A 65-year-old man presented with bilateral, painless, progressive blurring of vision over 9 years. Slit-lamp examination revealed bilateral subepithelial corneal opacities in clusters located at the mid-periphery. Anterior segment optical coherence tomography, in vivo confocal microscopy (IVCM), serum protein electrophoresis, and molecular genetic testing were performed to evaluate the cause of corneal opacities. Anterior segment optical coherence tomography revealed a band-like, hyperreflective lesion in the Bowman layer and anterior stroma of both corneas. IVCM revealed hyperreflective deposits in the epithelium, anterior stroma, and endothelium. Serum protein electrophoresis identified the presence of paraproteins (immunoglobulin kappa), and molecular genetic testing revealed absence of mutations in the transforming growth factor beta-induced gene (<i>TGFBI</i>) and collagen type XVII alpha 1 gene (<i>COL17A1</i>). The ocular diagnosis of paraproteinemic keratopathy eventually led to a systemic diagnosis of monoclonal gammopathy of undetermined significance by our hematologist/oncologist. Paraproteinemic keratopathy is a rare differential diagnosis in patients with bilateral corneal opacities and therefore may be misdiagnosed as corneal dystrophy or neglected as scars. In patients with bilateral corneal opacities of unknown cause, serological examination, adjunct anterior segment imaging, and molecular genetic testing play a role in establishing the diagnosis.

To study the changes in corneal nerves and corneal sensitivity over a 6-month period in patients with herpes zoster ophthalmicus (HZO) compared with healthy subjects. METHODS: This was a prospective longitudinal study on patients with newly diagnosed HZO. In vivo confocal microscopy (IVCM) corneal nerve parameters and corneal sensitivity were measured and compared between eyes with HZO, contralateral eyes and controls at baseline, 2 and 6 months. RESULTS: Fifteen subjects with HZO and 15 healthy age and sex matched controls were recruited. HZO eyes revealed a reduction in corneal nerve branch density (CNBD) from baseline to 2 months (9.65 ± 5.75 vs. 5.90 ± 6.87/mm 2 , p = 0.018), and decreased corneal nerve fibre density (CNFD) at 2 months when compared with control (p = 0.025). However, these differences resolved by 6 months. HZO fellow eyes demonstrated increased corneal nerve fibre area (CNFA), corneal nerve fibre width (CNFW) and corneal nerve fractal dimension (CNFrD) at 2 months compared with baseline (p = 0.025, 0.031, 0.009). There was no change in corneal sensitivity for both HZO affected and HZO fellow eyes from baseline or over time, nor was it different from sensitivity in controls. CONCLUSION: Corneal denervation was present at 2 months in HZO eyes, with an observed recovery by 6 months. HZO fellow eyes demonstrated increased corneal nerve parameters at 2 months, which could represent a proliferative response to nerve degeneration. IVCM is useful in monitoring corneal nerve changes, and is more sensitive in detecting nerve alterations than esthesiometry.