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Pathophysiologic Mechanisms of Cerebral Ischemia and Diffusion Hypoxia in Traumatic Brain Injury
Author(s) -
Tonny Veenith,
Eleanor L. Carter,
Thomas Geeraerts,
Julia Grossac,
Virginia Newcombe,
Joanne Outtrim,
Gloria S. Gee,
Victoria Lupson,
Rob Smith,
Franklin I. Aigbirhio,
Tim D. Fryer,
Young T. Hong,
David Me,
Jonathan Coles
Publication year - 2016
Publication title -
jama neurology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 5.298
H-Index - 231
eISSN - 2168-6157
pISSN - 2168-6149
DOI - 10.1001/jamaneurol.2016.0091
Subject(s) - hypoxia (environmental) , pathophysiology , ischemia , medicine , traumatic brain injury , cerebral hypoxia , cerebral ischaemia , neuroscience , cardiology , psychology , psychiatry , oxygen , chemistry , organic chemistry
Combined oxygen 15-labeled positron emission tomography (15O PET) and brain tissue oximetry have demonstrated increased oxygen diffusion gradients in hypoxic regions after traumatic brain injury (TBI). These data are consistent with microvascular ischemia and are supported by pathologic studies showing widespread microvascular collapse, perivascular edema, and microthrombosis associated with selective neuronal loss. Fluorine 18-labeled fluoromisonidazole ([18F]FMISO), a PET tracer that undergoes irreversible selective bioreduction within hypoxic cells, could confirm these findings.

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