Low-Tension Glaucoma: An Oxymoron in Ophthalmology

Ciro Costagliola, MD; Luca Agnifili, MD, PhD; Leonardo Mastropasqua, MD; Alfonso di Costanzo, MD


Prev Chronic Dis. 2019;16(1):e10 

In This Article

Should LTG be Included in a Spectrum of Congenital and Acquired Optic Neuropathies That can Simulate a Glaucomatous Optic Neuropathy?

When the more frequent causes of optic disc cupping have been excluded, the possibility of a neurodegenerative optic neuropathy should be considered. These cases are the most frustrating, because optic disc damage progresses even after IOP has been lowered. Many congenital and acquired optic neuropathies are included in this group of cases, and differentiation between glaucomatous and nonglaucomatous cupping can be challenging even for experienced observers.[13] Among the congenital forms of optic disc cupping, megalopapilla, autosomal dominant optic atrophy, and Leber hereditary optic neuropathy could produce an optic disc excavation simulating glaucomatous optic neuropathy.

The acquired neuropathies might be secondary to inflammatory, compressive, toxic, and traumatic causes. Optic neuritis may produce an increase of the cup-to-disc ratio that, although unilateral, may be confused with glaucomatous optic neuropathy. Compressive lesions including meningioma, pituitary adenoma, craniopharyngioma, and internal carotid artery aneurysm may lead to asymmetric optic disc cupping and erroneously attributed to LTG. Methanol and ethambutol poisoning might produce a bilateral optic disc cupping similar to glaucomatous optic neuropathy, secondary to axonal loss. Thus, when an asymmetric enlarged cup is observed, further neuro-ophthalmologic investigation is necessary.[13]

Lastly, among conditions leading to optic disc cupping, aging has a main role. Harju et al found that the degree of optic disc cupping increased in healthy older study participants because of physiological fiber loss. Their study population was appropriate and represented a set of healthy eyes without glaucoma; throughout 11 years of follow-up, no study participants developed visual field changes, and no significant rise in IOP was recorded.[14] In this latter case, a complete diagnostic examination for neurological diseases must be conducted, with the help of a neurologist (Figure).

Improvements in diagnostic techniques make it easier than before to classify optic disc cupping; a description of optic disc characteristics combined with the imaging of the retinal nerve fiber layer and optic disc topography permits differentiation between glaucomatous and nonglaucomatous optic disc cupping. Moreover, a careful analysis of patient history, together with morphologic and functional assessment of the optic nerve, helps to identify disorders.

The term LTG could be an oxymoron, a nostalgic memory of the past when a defined diagnosis was not possible. Using the term is like using the word "fever" when there is no high temperature or saying festina lente ("more haste, less speed"). The term LTG may be misleading or inaccurate, because it refers to a mechanical problem of IOP, whereas optic disc cupping and visual field loss in eyes with normal intraocular pressure are caused by other factors. Therefore, in the presence of optic disc cupping with normal IOP, ophthalmologists should investigate other plausible causes of optic nerve damage besides intraocular pressure.