Mechanisms of Cupping in Non-Glaucomatous Optic Neuropathies The term “cupping” in this review will refer to the enlargement of the cup-to-disc ratio determined by clinical examination. 4 The focus of this review is to describe the non-glaucomatous optic neuropathies that may present with cupping and review clinical features that may help differentiate nonglaucomatous cupping from glaucoma. 5 Trobe et al showed that 44% of eyes with nonglaucomatous optic atrophy were misdiagnosed as showing glaucoma in fundus stereophotographs by at least one observer. The highest payouts for medicolegal insurance claims were found to involve missed or poorly followed intracranial tumors causing optic nerve and visual field changes. Reviewing old records is also usually helpful since previous optic disc edema or a normal appearance of the optic nerve with vision loss argue against glaucoma. The history of presenting illness is also important since acute vision loss and rapid vision loss are less likely to be glaucomatous unless there is a corresponding high intraocular pressure. When there is advanced cupping and the visual function is severely depressed, this can be even more challenging and ancillary testing such as magnetic resonance imaging of the orbits with contrast may be necessary. 4 However, clinically differentiating glaucomatous and non-glaucomatous optic nerve cupping remains challenging even for experienced observers, especially since pallor is a subjective sign. Nonglaucomatous optic disc cupping is well known to occur with greater neuroretinal rim pallor and less profound excavation than seen in glaucoma and often has different visual manifestations. This cupping may be physiologic or related to a non-glaucomatous process and the better recognized processes include compressive optic neuropathies, hereditary optic neuropathies and arteritic anterior ischemic optic neuropathy. Diagnosis may become challenging if intraocular pressure remains within the generally considered normal limits and optic disc cupping is present. It also produces characteristic visual field defects such as nasal steps and arcuate defects. Glaucoma is also well known to spare central visual acuity and color vision until late stages. 1–3 When intraocular pressure is high, diagnosis of glaucoma is relatively easy. Based on initial histopathological studies, the optic nerve cupping in glaucoma was thought to result from the loss of ganglion cell axon fibers and thinning and the posterior displacement of the lamina cribrosa. Since its discovery over 170 years ago, a large volume of the literature on optic disc cupping has accumulated, yet the mechanism is still not fully understood. “Cupping” is a term used to describe enlargement of the cup-to-disc ratio and is widely recognized as a feature of glaucoma however, it is not pathognomonic. In this review, we review the non-glaucomatous causes of cupping and provide an approach to evaluating a patient that presents with an enlarged cup-to-disc ratio. Ancillary testing such as optical coherence tomography of the retinal nerve fiber layer and ganglion cell layer-inner plexiform layer may also be helpful in localizing the disease. The patient’s medical history, history of presenting illness, visual function (visual acuity, color vision and visual field testing) and ocular examination also need to be considered. Classically, the optic nerve in non-glaucomatous causes has pallor of the neuroretinal rim, but the optic nerve should not be examined in isolation. Differentiating glaucomatous and non-glaucomatous optic nerve cupping remains challenging even for experienced observers. The former is a shallow form of cupping and related to loss of retinal ganglion cells, whereas the latter involves damage to the lamina cribrosa and peripapillary scleral connective tissue. Cupping is thought to consist of two main components: prelaminar and laminar thinning. ![]() The most well-recognized non-glaucomatous optic neuropathies that cause cupping include compressive optic neuropathies, arteritic anterior ischemic optic neuropathies, hereditary optic neuropathies, and optic neuritis. Optic nerve cupping or enlargement of the cup-to-disc ratio is widely recognized as a feature of glaucoma, however it may also occur in non-glaucomatous optic neuropathies.
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