normal pressure glaucoma
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2021 ◽  
Vol 62 (11) ◽  
pp. 1527-1538
Author(s):  
Joon Hyuck Jang ◽  
Kyung Wha Lee ◽  
Sung Uk Baek

Purpose: As routine health examinations become more common, many patients first diagnosed with glaucoma have advanced glaucoma. We analyzed the routes to diagnosis and the characteristics of patients initially diagnosed with advanced glaucoma.Methods: We retrospectively retrieved the medical records of patients first diagnosed with advanced glaucoma in our tertiary care center. The inclusion criteria were a mean deviation (MD) less than -12 dB on the visual field test, accompanied by structural damage. All patients were classified in terms of unilateral/bilateral disease, the intraocular pressure before medication, and lens status. We divided patients into those with monocular or binocular advanced glaucoma, high- or normal-pressure glaucoma, and those who were pseudophakic or phakic.Results: We included 73 patients of mean age 69.3 years. The visual field test MD was -19.6 dB. In those with binocular advanced glaucoma, incidental ophthalmic examination was the most common means of diagnosis (52.2%). Central-island visual field defects were the most common defects (54.2%). In those with monocular advanced glaucoma, glaucoma-associated symptoms most commonly triggered diagnosis (46.9%). Both superior and inferiorvisual field defects were the most common defects (42.8%). Glaucoma-associated symptoms were present in 68.2 and 22.8% of patients with high- and normal-pressure glaucoma, respectively. Central-island visual field defects were present in 43.6 and 29.4% of those with high- and normal-pressure glaucoma, respectively.Conclusions: We analyzed the routes to diagnosis and the clinical characteristics of patients with advanced glaucoma. In those with binocular disease, glaucoma was most commonly diagnosed on incidental ophthalmic examination. Central-island visual field defects were the most common defects in patients with binocular and high-pressure glaucoma, and the pseudophakic group. A multi-center longitudinal study on risk factors for delayed glaucoma diagnosis is needed.


Biomolecules ◽  
2021 ◽  
Vol 11 (9) ◽  
pp. 1258
Author(s):  
Shayshadri Mallick ◽  
Malini Sharma ◽  
Ajay Kumar ◽  
Yiqin Du

Glaucoma is clinically characterized by elevated intraocular pressure (IOP) that leads to retinal ganglion cell (RGC) and optic nerve damage, and eventually blindness if left untreated. Even in normal pressure glaucoma patients, a reduction of IOP is currently the only effective way to prevent blindness, by either increasing aqueous humor outflow or decreasing aqueous humor production. The trabecular meshwork (TM) and the adjacent Schlemm’s canal inner wall play a key role in regulating IOP by providing resistance when aqueous humor drains through the tissue. TM dysfunction seen in glaucoma, through reduced cellularity, abnormal extracellular matrix accumulation, and increased stiffness, contributes to elevated IOP, but current therapies do not target the TM tissue. Stem cell transplantation for regeneration and re-functionalization of damaged TM has shown promise in providing a more direct and effective therapy for glaucoma. In this review, we describe the use of different types of stem cells for TM regeneration in glaucoma models, the mechanisms of regeneration, and the potential for glaucoma treatment using autologous stem cell transplantation.


2019 ◽  
Vol 8 (6) ◽  
pp. 457-468 ◽  
Author(s):  
Jacky W.Y. Lee ◽  
Poemen P. Chan ◽  
XiuJuan Zhang ◽  
Li Jia Chen ◽  
Jost B. Jonas

2019 ◽  
Vol 8 (6) ◽  
pp. 419-421 ◽  
Author(s):  
Dennis S.C. Lam ◽  
Clement C.Y. Tham ◽  
Robert Ritch

2019 ◽  
Vol 97 (7) ◽  
Author(s):  
Karin R. Pillunat ◽  
Robert Herber ◽  
Eberhard Spoerl ◽  
Carl Erb ◽  
Lutz E. Pillunat

2018 ◽  
Vol 24 ◽  
pp. 1988-1996 ◽  
Author(s):  
Chunyu Guo ◽  
Ningbo Wu ◽  
Xiaoyin Niu ◽  
Yue Wu ◽  
Dongfeng Chen ◽  
...  

2016 ◽  
Vol 36 (3) ◽  
pp. 344-353 ◽  
Author(s):  
Christine C. Boucard ◽  
Sandra Hanekamp ◽  
Branislava Ćurčić-Blake ◽  
Masahiro Ida ◽  
Masaki Yoshida ◽  
...  

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