April 2014
Volume 55, Issue 13
Free
ARVO Annual Meeting Abstract  |   April 2014
Determination of Injury Thresholds for Torsional Indirect Traumatic Optic Neuropathy in a Rat Model
Author Affiliations & Notes
  • Brooke Ivie Asemota
    Biomedical Engineering, University of Texas at San Antonio, San Antonio, TX
  • Randolph D Glickman
    University of Texas Health Science Center at San Antonio, San Antonio, TX
  • William Eric Sponsel
    Biomedical Engineering, University of Texas at San Antonio, San Antonio, TX
  • Matthew Aaron Reilly
    Biomedical Engineering, University of Texas at San Antonio, San Antonio, TX
Investigative Ophthalmology & Visual Science April 2014, Vol.55, 6194. doi:
  • Views
  • Share
  • Tools
    • Alerts
      ×
      This feature is available to authenticated users only.
      Sign In or Create an Account ×
    • Get Citation

      Brooke Ivie Asemota, Randolph D Glickman, William Eric Sponsel, Matthew Aaron Reilly; Determination of Injury Thresholds for Torsional Indirect Traumatic Optic Neuropathy in a Rat Model. Invest. Ophthalmol. Vis. Sci. 2014;55(13):6194.

      Download citation file:


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

      ×
  • Supplements
Abstract
 
Purpose
 

Traumatic optic neuropathy (TON) occurs in up to 5% of all head traumas resulting in severe visual deficit or blindness. In this study we imposed torsional indirect TON in a physiologically relevant rat model, which may be used for development of novel therapeutics.

 
Methods
 

Flash visual evoked potentials (fVEPs) were used before and after injury stimulus to characterize the visual performance of the visual track. A torsional indirect TON insult was applied using a robot described previously (Reilly et al., ARVO 2013 E-abstract 54:5757). The amplitude and velocity of this insult was varied to modulate the degree of irreversible TON. Histopathology was also used to examine optic nerve sections.

 
Results
 

Application of super-saccade rotation induced TON (Fig. 1). The torsion parameters correlated with fVEP amplitude and latency (Fig. 2).

 
Conclusions
 

The difference between pre- and post-traumatic event fVEPs directly corresponds to optic nerve damage because the signal relay producing the fVEP is dependent on the conductivity of the optic nerve with regards to amplitude, period, and phase number. Because the optic nerve is a part of the Central Nervous System (CNS), the neuroprotectives that are effective in preventing blindness in our TON rat model may be applicable to other neurodegenerative diseases and disorders.

 
 
Figure 1: Difference in fVEP between Normal (Pre-TITON) and Injured (Post-TITON) Eye
 
Figure 1: Difference in fVEP between Normal (Pre-TITON) and Injured (Post-TITON) Eye
 
 
Figure 2: Correlation of Torsion Parameters with fVEP Amplitude
 
Figure 2: Correlation of Torsion Parameters with fVEP Amplitude
 
Keywords: 629 optic nerve • 742 trauma  
×
×

This PDF is available to Subscribers Only

Sign in or purchase a subscription to access this content. ×

You must be signed into an individual account to use this feature.

×