title: Thickness, phase retardation, birefringence, and reflectance of the retinal nerve fiber layer in normal and glaucomatous non-human primates.
abstract: OBJECTIVE
  We identified candidate optical coherence tomography (OCT) markers for early glaucoma diagnosis. Time variation of retinal nerve fiber layer (RNFL) thickness, phase retardation, birefringence, and reflectance using polarization sensitive optical coherence tomography (PS-OCT) were measured in three non-human primates with induced glaucoma in one eye. We characterized time variation of RNFL thickness, phase retardation, birefringence, and reflectance with elevated intraocular pressure (IOP).
  
  
  METHODS
  One eye of each of three non-human primates was laser treated to increase IOP. Each primate was followed for a 30-week period. PS-OCT measurements were recorded at weekly intervals. Reflectance index (RI) is introduced to characterize RNFL reflectance. Associations between elevated IOP and RNFL thickness, phase retardation, birefringence, and reflectance were characterized in seven regions (entire retina, inner and outer rings, and nasal, temporal, superior and inferior quadrants) by linear and non-linear mixed-effects models.
  
  
  RESULTS
  Elevated IOP was achieved in three non-human primate eyes with an average increase of 13 mm Hg over the study period. Elevated IOP was associated with decreased RNFL thickness in the nasal region (P = 0.0002), decreased RNFL phase retardation in the superior (P = 0.046) and inferior (P = 0.021) regions, decreased RNFL birefringence in the nasal (P = 0.002) and inferior (P = 0.029) regions, and loss of RNFL reflectance in the outer rings (P = 0.018). When averaged over the entire retinal area, only RNFL reflectance showed a significant decrease (P = 0.028).
  
  
  CONCLUSIONS
  Of the measured parameters, decreased RNFL reflectance was the most robust correlate with glaucomatous damage. Candidate cellular mechanisms are considered for decreased RNFL reflectance, including mitochondrial dysfunction and retinal ganglion cell apoptosis.
authors.affiliation: Department of Biomedical Engineering, University of Texas at Austin, Austin, Texas, USA.
authors.forename: Jordan
authors.initials: J
authors.lastname: Dwelle
authors.forename: Shuang
authors.initials: S
authors.lastname: Liu
authors.forename: Bingqing
authors.initials: B
authors.lastname: Wang
authors.forename: Austin
authors.initials: A
authors.lastname: McElroy
authors.forename: Derek
authors.initials: D
authors.lastname: Ho
authors.forename: Mia K
authors.initials: MK
authors.lastname: Markey
authors.forename: Thomas
authors.initials: T
authors.lastname: Milner
authors.forename: H Grady
authors.initials: HG
authors.lastname: Rylander
mesh_terms: D000818:Animals; D001718:Birefringence; D004195:Disease Models, Animal; D018450:Disease Progression; D005901:Glaucoma / Q000175:diagnosis*; D007429:Intraocular Pressure; D008252:Macaca fascicularis; D008253:Macaca mulatta; D009412:Nerve Fibers / Q000473:pathology*; D009901:Optic Nerve Diseases / Q000175:diagnosis*; D010865:Pilot Projects; D012165:Retinal Ganglion Cells / Q000473:pathology*; D041623:Tomography, Optical Coherence