September 2016
Volume 57, Issue 12
Open Access
ARVO Annual Meeting Abstract  |   September 2016
Examining retinal structure and function in brain injury patients with homonymous hemianopia
Author Affiliations & Notes
  • Jakaria Mostafa
    College of Optometry, University of Houston, Houston, Texas, United States
  • Suzanne Wickum
    College of Optometry, University of Houston, Houston, Texas, United States
  • Laura J Frishman
    College of Optometry, University of Houston, Houston, Texas, United States
  • Jason Porter
    College of Optometry, University of Houston, Houston, Texas, United States
  • Footnotes
    Commercial Relationships   Jakaria Mostafa, None; Suzanne Wickum, None; Laura Frishman, None; Jason Porter, None
  • Footnotes
    Support  NIH Grant P30 EY007551, Fight for Sight Summer Student Fellowship, University of Houston College of Optometry
Investigative Ophthalmology & Visual Science September 2016, Vol.57, 5989. doi:
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      Jakaria Mostafa, Suzanne Wickum, Laura J Frishman, Jason Porter; Examining retinal structure and function in brain injury patients with homonymous hemianopia. Invest. Ophthalmol. Vis. Sci. 2016;57(12):5989.

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

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Abstract

Purpose : Recent studies report structural damage to retinal ganglion cells and their axons following an acquired cortical lesion, possibly due to retrograde degeneration. Building on these works, we sought to quantify (1) the extent to which abnormalities exist in inner retinal structure and function in brain injury patients with homonymous hemianopias (HHs) and (2) how retinal alterations relate to functional abnormalities of the central visual pathway.

Methods : Volume scans of the macula and optic nerve head were acquired with spectral domain optical coherence tomography in 24 eyes of 12 HH patients (5 stroke, 7 traumatic brain injury [TBI]; time post-injury = 2.5 ± 2.8 years, range: 6 months – 9 years). Peripapillary retinal nerve fiber layer thickness (RNFLT) and macular ganglion cell-inner plexiform layer thickness (GCIPLT) were quantified globally and in sectors, and compared with instrument-based normative data. Photopic negative response (PhNR) amplitudes were measured using the full-field flash electroretinogram and compared to normative data. Mean deviation (MD) was quantified via 30-2 standard automated perimetry. Structural and functional measures were related on global and local scales.

Results : Global or sectoral GCIPLT, RNFLT and PhNR amplitude were reduced in 79%, 71% and 50% of eyes, respectively. Global measures of inner retinal (GCIPLT) and axonal (RNFLT) structure were thinner in eyes in which more time elapsed since injury (R2=0.42 and 0.62, respectively). The significant linear relationships (P<.05) found across eyes between MD and (1) global GCIPLT (R2=0.29), (2) global RNFLT (R2=0.17) and (3) PhNR amplitude (R2=0.19) support that eyes with more extensive field loss tend to have more abnormalities in inner retinal structure and function. GCIPLT measures were abnormal with significantly greater frequency in retinal sectors corresponding to the side of hemianopic field loss versus those corresponding to the side with spared vision (P<.05, chi-squared test).

Conclusions : Preferential damage of inner retinal structure in locations corresponding to the side of hemianopic field loss and the higher prevalence of inner retinal structural damage in long-standing brain injury patients are suggestive of retrograde degeneration. A better understanding of changes in inner retinal structure and function may provide insights on the pathology involved in visual impairment following brain injury.

This is an abstract that was submitted for the 2016 ARVO Annual Meeting, held in Seattle, Wash., May 1-5, 2016.

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