DOI: 10.1002/ana.26785 ISSN:

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

Ethem Murat Arsava, Ken Chang, Ahmed Tawakol, Marco L. Loggia, Joshua N. Goldstein, James Brown, Kwang‐Yeol Park, Aneesh B. Singhal, Jayashree Kalpathy‐Cramer, Alma Gregory Sorensen, Bruce R. Rosen, Martin Allen Samuels, Hakan Ay
  • Neurology (clinical)
  • Neurology

Objective

Functional 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 (CSA) in a regionally‐specific manner.

Methods

We generated voxel‐wise p‐value maps of brain infarcts for post‐stroke plasma troponin T elevation (cTnT), QTc prolongation, in‐hospital infection, and acute stress hyperglycemia (ASH) in 1208 acute ischemic stroke patients prospectively recruited into the Heart‐Brain Interactions Study. We examined the relationship between infarct location and CSA using a permutation‐based approach and identified clusters of contiguous voxels associated with a p‐value <0.05.

Results

cTnT 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 post‐stroke 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 two clusters for post‐stroke infection, one associated with pneumonia in the left and one with urinary tract infection in the right hemisphere. The relationship between infarct location and CSA persisted after adjusting for infarct volume.

Interpretation

Our results show that there are discrete regions of brain infarcts associated with CSA. This information could be used to bootstrap towards new markers for better differentiation between neurogenic and non‐neurogenic mechanisms of post‐stroke CSA.

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