Normal-tension glaucoma: an update

Abstract

However, several structural and functional differences support the fact that different mechanisms may have a stronger role in the pathogenesis of NTG versus high-pressure POAG. Also, a recent study reported genetic variants associated with different tendencies towards POAG with lower or higher IOP (6) . Furthermore, clinical impression and anecdotal evidence suggest that NTG with mean IOP in the high teens (>15 mmHg), in which circadian fluctuation and CCT could lead to a possible misdiagnosis of an IOP ≤21 mmHg, would differ from NTG with mean IOP in the low teens (≤15 mmHg), with different ABSTRACT Descritores: Glaucoma de ângulo aberto; Pressão in traocular; Doenças do nervo óptico; Anti-hipertensivos/uso terapêuticopathogenesis and progression patterns, harder to achieve target IOP, and higher incidence of disc hemorrhages. Nonetheless, a recent report does not support this assumption and underscores low-teens NTG as an important entity (7) . The proportion of NTG varies depending on different population studies. In Asian epidemiological protocols, NTG constituted the majority of open-angle glaucomas (52%-92%), depending on the country and study methodology (8) . Normal IOP was measured in 57.1% cases of POAG in a South African study (9) . In white populations, the proportion of NTG was lower than that observed in Asian and African populations. In studies conducted in the United States, Netherlands, and Italy, NTG presented proportions of 31. 7%, 38.9%, and 30%, respectively (10-12) . The etiology of NTG is most likely multifactorial and still not well defined. Moreover, several alternative treatments based on this different pathogenesis have been discussed. The objective of this study was to review the mechanisms involved in the onset and progression of NTG and the efficacy of established and alternative therapies for NTG treatment. PathogenesisThe pathogenesis of NTG is unclear, and perhaps the development of the disease is a consequence of a complex interaction of several systemic and ocular factors. Different studies have shown that the cardiovascular system and intracranial pressure may be involved in the main pathways of optic nerve damage. Nevertheless, the complex relationship between these mechanisms and glaucoma pro gression continues to be debated.

Investigation of lateral geniculate nucleus volume and diffusion tensor imaging in patients with normal tension glaucoma using 7 tesla magnetic resonance imaging

“…The idea of glaucoma being always related to an elevated intraocular pressure (IOP) with the mechanistic explanation of pressure induced damage of the optic nerve is widespread, however, up to 40% of glaucoma patients in Caucasian populations present with an IOP within the physiological range (≤ 21 mmHg). This subtype of normal tension glaucoma (NTG) shows the same peripapillary retinal nerve fiber layer (RNFL) thinning and subsequent visual field defects as the high pressure glaucoma phenotype [ 15 ].…”

Laser speckle flowgraphy derived characteristics of optic nerve head perfusion in normal tension glaucoma and healthy individuals: a Pilot study

“…(≤21 mmHg) 1 . Even though the exact pathogenesis of NTG remains uncertain, it is understood that the disease develops as a consequence of several systemic and ocular factors 3 . There is some evidence that reduced optic nerve head microcirculation is associated with glaucoma progression 4 , 5 but the exact relation between reduced blood flow and the disease process remains unknown 6 , 7 .…”

The association of toll-like receptor 4 gene polymorphisms with primary open angle glaucoma susceptibility: a meta-analysis

“…Our meta-analysis was based on systematic collected studies relating to TLR4 gene polymorphisms and glaucoma. To our knowledge, this is the first study that attempted to combine the POAG and NTG studies because these two types of glaucoma are overlapping in some factors [5,6]. Interestingly, combined analysis showed rs1927911, rs12377632, and rs2149356 in the allele contrast model were strongly associated with glaucoma (POAG and NTG) suggesting that the POAG and NTG share some pathogenesis factors that may relate to TLR4.…”

“…POAG and NTG share similarities in phenotypes composed of having normal anterior chamber angles, peripapillary retinal nerve fiber layer (RNFL) thinning, glaucomatous optic neuropathy (GON), and corresponding visual field (VF) defects. Therefore, it is believed that POAG and NTG illustrate a continuum of open-angle glaucoma in which there is a difference in some causative factors and IOP [5,6]. Although the precise and accurate molecular mechanisms of POAG and NTG have not been investigated, it is possible that patients with POAG and NTG have some overlapping factors in both multiple genetic and environmental interactions.…”