Glaucoma pathophysiology: Difference between revisions
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief: Rohan Bir Singh, M.B.B.S.[2]
Pathophysiology
Primary Open Angle Glaucoma
The underlying pathogenesis of glaucoma is attributed to retinal ganglion cell death due to elevated the level of intraocular pressure. The intraocular pressure is determined by the balance between secretion of aqueous humor by the ciliary body and its drainage through the two pathways i.e. the trabecular meshwork and uveoscleral outflow pathway. The increased resistance to aqueous outflow via the trabecular meshwork leads to open angle glaucoma. However the angle-closure glaucoma occurs due to the obstruction in access to the drainage pathways .There is increasing evidence of ocular blood flow to be involved in the pathogenesis of glaucoma. Current data indicate that fluctuations in blood flow are more harmful in glaucomatous optic neuropathy than steady reductions. Unstable blood pressure and dips are linked to optic nerve head damage and correlate with visual field deterioration.
A number of studies also suggest that there is a correlation, not necessarily causal, between glaucoma and systemic hypertension (i.e. high blood pressure). In normal tension glaucoma, nocturnal hypotension may play a significant role. On the other hand there is no clear evidence that vitamin deficiencies cause glaucoma in humans, nor that oral vitamin supplementation is useful in glaucoma treatment[1].
References
- ↑ Rhee DJ, Katz LJ, Spaeth GL, Myers JS (2001). "Complementary and alternative medicine for glaucoma". Surv Ophthalmol. 46 (1): 43–55. PMID 11525790.