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Author response: BOLD cerebrovascular reactivity as a novel marker for crossed cerebellar diaschisis


van Niftrik, Christiaan H B; Sebök, Martina; Fierstra, Jorn (2019). Author response: BOLD cerebrovascular reactivity as a novel marker for crossed cerebellar diaschisis. Neurology, 93(4):182.

Abstract

We kindly thank Drs. Reidler and Kunz for their insightful comments regarding our article.1  The main objective was to study blood oxygen level–dependent cerebrovascular reactivity (BOLD-CVR) for crossed cerebellar diaschisis (CCD) detection. In this regard, worse clinical outcome in the CCD(+) group should indeed be interpreted with caution. Ideally, this association needs to be further investigated in a uniform stroke cohort with sequential follow-up studies.

We deliberately did not comment on supratentorial stroke volume because it is an inexact measurement and does not say anything about the infarct location.2 Besides, the concept that stroke volume is highly associated with the presence of CCD in the acute phase remains debatable, as the studies mentioned in the readers' comment appeared to be in disagreement.3,4 Nevertheless, we agree that stroke location would be a better variable for an adjusted analysis.

The statement made by Drs. Reidler and Kunz about “inferior cerebrovascular response indicating more severe supratentorial lesions”  is, however, erroneous. We have only shown the presence of more impaired supratentorial BOLD-CVR in the CCD(+) group. This finding has led us to believe that hemodynamic alterations may also cause CCD rather than a functional disruption alone. In general, BOLD imaging enables investigations on resting-state functional connectivity and the influence of CCD-induced altered metabolism in patients with stroke.5

Abstract

We kindly thank Drs. Reidler and Kunz for their insightful comments regarding our article.1  The main objective was to study blood oxygen level–dependent cerebrovascular reactivity (BOLD-CVR) for crossed cerebellar diaschisis (CCD) detection. In this regard, worse clinical outcome in the CCD(+) group should indeed be interpreted with caution. Ideally, this association needs to be further investigated in a uniform stroke cohort with sequential follow-up studies.

We deliberately did not comment on supratentorial stroke volume because it is an inexact measurement and does not say anything about the infarct location.2 Besides, the concept that stroke volume is highly associated with the presence of CCD in the acute phase remains debatable, as the studies mentioned in the readers' comment appeared to be in disagreement.3,4 Nevertheless, we agree that stroke location would be a better variable for an adjusted analysis.

The statement made by Drs. Reidler and Kunz about “inferior cerebrovascular response indicating more severe supratentorial lesions”  is, however, erroneous. We have only shown the presence of more impaired supratentorial BOLD-CVR in the CCD(+) group. This finding has led us to believe that hemodynamic alterations may also cause CCD rather than a functional disruption alone. In general, BOLD imaging enables investigations on resting-state functional connectivity and the influence of CCD-induced altered metabolism in patients with stroke.5

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Additional indexing

Item Type:Journal Article, refereed, original work
Communities & Collections:04 Faculty of Medicine > University Hospital Zurich > Clinic for Neurosurgery
Dewey Decimal Classification:610 Medicine & health
Scopus Subject Areas:Health Sciences > Neurology (clinical)
Language:English
Date:23 July 2019
Deposited On:17 Oct 2019 11:55
Last Modified:29 Jul 2020 11:29
Publisher:Lippincott Williams & Wilkins
ISSN:0028-3878
OA Status:Green
Publisher DOI:https://doi.org/10.1212/WNL.0000000000007841
PubMed ID:31332089

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