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H. Zwick, B.E. Stuck, J. Brown, S. Ruiz, B.J. Lund; Neural plasticity and accidental human laser macular injury. Journal of Vision 2002;2(7):62. doi: 10.1167/2.7.62.
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© ARVO (1962-2015); The Authors (2016-present)
Purpose: To evaluate mechanisms of long term recovery of visual function based on three human laser accident cases and the remarkable recovery these cases demonstrated in the presence of macular damage. Methods: Visual acuity, contrast sensitivity, eye movement fixation pattern, the FM 100 hue color discrimination test and anomaloscope matches were used in analysis of visual function. CSLO Ophthalmoscopy and Optical Coherence Tomography (OCT) characterized the presence of retinal traction, scar, thickness and hole formation. Ophthalmoscopy was used to evaluate preferred retinal location (PRL) in focal contrast sensitivity tests. Results: Visual acuity, contrast sensitivity and color vision recovered within 3 months (cases 1 and 2). In case 1, a thinner than normal foveal thickness was measured with OCT. Foveal OCT measurements (case 2) showed a break in foveal thickness. Foveal PRL measurements indicated functionality for case 1 and non foveal functionality for case 2 which developed a new PRL superior temporal to the fovea. Color vision metrics (case 3) recovered completely within 12 months post. Visual acuity and contrast sensitivity were near full recovery at two years post. OCT imaging revealed a macular hole at 3 months post and ophthalmoscopy revealed the presence of traction about the hole. At 12–24 months considerable “filling” of the hole appeared with the absence of traction. Ocular motility involved foveal and parafoveal retina. Conclusion: These cases suggest that morphological changes in retinal recovery may induce higher order visual brain centers to accept weaker retinal afferent signals from damaged retinal sites. More severe scar and traction limit retinal and cortical neural plasticity.
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