Low-Tension Glaucoma: An Oxymoron in Ophthalmology

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

Disclosures

Prev Chronic Dis. 2019;16(1):e10 

In This Article

Is Low-tension Glaucoma a Disease on the Spectrum of Primary Open-angle Glaucoma?

When in 1857 Albrecht von Graefe described a form of glaucoma manifesting damage to the optic nerve head and an open anterior chamber angle, with IOP within the reference range, digital palpation tonometry was considered the gold standard. If he had used an impression tonometer to measure IOP, the major shortcoming of the tonometry would have been that it displaced so much fluid upon contact with the eye that the measured readings would be highly variable and inaccurate. Conversely, if he had used indentation tonometry, it would not have considered the misclassification resulting from the presence of a thin central corneal.[1] Many diagnoses of LTG were for eyes with thin corneas and were based on false low values for IOP, a finding that casts some doubts on the diagnosis of LTG.[5] Furthermore, the absence of elevated IOP must be found on measurements performed more than one time or during daytime, since IOP shows diurnal and nocturnal fluctuations in healthy subjects, and even more in patients with POAG or LTG.[6] For variations in IOP, 3 populations of LTG patients may be distinguished: patients without IOP fluctuations, patients with diurnal IOP acrophase (the crest or peak of a cycle), and patients with nocturnal IOP acrophase.[7] Patients in the 2 last categories should be considered true POAG patients rather than LTG patients, in whom glaucomatous optic neuropathy occurs despite normal IOP. It is likely that patients with a diurnal or nocturnal acrophase have been enrolled in studies based on the mechanical theory; reduction of IOP might slow down the progression of visual field loss only in these patients.[8] Data from the Low-Pressure Glaucoma Treatment Study highlighted the role of IOP in LTG pathogenesis; the progression of visual field loss was reduced by 9.1% with timolol 0.5% and by 39.1% with brimonidine 0.2% after 2 years of treatment.[8] However, in this study, IOP values were recorded exclusively during daytime. Thus, whether patients with a worse visual field had IOP nocturnal acrophase is unknown. Other studies on asymmetric LTG reported that the eye with higher IOP shows greater glaucomatous damage than the eye with lower IOP, which sustains the role of IOP in the pathogenesis.[9] Yet, in all these clinical trials IOP was measured only during office hours; thus, the behavior of nocturnal IOP was not recorded. A recent study in which nychthemeral IOP curves were evaluated with a telemetric sensor showed a nocturnal acrophase with IOP spikes in patients with LTG, although these spikes were at significantly lower levels than the spikes found among patients with POAG.[7] This study reported that IOP peaked at night in 40% to 80% of patients with normal-tension glaucoma, and the pattern in these patients was similar to the pattern in patients with POAG. In 24-hour curves, patients with LTG and POAG had more pronounced patterns of IOP in the evening and night than in the morning, with more peaks and greater IOP fluctuation during the night than during the evening.[7] Other factors may corroborate the hypothesis of a primary IOP-related mechanical stress in LTG, such as the presence of changes in the aqueous humor outflow pathways similar to those occurring in POAG.[10]

In patients where LTG can be considered a disease on the spectrum of POAG, diagnostic and therapeutic strategies similar to those for patients with hyperbaric glaucoma must be implemented, with the help of an ophthalmologist (Figure).

Figure.

Proposed flowchart of optic neuropathy, with specialist referral, according to the nychthemeral IOP characteristics. Abbreviations: CCT, central corneal thickness; IOP, intraocular pressure; POAG, primary open-angle glaucoma.

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