April 2010
Volume 51, Issue 13
Free
ARVO Annual Meeting Abstract  |   April 2010
Early Functional and Structural Optic Nerve Deficits in a Canine Model of Compressive Optic Neuropathy
Author Affiliations & Notes
  • R. N. Nzokwe
    Veterinary Clinical Sciences, Iowa State University, Ames, Iowa
  • H. Kecova
    Veterinary Clinical Sciences, Iowa State University, Ames, Iowa
  • R. H. Kardon
    Ophthalmology and Visual Sciences, University of Iowa, Iowa City, Iowa
  • S. A. Park
    Veterinary Clinical Sciences, Iowa State University, Ames, Iowa
  • K. Hamouche
    Veterinary Clinical Sciences, Iowa State University, Ames, Iowa
  • S. Jacobson
    Veterinary Clinical Sciences, Iowa State University, Ames, Iowa
  • E. Alward
    Veterinary Clinical Sciences, Iowa State University, Ames, Iowa
  • M. M. Harper
    Veterinary Clinical Sciences, Iowa State University, Ames, Iowa
    Veterans Administration Medical Center, Iowa City, Iowa
  • S. D. Grozdanic
    Veterinary Clinical Sciences, Iowa State University, Ames, Iowa
  • Footnotes
    Commercial Relationships  R.N. Nzokwe, None; H. Kecova, None; R.H. Kardon, None; S.A. Park, None; K. Hamouche, None; S. Jacobson, None; E. Alward, None; M.M. Harper, None; S.D. Grozdanic, None.
  • Footnotes
    Support  Veterans Administration Rehabilitation Division Merit Grant #C4702R and Iowa City VA Center for the Prevention and Treatment of Vision Loss
Investigative Ophthalmology & Visual Science April 2010, Vol.51, 3842. doi:https://doi.org/
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      R. N. Nzokwe, H. Kecova, R. H. Kardon, S. A. Park, K. Hamouche, S. Jacobson, E. Alward, M. M. Harper, S. D. Grozdanic; Early Functional and Structural Optic Nerve Deficits in a Canine Model of Compressive Optic Neuropathy. Invest. Ophthalmol. Vis. Sci. 2010;51(13):3842. doi: https://doi.org/.

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

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Abstract

Purpose: : To evaluate functional and structural optic nerve deficits in a canine model of compressive optic neuropathy (CON).

Methods: : CON was induced in healthy laboratory beagles (n=10) by implanting an expandable silicone implant into the orbital space. Controlled optic nerve compression was achieved by inflation of the implant with saline injection. Fluorescein angiography was performed to demonstrate perfusion of the optic nerve and retinal vasculature. Thickness of the retinal nerve fiber layer (RNFL) was evaluated using optical coherence tomography (Spectralis SD-OCT system), while pattern ERG (pERG) was recorded to evaluate retinal ganglion cell (RGC) function.

Results: : Despite relatively normal optic nerve perfusion observed by fluorescein angiography, orbital implant inflation resulted in significant pERG deficits immediately after induction of optic nerve compression (0.36+0.13 µV; mean+SEM; p<0.0001, Student’s t-test), when compared to control values (6.2+0.35 µV). OCT linear scans were obtained prior to pERG recordings and scan analysis showed significant increase in the RNFL thickness of area centralis (macula) region in CON dogs (39.54+1.849 µm) when compared to control dogs (26.35+1.53 µm, p<0.0001). Peripapillary circular scan analysis showed significantly decreased RNFL thickness in CON dogs (66.92+3.569 µm) when compared to controls (75.74+1.324 µm, p=0.0098). Linear correlation analysis showed statistically significant negative correlation between macular RNFL thickness and pERG amplitudes (r2= 0.43, p=0.03), while there was no statistically significant relationship between peripapillary RNFL thickness and pERG amplitudes.

Conclusions: : Experimental optic nerve compression resulted in macular RNFL thickening and correlated with pERG deficits. Inclusion of blood vessel profile in the peripapillary RNFL analysis seems to decrease detection sensitivity and specificity for RNFL changes associated with compressive optic nerve injury in the dog model.

Keywords: imaging methods (CT, FA, ICG, MRI, OCT, RTA, SLO, ultrasound) • electroretinography: clinical • ischemia 
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