Patterns of ganglion cell complex (GCC) loss detected by optical coherence tomography provide an objective measure of optic nerve injury. These patterns aid in early diagnosis and localization of chiasmal lesions.
Twenty-three patients with chiasmal compression seen between 2010 and 2015 were imaged with the Cirrus high-definition optical coherence tomography macular cube 512 × 128, retinal nerve fiber layer (RNFL) scan protocols and automated (30-2 Humphrey) visual fields (VFs). Age-matched controls were included for comparison. Generalized estimating equations were performed comparing RNFL and GCC thicknesses between patients and their controls. Effect size (d) was calculated to assess the magnitude of difference between patients and controls. The average GCC and RNFL thicknesses also were correlated with VF mean deviation (MD). Pre operative average GCC thickness was correlated to post operative VF MD.
Patterns of GCC thinning corresponded to VF defects. The average GCC thickness was 67 ± 9 μm in patients and 86 ± 5 μm in controls (P < 0.001). The effect size was the greatest for GCC thickness (d = 2.72). The mean deviation was better correlated with GCC thickness (r2 =0.25) than RNFL thicknesses (r2 =0.15). Postoperatively, VF MD improved in 7 of 8 patients with persistent nasal GCC thinning. Six patients had no VF defect and showed statistically significant loss of GCC compared with controls (P = 0.001).
Distinct patterns of GCC loss were identified in patients with chiasmal compression. Binasal GCC loss was typical and could be seen with minimal or no detectable VF loss. Thinning of the GCC may be detected before loss of the RNFL in some patients. After decompression, the majority of patients showed improvement in VF despite persistent GCC loss. Patients with less GCC loss before decompression had better postoperative VFs. Therefore, GCC analysis may be an objective method to diagnose and follow patients with chiasmal lesions.
New England Eye Center (MG, TRH, JH, NE, LNV, GKA, CEM), Tufts Medical Center, School of Medicine, Tufts University, Boston, Massachusetts
Dysautonomia Center (CEM), NYU Langone Medical Center, Schools of Medicine, New York University, New York, New York.
Address correspondence to Thomas R. Hedges III, MD, Department of Ophthalmology, Tufts Medical Center 800 Washington Street, Boston, MA 02111; E-mail: firstname.lastname@example.org
C. E. Mendoza-Santiesteban receives research support from The Dysautonomia Foundation, Inc. and The Massachusetts Lions Clubs/Research to Prevent Blindness Challenge Grant. He has served as a consultant/advisory board member for EISAI/H3, Roland Consult, and Carl Zeiss Meditec. T. R. Hedges receives research support from The Massachusetts Lions Clubs/Research to Prevent Blindness Challenge Grant. This work was supported in part by a Research to Prevent Blindness Challenge Grant to the New England Eye Center/Department of Ophthalmology, Tufts University School of Medicine, National Institutes of Health (NIH) contracts RO1-EY11289-24, R01-EY13178-10, R01-EY013516-07, Air Force Office of Scientific Research FA9550-07-1-0101 and FA9550-07-1-0014. The sponsors had no role in the design or conduct of this research. The project described was supported by the National Center for Advancing Translational Sciences, National Institutes of Health, award number UL1TR001064. The content is solely the responsibility of the authors and does not necessarily represent the official views of the NIH. The other authors report no conflict of interest.