July 2019
Volume 60, Issue 9
Free
ARVO Annual Meeting Abstract  |   July 2019
Evaluation of treatment for traumatic optic neuropathy
Author Affiliations & Notes
  • Boglarka Racz
    Ophthalmology, Columbia University Medical Center, New York, New York, United States
  • Pavel Iserovich
    Ophthalmology, Columbia University Medical Center, New York, New York, United States
  • Konstantin Petrukhin
    Ophthalmology, Columbia University Medical Center, New York, New York, United States
  • Footnotes
    Commercial Relationships   Boglarka Racz, None; Pavel Iserovich, None; Konstantin Petrukhin, The Trustees of Columbia University in the City of New York (P)
  • Footnotes
    Support  None
Investigative Ophthalmology & Visual Science July 2019, Vol.60, 2262. doi:
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      Boglarka Racz, Pavel Iserovich, Konstantin Petrukhin; Evaluation of treatment for traumatic optic neuropathy. Invest. Ophthalmol. Vis. Sci. 2019;60(9):2262.

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      © ARVO (1962-2015); The Authors (2016-present)

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Abstract

Purpose : Traumatic optic neuropathy (TON) is a common cause of significant visual loss after the combat-related frontal head trauma. The injury-induced edema of the canalicular portion of the optic nerve leads to neural compression that triggers development of an intracanalicular compartment syndrome. Reduction of swelling by inhibiting injury-induced edema in the intracanalicular portion of the optic nerve is a sound strategy for the prevention of TON-related loss of vision. B-3(+) is an abandoned fluorenone drug that has demonstrated significant efficacy in preventing mortality in animal models of concussive brain injury. B-3(+) acts as a polypharmacological agent capable of significantly reducing insult-induced astrocyte swelling in a number of experimental systems. We evaluated the ability of B-3(+) to confer axonal protection in the guinea pig optic nerve crush model and assessed the systemic exposure of B-3(+) following its intravitreal injections.

Methods : The exposed guinea pig optic nerve was partially crushed with a pair of self-closing forceps 2 mm behind the globe for 3 seconds. A sham-operated control group was treated in the same way without closing of the forceps. Compound was injected to the vitreous to the final concentration of 8 nM. Three weeks after the surgery animal eyes were enucleated and optic nerve fixed. One-micrometer ON sections were prepared and stained. Images were collected, and intact axons were counted at the 250 μm distance distal from the crush site using the commercial image analysis software. Guinea pig sera were analyzed for the biomarker of the systemic exposure of the test compound

Results : In the absence of treatment after inducing the crush only 23% of optic nerve axons survive at the 3 week post-injury time point. Intravitreal administration of B3(+)conferred significant axonal protection as the number of survived axons in the optic nerve significantly increased by 3-fold. Analysis of the serum biomarker revealed no systemic compound exposure after its intraocular administration

Conclusions : B3(+), previously evaluated as a treatment for traumatic brain injury, conferred protection in the guinea pig optic nerve crush model which provides rationale for its additional characterization as a potential treatment for traumatic optic neuropathy associated with combat-related traumatic head trauma.

This abstract was presented at the 2019 ARVO Annual Meeting, held in Vancouver, Canada, April 28 - May 2, 2019.

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