Citation

Ishaque M, Manning JH, Woolsey MD, Franklin CG, Tullis EW, Fox PT. Neuroimage (Amst) 2016; 11: 167-172.

Affiliation

Research Imaging Institute, University of Texas Health Science Center at San Antonio, 8403 Floyd Curl Drive, San Antonio, TX 78229, USA; Department of Radiological Sciences, University of Texas Health Science Center at San Antonio, 7703 Floyd Curl Drive, San Antonio, TX 78229, USA; South Texas Veterans Healthcare System, 7400 Merton Minter Boulevard, San Antonio, TX 78229, USA; Shenzhen University School of Medicine, Neuroimaging Laboratory, Nanhai Avenue 3688, Shenzhen, Guangong, 518060, People's Republic of China.

Copyright

(Copyright © 2016, Elsevier Publishing)

DOI

10.1016/j.nicl.2016.01.019

PMID

26937385

Abstract

Drowning is a leading cause of neurological morbidity and mortality in young children. Anoxic brain injury (ABI) can result from nonfatal drowning and typically entails substantial neurological impairment. The neuropathology of drowning-induced pediatric ABI is not well established. Specifically, quantitative characterization of the spatial extent and tissue distribution of anoxic damage in pediatric nonfatal drowning has not previously been reported but could clarify the underlying pathophysiological processes and inform clinical management. To this end, we used voxel-based morphometric (VBM) analyses to quantify the extent and spatial distribution of consistent, between-subject alterations in gray and white matter volume. Whole-brain, high-resolution T1-weighted MRI datasets were acquired in 11 children with chronic ABI and 11 age- and gender-matched neurotypical controls (4-12 years). Group-wise VBM analyses demonstrated predominantly central subcortical pathology in the ABI group in both gray matter (bilateral basal ganglia nuclei) and white matter (bilateral external and posterior internal capsules) (P < 0.001); minimal damage was found outside of these deep subcortical regions. These highly spatially convergent gray and white matter findings reflect the vascular distribution of perforating lenticulostriate arteries, an end-arterial watershed zone, and suggest that vascular distribution may be a more important determinant of tissue loss than oxygen metabolic rate in pediatric ABI. Further, these results inform future directions for diagnostic and therapeutic modalities.

Language: en