Pedram Hamrah, MD is the Interim Chairman, Department of Ophthalmology and Professor of Ophthalmology at Tufts University School of Medicine in Boston. Dr. Hamrah trained in Ocular and Transplantation Immunology at the Schepens Eye Research Institute of Mass. Eye and Ear. He has authored over 50 peer-reviewed articles, over 30 reviews, and book chapters, and has given more than 60 lectures and presentations worldwide. He serves on numerous editorial boards and is a peer reviewer for over 45 ophthalmology, immunology, and transplantation journals.
This abstract was originally presented at the 2019 ARVO Annual Meeting, held in Vancouver, Canada, April 28 – May 2, 2019.
Structural and Functional Corneal Nerve Abnormalities suggest the Neurosensory Origin of Contact Lens Discomfort
Gabriela Dieckmann, Yashar Seyed-Razavi, Neslihan Dilruba Koseoglu, Arsia Jamali, Cecilia Chao, Anam Akhlaq, Afsun Sahin, Stephanie Cox, Ricardo Nos, Pedram Hamrah
Contact lens discomfort (CLD) results in discontinuation of contact lens wear. However, due to a lack of understanding on the mechanisms of CLD, interventions to alleviate CLD have failed in many patients. This study aims to assess the morphological and functional changes in sensory corneal nerves in order to understand CLD pathophysiology.
91 subjects were recruited in this prospective, cross-sectional, single-center study, and divided into 5 groups: asymptomatic contact lens wearers (ACLW, n=18); symptomatic contact lens wearers (SCLW, n=19); intolerant contact lens wearers (ICLW, n=18); neuropathic corneal pain patients (NCP, n=18) and normal controls (n=18). Cold and polymodal corneal nociceptors were stimulated applying topical cold 0.9% saline or hypertonic 5% sodium chloride. Evoked responses were registered according to the visual analogues scale (VAS) for pain (0-10). Analysis was performed based on the changes of VAS before and after instillation. Corneal in vivo confocal microscopy was performed to analysis of nerve density and number of micro-neuromas in a masked fashion.
Mean total nerve density was reduced in SCLW and ICLW groups (14.8±4.9, 13.6±3.0) compared to controls (19.0±4.5, p<0.05) and were similar to NCP patients (13.0±5.6). Analysis of micro-neuromas revealed an increased density in SCLW and ICLW (0.44±0.46, 0.96±0.68, p<0.05) compared to controls (0.03±0.10), at similar levels to NCP (0.79±0.91). The number of patients with micro-neuromas increased between groups (controls: 7.7%, ACLW: 27.8%, SCLW: 68.4%, ICLW: 83.3% and NCP: 94.4%). Baseline VAS scores were only increased in symptomatic SCLW, ICLW, and NCP groups (2.6 ± 3.2, 2.7 ± 2.2, 5.4 ± 2.7, p<0.001). Changes in baseline VAS were increased for all symptomatic groups (by 2.3±2.5, 3.5±3.1, 2.7±2.3 respectively) compared to controls and ACLW (0.2±0.7, p<0.001). The response to cold saline was not significant between groups (p=0.38). Micro-neuromas density correlated with both hypertonic saline response (r=0.327, p=0.003) and baseline pain levels (r=0.325, p<0.02), hypertonic saline response correlated with baseline pain levels (r=0.457, p<0.001).
Morphological and functional changes of sensory corneal nerves present in SCLW and ICLW, suggest the neurosensory nature of the CLD pathophysiology.