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Introduction Yes – glaucoma often runs in families, but the story is far more complex than a single “glaucoma gene.” Having a first-degree relative (parent, sibling, or child) with glaucoma raises your own risk dramatically – by roughly 4 to 9 times compared with the general population (). In other words, family history is a very strong warning flag. However, most cases of glaucoma are not caused by one single inherited mutation. Instead, glaucoma is usually a polygenic, multifactorial disease – meaning that dozens or even hundreds of common genetic variants each add a little to risk, and environmental factors (age, blood pressure, steroid use, etc.) also play key roles. In this article we unpack the genetics: identifying the handful of rare genes that can cause glaucoma on their own, and explaining the vast network of other genes that subtly raise risk. We also explore how genetic risk varies among ethnic groups, what exciting new genetic tests and treatments are on the horizon, and what patients should do today with family history or genetic test results in hand.Monogenic Glaucoma – When One Gene Drives the Disease A few glaucoma genes follow classic “Mendelian” inheritance (like sickle cell or cystic fibrosis), especially in early‐onset cases. These are relatively rare but have very high impact. We highlight the major ones: MYOC (myocilin). This was the first glaucoma gene discovered. Mutations in MYOC cause juvenile and adult primary open-angle glaucoma (POAG). In juvenile-onset glaucoma (ages ~3–40), MYOC mutations appear in roughly 10% of patients () (up to ~30–36% in some early studies). In adult POAG (onset after age 40), MYOC mutations account for about 3–5% of cases (). These mutations act in a dominant way; if you have one bad copy of MYOC you have high lifetime risk of glaucoma (). For example, a common MYOC mutation called p.Gln368Ter is found almost exclusively in people of European descent and by itself gives a very high risk – population studies show that carriers of this variant have about a 7-fold higher odds of POAG than non-carriers () (). (Not everyone with the mutation gets glaucoma, illustrating that other factors matter too.) OPTN (optineurin) and TBK1 (TANK-binding kinase 1). These two genes are linked to normal‐tension glaucoma (NTG), a form of open-angle glaucoma that occurs even when eye pressure is not elevated. In rare families with aggressive NTG, mutations in OPTN or duplications of TBK1 have been found (). These mutations also act in a dominant fashion. Because OPTN and TBK1 are involved in cellular stress and death pathways, their discovery showed that neurodegenerative mechanisms (not just high pressure) can drive glaucoma (). CYP1B1. This gene (encoding a cytochrome P450 enzyme) is the major cause of primary congenital glaucoma (PCG) – glaucoma that appears at birth or in infancy. Mutations in CYP1B1 are autosomal recessive, meaning a child must inherit two bad copies (one from each parent) to develop the disease. Worldwide, CYP1B1 mutations are by far the most common cause of PCG, especially in populations with high family marriage rates (). (In one large review, over 70 different CYP1B1 mutations were identified in PCG patients from many countries ().) Because this is a well-established cause, any child with true congenital glaucoma is usually offered genetic

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This audio article is from VisualFieldTest.com.

Read the full article here: https://visualfieldtest.com/en/what-is-narrow-angle-glaucoma

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What Is Narrow-Angle Glaucoma?Primary glaucoma is usually thought of as “open-angle” glaucoma, where the eye’s drainage system (the trabecular meshwork in the angle between the cornea and iris) remains open. Narrow-angle glaucoma – also called angle-closure glaucoma – is different. In these eyes the front part of the eye is crowded: the iris (the colored part) sits too close to the drainage angle, blocking fluid outflow. Tiny pores in the drainage tissue can become partially or fully sealed by the iris. This stops aqueous humor from draining normally and causes eye pressure (intraocular pressure, or IOP) to rise quickly () (). In open-angle glaucoma, pressure usually rises slowly over years and damages nerves little by little. In contrast, narrow angles can abruptly trap fluid, driving IOP sky-high in hours – a spike that can destroy optic nerve fibers very quickly if untreated () (). High pressure in the eye leads to irreversible vision loss if not relieved. In fact, studies show angle-closure glaucoma causes blindness far more often than open-angle disease (). Although rare compared to open-angle glaucoma, angle-closure attacks can be catastrophic. It is one of the few true eye emergencies, because vision can be lost in a matter of hours without treatment () (). Anatomy: Closed Angle vs. Open AngleTo understand narrow angles, imagine the anterior chamber of the eye (space between cornea and iris) as a bowl. In open-angle glaucoma this bowl is deep enough that fluid (the aqueous humor) easily flows through the angle at the periphery. In narrow-angle glaucoma, the inner wall of the bowl (iris) bows forward toward the outer wall (cornea). This flattens and narrows the angle through which fluid drains () (). A helpful way ophthalmologists define angle-closure is by how much the iris touches the trabecular meshwork. If more than half of the meshwork is blocked by iris contact, the angle is considered “closed” (). In practice, doctors use gonioscopy – a special contact lens with mirrors – to shine light into the angle and see how open it is (). With gonioscopy they can see if the iris is bumping into the drainage site. In short, angle-closure glaucoma means the drainage pathway is physically narrowed or sealed off by the iris, whereas open-angle glaucoma means the pathway remains open but becomes clogged or inefficient in other ways.The Spectrum of Angle-Closure DiseaseNarrow angles come in degrees. Some people are “angle-closure suspects” with anatomically narrow angles but no glaucoma damage yet. Others progress to chronic or acute closure. Narrow Angles (Angle-Closure Suspect) Some eyes simply have naturally shallow anterior chambers. These eyes are at risk: the iris is closer to the angle than normal, but fluid still drains (though a little slower). Many people with narrow angles never have symptoms or vision loss. We call them “suspects” or “pre-glaucoma.” They have narrow angles on exam, but pressure and nerve health remain normal. Such eyes need monitoring and often preventive treatment because they can progress to true angle-closure. Chronic Angle-Closure Glaucoma (Subacute, Insidious) Over time, a narrow angle can develop synechiae (iris adhesions) – patches where the iris sticks to the meshwork. This can block drainage bit by bit. Chronic angle-closure glaucoma often has no warning p

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Glaucoma is often called the “silent thief of sight.” In primary open-angle glaucoma (POAG) – the most common form worldwide – patients usually notice nothing at all until the disease is advanced (). In fact, eye doctors warn that POAG is essentially asymptomatic in early stages. The optic nerve slowly deteriorates over years, chipping away at peripheral vision without causing any pain or obvious change in sharpness. Imagine bumping into objects at the edges of your vision, missing curb steps, or failing to see people approaching from the side – these subtle clues can appear, but often go unnoticed for so long that about 40% of retinal nerve fibers are already lost before patients report any “tunnel vision” or vision loss (). By then, glaucoma’s real symptom is finally felt: the absence of any warning at all. As POAG progresses, symptoms emerge only gradually. Patients may describe difficulty discriminating contrast, or an unusual glare or halo around lights – especially when driving at night. In fact, research shows many people with glaucoma have trouble with glare and low-contrast vision (). Bright headlights or sunlit road signs may seem to wash out, and vision transition from dark to light can become jarring. These symptoms are often dismissed as normal aging or unrecognized cataracts. Over time, the visual field continues to constrict like tunnel vision, and central vision can slowly be affected. Reading small print, recognizing faces, or navigating unfamiliar routes then become more challenging. By the late stages of POAG, even straight-ahead vision can blur, greatly impacting daily activities. Acute Angle-Closure Glaucoma Unlike POAG’s silent course, acute angle-closure glaucoma presents suddenly and dramatically. This is a true emergency. Patients develop a sprinter’s warning sign of symptoms: intense eye pain, severe headache, and visual disturbances all at once. The affected eye turns red and feels very hard. Vision blurs and patients often see colored halos around lights. The episode may trigger nausea, vomiting, and even abdominal pain. In fact, one eye care protocol notes that acute angle-closure can mimic a neurological or gastrointestinal emergency: patients can be misdiagnosed with migraine, sinus headache or severe stomach sickness (). This is dangerous – without immediate treatment (often within hours) to lower the eye’s pressure, permanent vision loss can result (). In short, sudden eye pain plus headache and nausea demands an immediate emergency response. Subacute (“Intermittent”) Angle-Closure Glaucoma Some people experience intermittent angle-closure attacks – shorter, milder episodes that come and go. These attacks can cause dull brow or eye ache, foggy/blurry vision, and exploitable haloes around lights, especially after activities that dim the pupil (for example, moving into a dark room). Each episode may resolve on its own, so patients often ignore it or think it was just a bad headache. Indeed, studies found that many people with subacute angle-closure glaucoma first complain of recurring headaches and are mistakenly treated for migraines (). Because each attack is brief, it’s easy to blame them on stress or sinus troubles instead of underlying eye pressure spikes. Over time, however, these repeated IOP surges cause adhesions in the angle and l

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