Document Type

Article

Peer Reviewed

1

Publication Date

3-2018

NLM Title Abbreviation

Ann Clin Transl Neurol

Journal/Book/Conference Title

Annals of Clinical and Translational Neurology

PubMed ID

29560370

DOI of Published Version

10.1002/acn3.523

Start Page

240

End Page

251

Abstract

Objective: Limited attention has been given to ocular injuries associated with traumatic brain injury (TBI). The retina is an extension of the central nervous system and evaluation of ocular damage may offer a less-invasive approach to gauge TBI severity and response to treatment. We aim to characterize acute changes in the mouse eye after exposure to two different models of TBI to assess the utility of eye damage as a surrogate to brain injury.

Methods: A model of blast TBI (bTBI) using a shock tube was compared to a lateral fluid percussion injury model (LFPI) using fluid pressure applied directly to the brain. Whole eyes were collected from mice 3 days post LFPI and 24 days post bTBI and were evaluated histologically using a hematoxylin and eosin stain.

Results: bTBI mice showed evidence of vitreous detachment in the posterior chamber in addition to vitreous hemorrhage with inflammatory cells. Subretinal hemorrhage, photoreceptor degeneration, and decreased cellularity in the retinal ganglion cell layer was also seen in bTBI mice. In contrast, eyes of LFPI mice showed evidence of anterior uveitis and subcapsular cataracts.

Interpretation: We demonstrated that variations in the type of TBI can result in drastically different phenotypic changes within the eye. As such, molecular and phenotypic changes in the eye following TBI may provide valuable information regarding the mechanism, severity, and ongoing pathophysiology of brain injury. Because vitreous samples are easily obtained, molecular changes within the eye could be utilized as biomarkers of TBI in human patients.

Keywords

Traumatic Brain Injuries, lateral fluid percussion injury model, Immunohistochemistry, central nervous system, Pediatrics, Neurology, Ophthalmology, TBI, LFBI

Comments

VBM and AGB are supported by NIH grants [R01EY026682, R01EY024665, R01EY025225, R01EY024698 and R21AG050437]. VBM is supported by Research to Prevent Blindness (RPB), New York, NY. SHT is supported by the Barbara & Donald Jonas Laboratory of Regenerative Medicine and Bernard & Shirlee Brown Glaucoma Laboratory are supported by the National Institute of Health [5P30EY019007 R01EY018213, R01EY024698, R21AG050437], National Cancer Institute Core [5P30CA013696], the Research to Prevent Blindness (RPB) Physician‐Scientist Award, unrestricted funds from RPB, New York, NY, USA. PJF is supported by NIH R01AR059703. CDH, EWV, and BM were supported by a Multi‐University Research Initiative from the Army Research Office (W911NF‐10‐1‐0526). EWV was supported by a National Defense Science & Engineering Graduate Fellowship from the Department of Defense (EWV‐2012). OA and RN were supported by the Dept. of the Army – USAMRAA (W81XWH12‐1‐0579).

Journal Article Version

Version of Record

Published Article/Book Citation

Ann Clin Transl Neurol. 2018 Feb 26;5(3):240-251. doi: https://doi.org/10.1002/acn3.523

Rights

© 2018 The Authors

Creative Commons License

Creative Commons License
This work is licensed under a Creative Commons Attribution-Noncommercial-No Derivative Works 4.0 License.

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URL

https://ir.uiowa.edu/pediatrics_pubs/16