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Related Concept Videos

Glaucoma: Overview01:25

Glaucoma: Overview

665
Glaucoma is an eye condition characterized by increased intraocular pressure that damages the retina and optic nerve, leading to irreversible blindness if left untreated. The human eye has various components, including the cornea, iris, pupil, lens, and optic nerve. Aqueous humor is secreted by the epithelium of the ciliary body in the posterior chamber and flows through the trabecular meshwork and canal of Schlemm, maintaining normal intraocular pressure. The trabecular meshwork and the canal...
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Open Angle Glaucoma: Treatment01:27

Open Angle Glaucoma: Treatment

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In open-angle glaucoma, the iridocorneal angle remains open, but the trabecular meshwork becomes stiff, slowing down the outflow of aqueous humor. This causes a buildup of aqueous humor in the anterior chamber, leading to a sudden increase in intraocular pressure. The treatment for open-angle glaucoma focuses on reducing the elevated intraocular pressure by either decreasing the secretion of aqueous humor or increasing its outflow.
Drugs such as carbonic anhydrase inhibitors, α2- and...
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Angle Closure Glaucoma: Treatment01:28

Angle Closure Glaucoma: Treatment

600
Angle-closure glaucoma, or closed-angle glaucoma, is an eye condition where the iris bulges out and blocks the iridocorneal angle, resulting in a buildup of aqueous humor and increased intraocular pressure. Immediate medical attention is necessary due to the sudden onset of symptoms. The treatment for angle-closure glaucoma includes short-term and long-term approaches. Short-term treatment involves using eye drops like pilocarpine to lower intraocular pressure by increasing aqueous humor...
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Updated: Aug 7, 2025

Full-Circle Cauterization of Limbal Vascular Plexus for Surgically Induced Glaucoma in Rodents
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Choroidal Microvasculature Dropout in Glaucoma.

Yanzhi Guo1, Shouyue Huang1, Shushu Xu1

  • 1Department of Ophthalmology, Ruijin Hospital Affiliated Medical School, Shanghai Jiaotong University, Shanghai, China.

Seminars in Ophthalmology
|March 7, 2023
PubMed
Summary
This summary is machine-generated.

Parapapillary choroidal microvasculature dropout (CMvD) is linked to optic nerve head perfusion issues, potentially worsening glaucoma. This review explores CMvD

Keywords:
Choroidal microvasculature dropoutGlaucoma prognosisglaucoma pathogenesispathological changesvisual field loss

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Area of Science:

  • Ophthalmology
  • Neuroscience
  • Vascular Biology

Background:

  • Glaucoma, a leading cause of irreversible blindness, involves optic nerve atrophy and visual field defects, often linked to elevated intraocular pressure (IOP).
  • Vascular factors are increasingly recognized as crucial in glaucoma pathogenesis, influencing disease development and progression.
  • Parapapillary choroidal microvasculature dropout (CMvD) is associated with impaired optic nerve head (ONH) perfusion, suggesting a role in glaucoma progression.

Approach:

  • This review synthesizes current literature to comprehensively understand the relationship between CMvD and glaucoma.
  • It examines how CMvD relates to key glaucomatous pathological processes and clinical outcomes.
  • The review focuses on up-to-date research to elucidate the pathogenic role and prognostic implications of CMvD in glaucoma.

Key Points:

  • CMvD is closely associated with changes in retinal nerve fiber layer (RNFL) thickness and lamina cribrosa (LC) morphology.
  • Impaired optic nerve head perfusion, indicated by CMvD, correlates with reduced peripapillary vessel density (cpVD).
  • CMvD is linked to visual field (VF) defects and impacts the overall prognosis of glaucoma.

Conclusions:

  • CMvD is a significant factor in glaucoma, affecting ONH perfusion and contributing to disease progression.
  • Understanding the link between CMvD and glaucoma pathogenesis is vital for improving diagnostic and prognostic capabilities.
  • Further research is needed to fully elucidate the pathogenic role of CMvD and its clinical implications for glaucoma management and patient outcomes.