ABSTRACT
Dark adaptation (DA) refers to the slow recovery of visual sensitivity in darkness following exposure to intense or prolonged illumination, which bleaches a significant amount of the rhodopsin. This natural process also offers an opportunity to understand cellular function in the outer retina and evaluate for presence of disease. How our eyes adapt to darkness can be a key indicator of retinal health, which can be altered in the presence of certain diseases, such as age-related macular degeneration (AMD). A specific focus on clinical aspects of DA measurement and its significance to furthering our understanding of AMD has revealed essential findings underlying the pathobiology of the disease. The process of dark adaptation involves phototransduction taking place mainly between the photoreceptor outer segments and the retinal pigment epithelial (RPE) layer. DA occurs over a large range of luminance and is modulated by both cone and rod photoreceptors. In the photopic ranges, rods are saturated and cone cells adapt to the high luminance levels. However, under scotopic ranges, cones are unable to respond to the dim luminance and rods modulate the responses to lower levels of light as they can respond to even a single photon. Since the cone visual cycle is also based on the Muller cells, measuring the impairment in rod-based dark adaptation is thought to be particularly relevant to diseases such as AMD, which involves both photoreceptors and RPE. Dark adaptation parameters are metrics derived from curve-fitting dark adaptation sensitivities over time and can represent specific cellular function. Parameters such as the cone-rod break (CRB) and rod intercept time (RIT) are particularly sensitive to changes in the outer retina. There is some structural and functional continuum between normal aging and the AMD pathology. Many studies have shown an increase of the rod intercept time (RIT), i.e., delays in rod-mediated DA in AMD patients with increasing disease severity determined by increased drusen grade, pigment changes and the presence of subretinal drusenoid deposits (SDD) and association with certain morphological features in the peripheral retina. Specifications of spatial testing location, repeatability of the testing, ease and availability of the testing device in clinical settings, and test duration in elderly population are also important. We provide a detailed overview in light of all these factors.
ABSTRACT
PURPOSE: To report the successful treatment of a 78-year-old woman with bilateral mantle cell lymphoma involving the optic nerves. Chemotherapy initially was administered in the form of intravitreal methotrexate (MTX) monotherapy and was subsequently combined with systemic ibrutinib. METHODS: Retrospective case report. The diagnosis of CD5-negative mantle cell lymphoma was confirmed via immunohistopathological analysis of an axillary lymph node. Serial ophthalmologic examinations in conjunction with fluorescein angiography, fundus photography, and spectral domain optical coherence tomography were used to assess the treatment response. RESULTS: Prompt improvement in optic nerve infiltration, no significant side effects, and excellent tolerability were noted after two weekly injections of unilateral intravitreal MTX monotherapy. Combined systemic treatment with ibrutinib and bilateral weekly MTX intravitreal injections then resulted in continued regression of optic nerve infiltration bilaterally as confirmed by serial fundus photography and optical coherence tomography. After eight additional bilateral weekly injections, a mild MTX-associated keratopathy developed, which resolved promptly with cessation of injections and administration of topical lubrication. Six weeks after MTX cessation, but with continued ibrutinib treatment, the optic nerves revealed near-complete resolution of the lymphomatous infiltration and the visual acuity improved. CONCLUSION: Intravitreal MTX injections and systemic ibrutinib may represent effective treatment options for patients diagnosed with intraocular mantle cell lymphoma.