Stroke‐Related Visceral Alterations: A Voxel‐Based Neuroanatomic Localization Study

Author:

Arsava Ethem Murat1ORCID,Chang Ken12,Tawakol Ahmed3,Loggia Marco L.1,Goldstein Joshua N.4,Brown James5,Park Kwang‐Yeol16,Singhal Aneesh B.7,Kalpathy‐Cramer Jayashree1,Sorensen Alma Gregory1,Rosen Bruce R.1,Samuels Martin Allen8,Ay Hakan1

Affiliation:

1. Athinoula A. Martinos Center for Biomedical Imaging, Department of Radiology Massachusetts General Hospital Charlestown MA USA

2. Department of Medicine Memorial Sloan Kettering Cancer Center New York NY USA

3. Cardiology Division and Cardiovascular Imaging Research Center Massachusetts General Hospital Boston MA USA

4. Department of Emergency Medicine Massachusetts General Hospital Boston MA USA

5. School of Computer Science University of Lincoln Lincoln UK

6. Department of Neurology Chung‐Ang University Hospital Seoul Republic of Korea

7. Department of Neurology Massachusetts General Hospital Boston MA USA

8. Department of Neurology Brigham and Women's Hospital Boston MA USA

Abstract

ObjectiveFunctional and morphologic changes in extracranial organs can occur after acute brain injury. The neuroanatomic correlates of such changes are not fully known. Herein, we tested the hypothesis that brain infarcts are associated with cardiac and systemic abnormalities (CSAs) in a regionally specific manner.MethodsWe generated voxelwise p value maps of brain infarcts for poststroke plasma cardiac troponin T (cTnT) elevation, QTc prolongation, in‐hospital infection, and acute stress hyperglycemia (ASH) in 1,208 acute ischemic stroke patients prospectively recruited into the Heart–Brain Interactions Study. We examined the relationship between infarct location and CSAs using a permutation‐based approach and identified clusters of contiguous voxels associated with p < 0.05.ResultscTnT elevation not attributable to a known cardiac reason was detected in 5.5%, QTc prolongation in the absence of a known provoker in 21.2%, ASH in 33.9%, and poststroke infection in 13.6%. We identified significant, spatially segregated voxel clusters for each CSA. The clusters for troponin elevation and QTc prolongation mapped to the right hemisphere. There were 3 clusters for ASH, the largest of which was in the left hemisphere. We found 2 clusters for poststroke infection, one associated with pneumonia in the left and one with urinary tract infection in the right hemisphere. The relationship between infarct location and CSAs persisted after adjusting for infarct volume.InterpretationOur results show that there are discrete regions of brain infarcts associated with CSAs. This information could be used to bootstrap toward new markers for better differentiation between neurogenic and non‐neurogenic mechanisms of poststroke CSAs. ANN NEUROL 2023;94:1155–1163

Funder

National Institutes of Health

Publisher

Wiley

Subject

Neurology (clinical),Neurology

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