ABSTRACT
PURPOSE: Refined data analysis was performed to assess binocular visual field conservation in patients with bilateral glaucomatous damage to determine whether unilateral visual field loss is random, anatomically symmetric, or nonrandom in relation to the fellow eye. METHODS: This was a case-control study of 47 consecutive patients with bilaterally severe glaucoma; each right eye visual field locus was paired with randomly selected coisopteric left eye loci, with 760,000 (10,000 complete sets of 76 loci) such iterations performed per subject. The potential role of anatomic symmetry in bilateral visual field conservation was also assessed by pairing mirror-image loci of the paired fields. The mean values of the random coisopteric and the symmetric mirror pairings were compared with natural point-for-point pairings of the two eyes by paired t-test. RESULTS: Mean unilateral thresholds across the entire visual field were 18.9 dB left and 19.9 dB right (average 19.4), 4 dB lower than the better of the naturally paired concomitant loci of 23.4 dB (P < 10-15). A remarkable natural tendency for conservation of the binocular visual field was confirmed, far stronger than explicable by random chance or anatomic symmetry (P < 0.0001), and reaffirmed by subsequent prospective simultaneous binocular visual field retesting of an arbitrary subset (n = 16) of the study population (P < 0.0001). CONCLUSIONS: Refined data analysis of paired visual fields confirms the existence of a natural optimization of binocular visual function in severe bilateral glaucoma via interlocking fields that could be created only by central nervous system (CNS) involvement. TRANSLATIONAL RELEVANCE: Integrated bilateral visual field analysis should better define actual visual disability and more accurately reflect the functional efficacy of current ocular and future CNS-oriented therapeutic approaches to the treatment of glaucoma. Glaucomatous eyes provide a highly accessible paired-organ study model for developing therapeutics to optimize conservation of function in neurodegenerative disorders.