acute Ischaemic Stroke
title_full The Longitudinal Evolution of Cerebral Blood Flow Regulation after Acute Ischaemic Stroke
title_fullStr The Longitudinal Evolution of Cerebral Blood Flow Regulation after Acute Ischaemic Stroke
title_full_unstemmed The Longitudinal Evolution of Cerebral Blood Flow Regulation after Acute Ischaemic Stroke
title_short The Longitudinal Evolution of Cerebral Blood Flow Regulation after Acute Ischaemic Stroke
title_sort longitudinal evolution of cerebral blood flow regulation after acute ischaemic stroke
topic Original Paper
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4176407/
https://www.ncbi.nlm.nih.gov/pubmed/25298773
http://dx.doi.org/10.1159/000366017
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