What Causes Glaucoma

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Elevated Eye Pressure: The Main Driver of Glaucoma Glaucoma often begins when aqueous humor (the eye’s clear fluid) builds up, raising intraocular pressure (IOP). Normally this fluid drains freely from the front of the eye through the trabecular meshwork and a secondary uveoscleral pathway. If these drainage channels become blocked or less efficient – due to age-related changes or other damage – fluid cannot exit fast enough and pressure rises (). This chronic pressure pushes on the optic nerve at the back of the eye. Over time, the nerve fibers (which carry vision to the brain) are compressed and die, leading to the classic “cupping” of glaucoma and blind spots. For example, mutations in the MYOC gene cause a misfolded protein in the trabecular meshwork that raises IOP (), directly illustrating how fluid outflow problems lead to glaucoma.Normal-Tension Glaucoma: Beyond Pressure Not all glaucoma patients have high eye pressure. In normal-tension glaucoma (NTG), IOP remains in the normal range, yet optic nerve damage still occurs. Research suggests reduced blood flow to the optic nerve plays a key role. Insufficient eye or brain blood supply (for instance from vascular disease, nocturnal low blood pressure or migraine) starves nerve fibers of oxygen () (). In support, studies show NTG patients often have signs of poor circulation or systemic blood pressure dips, making the optic nerve more vulnerable. Another theory is low cerebrospinal fluid (CSF) pressure around the optic nerve may increase the pressure difference across the nerve head, squeezing it even when eye pressure is “normal.” Indeed, NTG patients were found to have lower CSF pressure than healthy people (). In short, NTG likely involves a “bad blood flow/bad fluid environment” effect: optic nerve cells are inherently sensitive, and factors like low blood or CSF pressure, plus other insults, can injure them even without high IOP () ().Genetic Causes of Glaucoma Family history is one of the strongest risks for glaucoma (). Specific gene mutations have been identified for different glaucoma types. For primary open-angle glaucoma (POAG), three genes stand out: MYOC, OPTN, and TBK1. MYOC (first discovered glaucoma gene) accounts for about 3–4% of typical open-angle cases with high IOP (). Mutant MYOC protein clogs the drainage meshwork, raising pressure (). The other genes, OPTN and TBK1, each cause roughly 1% of cases, usually in NTG (normal-pressure) patients (). These genes normally help cells clear waste and regulate survival, so when mutated they may impair cell housekeeping (autophagy) and trigger nerve-cell failure (). For congenital glaucoma (seen in babies and young children), the CYP1B1 gene is a leading cause (). CYP1B1 is involved in eye development; recessive mutations disrupt the drainage system before birth, so pressure builds early (). Other genes tied to childhood glaucoma include FOXC1 and PITX2, which guide eye/front structure development – mutations in these (often in Axenfeld-Rieger syndrome) lead to abnormal angles and drainage block () (). Rare TEK/ANGPT1 mutations (involved in forming fluid channels during development) also cause juvenile glaucoma (). For angle-closure glaucoma, the genetics are more complex and less clear-cut. This form depends on eye shape (shallow front chamber) more than one gene. Some studies have found key variants