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Editors Selection IGR 7-3

Clinical Forms of Glaucoma: Edema of the Outflow Pathway May Be the Cause Hypertension in Posner-Schlossman Syndrome

Comment by Ursula Schlötzer-Schrehardt on:

98432 Morphology of the Trabecular Meshwork and Schlemm's Canal in Posner-Schlossman Syndrome, Yan X; Li M; Wang J et al., Investigative Ophthalmology and Visual Science, 2022; 63: 1

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Posner-Schlossman syndrome (PSS), also known as glaucomatocyclitic crisis, is a rare unilateral disease characterized by recurrent episodes of anterior uveitis and acute rises in IOP, which may lead to chronic secondary glaucoma. Although etiology and pathophysiology of PSS are still unclear, infectious and autoimmune causes have been proposed as potential triggers. Structural alterations of the trabecular meshwork, including trabeculitis and trabecular outflow obstruction by inflammatory cells or pigment, have been suggested as potential causes of IOP elevation.¹

This cross-sectional observational study presents the first description of morphological changes of trabecular meshwork (TM) and Schlemm's canal (SC) in 45 patients with PSS using in-vivo SS-OCT imaging. The patients revealed transient episodes of IOP elevation, mild anterior chamber inflammation and open chamber angles and were divided into two subgroups with ocular hypertension (OHT) and ocular normal tension (ONT); their unaffected fellow eyes served as controls. TM and SC parameters were measured in nasal and temporal quadrants on 2D cross-sectional images. TM thickness, SC area and SC diameter were found to be significantly greater in the affected eyes of all PSS patients and the OHT subgroup only compared to the fellow eyes. TM thickness was either positively or negatively correlated with IOP in the OHT and ONT subgroups, respectively. From these observations, the authors conclude that edematous thickening of TM, by narrowing trabecular outflow spaces, may contribute to IOP elevation in PSS patients.

The strength of this study is that it is the first to analyze the morphological changes of TM and SC using high-resolution in-vivo imaging of anterior segment structures in PSS patients. However, there are several weaknesses, which include: (1) the use of 2D cross-sectional images instead of 3D volumetric scans; (2) the lack of intra- and interobserver reproducibility measurements; (3) no correlation of findings with the presence of viral infection and keratic precipitates; and (4) insufficient methodological details on image acquisition, such as light conditions, anatomical landmarks to ensure comparable area scans, etc. Most importantly, anti-inflammatory and IOP-lowering medications, which might have affected the morphology of TM and SC, have not been taken into account, even though several studies have reported that glaucoma treatments can change the TM and SC morphology.² Finally, it may be considered that TM thickening could be also caused by inflammatory infiltrations rather than edema. A histopathological analysis of a trabeculectomy specimen provided evidence of numerous mononuclear cells accumulating in the trabecular spaces, which were suggested to increase aqueous outflow resistance.³ Although the present study confirms involvement of the trabecular meshwork in PSS-associated hypertension, further studies are needed to provide a more accurate understanding of the mechanisms of IOP elevation in PSS patients.

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