December 2002
Volume 43, Issue 13
ARVO Annual Meeting Abstract  |   December 2002
Mechanism of Focal Optic Nerve Injury from Elevated Intraocular Pressure
Author Affiliations & Notes
  • JC Morrison
    Ophthalmology Casey Eye Inst/OHSU Portland OR
  • WO Cepurna
    Ophthalmology Casey Eye Inst/OHSU Portland OR
  • L Jia
    Ophthalmology Casey Eye Inst/OHSU Portland OR
  • J Aubert
    Ophthalmology Casey Eye Inst/OHSU Portland OR
  • EC Johnson
    Ophthalmology Casey Eye Inst/OHSU Portland OR
  • Footnotes
    Commercial Relationships   J.C. Morrison, None; W.O. Cepurna, None; L. Jia, None; J. Aubert, None; E.C. Johnson, None. Grant Identification: NIH grant #EY10145, Glaucoma Research Foundation, OHSU Foundation and Research to Prevent Blindness
Investigative Ophthalmology & Visual Science December 2002, Vol.43, 2885. doi:
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    • Get Citation

      JC Morrison, WO Cepurna, L Jia, J Aubert, EC Johnson; Mechanism of Focal Optic Nerve Injury from Elevated Intraocular Pressure . Invest. Ophthalmol. Vis. Sci. 2002;43(13):2885.

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

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Abstract: : Purpose: Regional injury is a hallmark of glaucomatous optic nerve damage. This study confirms that focal injury in rats with elevated intraocular pressure (IOP) preferentially occurs in the superior optic nerve and correlates it to early regional morphologic changes in the superior optic nerve head (ONH). The results suggest a mechanism of IOP-induced injury that explains regional injury in both rats and in human glaucoma. Methods: Optic nerve cross sections from 69 animals with partial optic nerve injury following episcleral vein sclerosis were reviewed in masked fashion by light microscopy to determine if injury occurred in the superior, inferior, central or diffuse portions of the optic nerve. In four additional animals with minimally elevated IOP, but no optic nerve injury, ONH cross sections were evaluated by electron microscopy in a masked, random fashion to determine the location of the earliest pathology. Findings were correlated with regional optic nerve head anatomy and statistically analyzed using Student's t-test and ANOVA. Results: 59% of focal optic nerve lesions were located superiorly, while only 6% were inferior. In ONH, the most identifiable early ultrastructural abnormality consisted of lucent vacuoles within astrocytes, consistent with some form of activation. These were much more commonly seen at the level of the sclera (p<0.0001), and were not present in normal eyes. They were also more likely to occur in the superior vs inferior the region of the ONH (p<0.01). In all eyes, only the superior ONH was physically connected to the peripapillary sclera; the inferior ONH was separated from the sclera by a broad central retinal vein. Conclusion: In rats, elevated IOP preferentially damages the superior optic nerve. This is highly correlated with changes in ONH astrocytes adjacent to the sclera. We propose that elevated IOP increases stress in the peripapillary sclera and that this is transmitted preferentially to astrocytes through physical attachments to the superior ONH. Astrocyte response to this stress may mediate optic nerve injury, either directly by damaging axons or indirectly by withdrawing their normal support. In humans, thinner, less dense connective tissue laminar beams in the superior and inferior ONH would provide less protection for astrocytes from stress than the larger, more numerous nasal and temporal beams. This could explain preferential superior and inferior ONH damage typically seen in glaucoma

Keywords: 316 animal model • 444 intraocular pressure • 472 microscopy: electron microscopy 

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