Primary Glaucoma

Primary glaucoma is a group of eye diseases that slowly injure the optic nerve without another eye problem causing it (that’s why we call it “primary”). The damage often happens because fluid inside the eye (aqueous humor) does not drain out properly. When drainage fails, pressure inside the eye (intra‑ocular pressure, or IOP) can rise, or the nerve may become vulnerable even at normal pressure. Over time, this pressure/stress kills the thin nerve fibers that make up the optic nerve. Once those fibers die, the blind spots in your side vision grow, and in late stages central vision can fail.

Think of the eye like a sink: the tap is the ciliary body making fresh fluid all the time, and the drain is the trabecular meshwork/Schlemm’s canal (main drain) and the uveoscleral pathway (backup drain). In primary glaucoma, the drain clogs, the flow out falls, or the nerve is too fragile—so pressure or strain hurts the nerve. The process is usually slow and painless, which is why many people don’t notice it until a lot of vision is gone. The goal of care is lowering the pressure/stress on the nerve and protecting nerve cells for life.

Types of Primary Glaucoma

1. Primary Open‑Angle Glaucoma (POAG). The drainage angle (where the cornea and iris meet) looks open on exam, but the inner drain (trabecular meshwork) doesn’t work well. IOP can be high or sometimes normal. Damage is slow and silent.
2. Primary Angle‑Closure Disease (PACD) / Primary Angle‑Closure Glaucoma (PACG). The drainage angle is physically narrow or closes. Fluid cannot reach the meshwork. Pressure may spike quickly (acute attack) or stay moderately high over time (chronic). Acute angle closure causes severe pain, halos, headache, and nausea—this is an emergency.
3. Normal‑Tension Glaucoma (NTG). Optic nerve damage and typical visual‑field loss happen even though IOP is in the “normal” range. The nerve is extra sensitive, or blood flow to the nerve is poor. Treatment still focuses on lowering IOP further and optimizing overall vascular health.
4. Primary Juvenile/Young‑Adult Open‑Angle Glaucoma. Similar mechanism to POAG but starts earlier (teens to 30s), often with higher pressures and a stronger genetic component.
5. Primary Congenital/Infantile Glaucoma (mentioned for completeness). A rare birth‑to‑early‑childhood form from developmental issues in the angle. It presents with light sensitivity, tearing, and enlarged, cloudy corneas. It requires urgent specialist surgery.

Causes and contributors

Glaucoma rarely has a single cause. Instead, many risk factors raise the chance that the optic nerve will be injured. Here are 20 important ones, explained simply.

1. Age (getting older).
   With age, the eye’s drainage filter can stiffen and clog, and the optic nerve becomes more vulnerable. Risk rises after age 40 and increases each decade.

2. Family history (genetics).
   If a parent or sibling has glaucoma, your risk is two to nine times higher. Certain gene changes (for example in MYOC, OPTN, TBK1) can increase risk in some families.

3. Race and ethnicity.
   People of African ancestry have higher risk of POAG and earlier onset. East and Southeast Asian populations have higher risk of angle-closure disease. Latino/Hispanic populations also have elevated POAG risk with age.

4. Elevated eye pressure (IOP).
   Higher IOP is the strongest modifiable risk. Not everyone with high IOP gets glaucoma, but lowering IOP slows damage for almost everyone who has glaucoma.

5. Thin central cornea (low CCT).
   A thin cornea can make measured pressure seem lower than true pressure and is also a biologic risk marker—eyes with thin corneas tend to have more fragile nerve support tissues.

6. Low corneal hysteresis (softer corneal “shock absorber”).
   Low corneal hysteresis suggests the eye’s tissues absorb stress poorly, which is linked to faster nerve damage at a given pressure.

7. Disc hemorrhages (tiny splinter bleeds on the optic disc).
   These small bleeds indicate ongoing stress at the nerve head and predict visual field worsening unless pressure is controlled.

8. Myopia (nearsightedness).
   In moderate to high myopia, the optic nerve head is stretched and structurally different, which can increase risk of POAG and complicate detection.

9. Hyperopia (farsightedness).
   Shorter, smaller eyes with shallow front chambers are prone to narrow or closed angles, raising the risk of angle-closure glaucoma.

10. Female sex (for angle-closure).
    Women are more likely to have narrow angles, partly because of eye anatomy differences, so angle-closure risk is higher.

11. Vascular dysregulation (poor blood flow control).
    Problems with small blood vessels—such as migraines, Raynaud-like symptoms, or night-time blood pressure dips—can starve the optic nerve of oxygen at critical times.

12. Low ocular perfusion pressure.
    If blood pressure is too low compared with eye pressure (especially at night), the optic nerve can be under-perfused, increasing damage risk even when IOP looks okay.

13. Obstructive sleep apnea.
    Sleep apnea causes oxygen drops and blood pressure swings at night. These changes can stress the optic nerve and worsen glaucoma in some people.

14. Diabetes mellitus.
    Diabetes can affect microcirculation and the quality of connective tissues, which may add risk and complicate management, though the link varies between studies.

15. Systemic hypertension and large BP variability.
    High blood pressure and big ups and downs in blood pressure can hurt the optic nerve’s steady flow needs—especially when over-treated at night.

16. Long-term steroid exposure (drops, pills, skin creams).
    Some people are steroid responders, meaning steroids make IOP climb. While steroid-induced glaucoma is technically secondary, the tendency to respond strongly is a personal risk you should tell your eye doctor about.

17. Eye anatomy that crowds the angle.
    A thick lens, forward iris, or plateau iris can narrow the angle and make angle closure more likely, especially in dim light or after certain medicines.

18. Oxidative stress and mitochondrial vulnerability.
    The optic nerve head is energy-hungry. Oxidative stress and mitochondrial strain may make nerve cells less able to handle pressure and blood-flow stress.

19. High fluctuation of IOP over 24 hours.
    Big swings in pressure, especially night-time peaks that clinic checks miss, can speed up damage. That’s why some people need 24-hour or home monitoring.

20. Earlier eye pressure spikes or trauma (even if remote).
    Past episodes of pressure spikes or blunt eye injury can leave the drain less efficient, nudging the eye toward glaucoma later in life.

Symptoms

Many people with primary glaucoma, especially open-angle types, feel fine until late. Still, there are warning signs and experiences worth knowing.

1. No symptoms at first.
   This is the most common “symptom.” You can feel normal while slow damage is happening.

2. Slow loss of side vision.
   You may start to miss things off to the side, bump into doorframes, or not notice a car in the next lane.

3. Trouble seeing in dim light.
   Driving at night, walking in a dark hallway, or moving from bright to dim rooms can feel unusually hard.

4. Needing more light to read.
   You may keep turning up lamps or using brighter bulbs to feel comfortable.

5. Glare and halos.
   Headlights or bright lights may cause glare or faint colored rings. (Halos are also common in angle-closure or with early cataract.)

6. Blurred or fluctuating vision.
   On some days or at some times, vision feels less crisp, then improves again.

7. Eye fatigue.
   Your eyes may feel tired after tasks that used to be easy, like reading or screen time.

8. Headaches or brow ache (especially with angle problems).
   A dull ache above the eye or brow can happen with pressure changes, more often in angle-closure situations.

9. Red eye during pressure spikes.
   The eye can look a bit red when pressure rises quickly.

10. Nausea or vomiting in acute angle closure.
    A sudden pressure attack from angle closure can cause severe pain, headache, nausea, and even vomiting—this is an emergency.

11. Sudden blurred vision with rainbow halos (acute angle closure).
    If the angle shuts quickly, vision can go foggy, with rainbow halos and a painful eye. Seek urgent care.

12. Frequent changes in glasses prescription.
    Repeated small changes, especially with myopia, can be a tip-off to check the optic nerve and pressure carefully.

13. Poor contrast sensitivity.
    Faint gray-on-gray details and low-contrast scenes become harder to see.

14. Difficulty with steps and curbs.
    Because side vision shrinks, judging edges and obstacles can become harder.

15. Late-stage tunnel vision.
    If untreated, side vision closes in, leaving tunnel vision; central vision can also be lost later.

Diagnostic tests

Your eye care team will mix and match tests from these groups. No single test tells the whole story. Doctors look for agreement between structure (imaging) and function (vision tests) over time.

Physical exam

1) Visual acuity (letters chart).
Measures how clearly you see at a distance. It doesn’t diagnose glaucoma by itself, but it sets a baseline and helps track other eye problems.

2) External and slit-lamp exam.
A slit-lamp microscope lets the doctor inspect the eyelids, cornea, anterior chamber, iris, and lens. They look for signs that mimic glaucoma (inflammation, pigment, pseudoexfoliation) and check for angle crowding clues.

3) Pupillary reactions (looking for RAPD).
Shining a light in each eye tests the afferent pathway. A relative afferent pupillary defect (RAPD) can suggest significant optic nerve or retinal damage in one eye.

4) Anterior chamber depth estimate (penlight/Van Herick).
A quick way to tell if the angle might be narrow. If the chamber is shallow, more detailed angle testing follows.

Manual/functional tests

5) Goldmann applanation tonometry (gold standard IOP).
A blue light probe gently touches a numbed cornea to measure eye pressure. It’s the most trusted clinic method.

6) Diurnal IOP curve or home IOP monitoring.
Pressure can spike outside clinic hours. Multiple readings across the day (or home measurements) reveal peaks and swings that matter for treatment.

7) Gonioscopy (static).
A mirrored contact lens lets the doctor look directly at the drainage angle. They note if it’s open, narrow, or closed and look for PAS (scar bands), pigment, or abnormal vessels.

8) Indentation gonioscopy (dynamic).
Gentle pressure with the lens can open a bowed-forward iris to see if closure is from pupil block or from plateau iris. This guides laser or surgical choices.

9) Standard automated perimetry (SAP).
You press a button when you see faint lights. The test maps your visual field to find and track blind spots typical of glaucoma. It’s key for monitoring change.

10) Central corneal thickness (pachymetry).
A small probe or optical device measures corneal thickness. Thin corneas mean higher true risk and can under-estimate pressure readings.

11) Corneal hysteresis (ocular biomechanics).
A specialized device gives a hysteresis number—a sign of how the cornea and, by proxy, the eye handles stress. Lower values are linked to faster progression.

Lab and pathological tests

These are not routine for most people with primary glaucoma, but can be used in special cases or to rule out other causes of optic nerve damage.

12) Genetic testing (selected families).
In early, severe, or strongly familial cases—especially in juvenile disease—testing for glaucoma-linked genes (like MYOC, OPTN, TBK1) may be considered to inform screening of relatives.

13) Systemic rule-out labs when the picture is atypical.
If the optic nerve looks unusual or vision loss is not matching glaucoma patterns, doctors may order labs (for example syphilis tests, autoimmune screens, B12) to rule out non-glaucoma neuropathies.

14) Medication history and steroid-response evaluation.
A careful review of steroid exposure (drops, pills, inhalers, creams) acts like a “functional lab”—identifying steroid responders who need special IOP strategies.

Electrodiagnostic tests

15) Pattern electroretinography (pERG).
Measures ganglion cell function directly. It can detect early dysfunction before visual field loss appears, helping confirm risk and track response.

16) Photopic negative response (PhNR, ERG component).
Another signal reflecting ganglion cell health. Lower PhNR amplitudes can support a glaucoma diagnosis and monitor progression.

17) Visual evoked potential (VEP/mfVEP).
Measures the brain’s response to visual patterns. Useful when fields are unreliable or to confirm asymmetry between eyes.

Imaging tests

18) Optical coherence tomography (OCT) of RNFL and macula (GCC/GCL+IPL).
OCT gives a cross-section picture of the retinal nerve fiber layer and ganglion cell complex. Thinning here correlates with damage and helps stage and follow glaucoma.

19) Stereoscopic optic disc photography / scanning laser ophthalmoscopy.
High-quality disc photos create a visual record of cupping, rim shape, and disc hemorrhages to compare over time.

20) Anterior segment OCT or ultrasound biomicroscopy (UBM).
These front-of-eye scans show the angle structures, iris position, and lens size. They help confirm plateau iris, pupil block, and angle crowding, guiding laser vs. surgical plans.

Non‑Pharmacological Treatments (Therapies & Others)

These methods support or, in some cases, replace drops. Always use them under your eye doctor’s guidance.

1. Selective Laser Trabeculoplasty (SLT). What: Gentle laser to the meshwork to improve drainage. Purpose: Lower IOP without daily drops; often first‑line in POAG/ocular hypertension. Mechanism: Biostimulation and remodeling of trabecular cells increases outflow.
2. Laser Peripheral Iridotomy (LPI). What: Tiny laser opening in the iris for narrow/closure‑prone angles. Purpose: Prevent or treat angle closure by letting fluid bypass the pupil block. Mechanism: Equalizes pressure between chambers so the angle opens.
3. Exercise Program (aerobic, moderate, regular). Purpose: Modestly lowers IOP and improves optic‑nerve blood flow. Mechanism: Lowers episcleral venous pressure, improves vascular health and insulin sensitivity.
4. Breath‑work/Yoga (avoid prolonged headstands). Purpose: Stress reduction without IOP spikes. Mechanism: Calms sympathetic tone; however, inverted poses raise IOP—avoid them.
5. Sleep Optimization (treat sleep apnea, elevate head ~20–30°). Purpose: Support nerve perfusion overnight; avoid nocturnal hypotension. Mechanism: Better oxygenation and stable perfusion pressure to the optic nerve.
6. Caffeine Moderation. Purpose: Prevent short‑term IOP spikes from large caffeine boluses. Mechanism: Caffeine can transiently raise IOP in some individuals.
7. Hydration Hygiene (avoid “water‑chugging”). Purpose: Prevent brief IOP spikes after rapid large fluid intake. Mechanism: Sudden aqueous production/venous changes increase pressure temporarily.
8. Smoking Cessation. Purpose: Improve micro‑circulation and reduce oxidative stress. Mechanism: Nicotine/carbon monoxide harm blood flow and mitochondria.
9. Weight and Cardiometabolic Care. Purpose: Better vascular health for the optic nerve. Mechanism: Blood‑sugar, lipid, and BP control stabilize perfusion.
10. Blue‑light/Glare Management. Purpose: Improve comfort and contrast in damaged fields. Mechanism: Filters and lighting reduce stray‑light glare around scotomas.
11. Low‑Vision Rehabilitation (as needed). Purpose: Maximize remaining vision with training/tools. Mechanism: Prism, contrast enhancement, orientation/mobility aids.
12. Medication Adherence Coaching. Purpose: Keep IOP low all the time; missed doses undo control. Mechanism: Reminders, app timers, and pairing drops with daily habits.
13. Steroid‑Smart Policy. Purpose: Avoid steroid‑induced IOP rise. Mechanism: Use the lowest dose, shortest time, or steroid‑sparing options; monitor IOP.
14. Dietary Nitrate‑Rich Foods (leafy greens, beet). Purpose: Support vasodilation to the optic nerve. Mechanism: Nitrates → nitric oxide → improved micro‑circulation.
15. Antioxidant‑rich Diet Pattern (berries, citrus, colorful veg). Purpose: Reduce oxidative stress on ganglion cells. Mechanism: Polyphenols and vitamins support mitochondrial defense.
16. Mindful BP Management (especially at night). Purpose: Avoid over‑lowering BP that starves the nerve in NTG. Mechanism: Coordinate with primary care to time meds and monitor nocturnal dips.
17. Proper Lighting & Contrast at Home. Purpose: Safer mobility, fewer falls. Mechanism: Increases visibility where side vision is weak.
18. Sunglasses/UV Protection Outdoors. Purpose: Comfort, glare reduction, and general ocular health. Mechanism: Blocks harsh light that worsens halos/glare.
19. Regular Follow‑Up Schedule. Purpose: Adjust treatment quickly if damage progresses. Mechanism: Serial OCT, fields, and IOP curves catch change early.
20. Education & Family Screening. Purpose: Catch disease earlier in relatives; improve your own self‑care. Mechanism: Awareness leads to earlier exams and lower lifetime IOP burden.

Drug Treatments

Always use exactly as your eye doctor prescribes. Doses below are typical adult examples; brands vary.

1. Prostaglandin analogs (latanoprost, travoprost, bimatoprost, tafluprost) Dose/Time: 1 drop nightly in affected eye(s). Purpose: First‑line IOP lowering; once‑daily convenience. Mechanism: Increases uveoscleral (and trabecular for bimatoprost) outflow. Side effects: Red eye, eyelash growth, darkening of iris/eyelids, peri‑orbital fat atrophy; rare inflammation.
2. Beta‑blockers (timolol, betaxolol, levobunolol) Dose/Time: 1 drop once or twice daily. Purpose: Add‑on or alternative when prostaglandin not enough/contraindicated. Mechanism: Decreases aqueous production. Side effects: Slow heart rate, low BP, bronchospasm (avoid in asthma/COPD), fatigue, depression; caution with systemic beta‑blockers.
3. Alpha‑2 agonists (brimonidine, apraclonidine) Dose/Time: 1 drop 2–3×/day. Purpose: Add‑on for extra IOP lowering; short‑term for pressure spikes. Mechanism: Lowers aqueous production and increases uveoscleral outflow; possible neuroprotective effects (studied). Side effects: Allergy/redness common, dry mouth, fatigue; avoid in infants.
4. Topical carbonic anhydrase inhibitors (dorzolamide, brinzolamide) Dose/Time: 1 drop 2–3×/day (often 2×/day in combos). Purpose: Add‑on therapy to reduce aqueous production. Mechanism: Blocks carbonic anhydrase in ciliary body → less fluid made. Side effects: Bitter taste, stinging, corneal issues rarely; sulfonamide cross‑reactivity is rare but possible.
5. Systemic carbonic anhydrase inhibitor (acetazolamide tablets) Dose/Time: 250 mg 2–4×/day (or 500 mg SR 2×/day) short‑term. Purpose: Rapid pressure reduction (e.g., acute angle closure or very high IOP) while definitive treatment is arranged. Mechanism: Strongly suppresses aqueous production. Side effects: Tingling, frequent urination, fatigue, metabolic acidosis, kidney stones, low potassium; avoid in sulfa allergy unless advised by specialist.
6. Rho‑kinase inhibitor (netarsudil) Dose/Time: 1 drop nightly. Purpose: Add‑on or alternative when others are not enough. Mechanism: Relaxes trabecular meshwork to increase outflow; lowers episcleral venous pressure. Side effects: Conjunctival redness, small corneal verticillata, mild discomfort.
7. Miotic (pilocarpine) Dose/Time: 1 drop 3–4×/day (varies by strength). Purpose: Helpful in angle‑closure mechanisms and post‑LPI plateau iris. Mechanism: Contracts the pupil and ciliary muscle to open the trabecular outflow. Side effects: Brow ache, small pupil (night vision issues), retinal detachment risk in predisposed patients.
8. Fixed‑combination drops (e.g., timolol/dorzolamide, brimonidine/timolol, brinzolamide/brimonidine, latanoprost/netarsudil) Dose/Time: Usually 2×/day (some nightly if prostaglandin combo). Purpose: Simplify multi‑drug regimens and improve adherence. Mechanism: Combines actions above. Side effects: Combination of each component; fewer preservatives if single bottle.
9. Hyperosmotic agents (mannitol IV, oral glycerol/isorbide) Dose/Time: Single course in emergency settings. Purpose: Rapidly reduce IOP in acute angle closure or before surgery. Mechanism: Draws fluid out of the eye by osmotic gradient. Side effects: Nausea, dehydration, electrolyte shifts; mannitol needs IV and monitoring.
10. Neuroprotective candidates (off‑label citicoline oral/eye, nicotinamide high‑dose with riboflavin co‑factor) Dose/Time: Varies (citicoline 500–1000 mg/day; nicotinamide often 1–3 g/day with B2 under supervision). Purpose: Support retinal ganglion cell metabolism in addition to pressure lowering. Mechanism: Mitochondrial support, membrane stabilization, NAD+ pathway support (research ongoing). Side effects: Nicotinamide can affect liver enzymes at high doses; use only with physician guidance.

Dietary Molecular & Supportive Supplements

Evidence varies; these are adjuncts, not cures. Discuss with your doctor, especially if pregnant, on blood thinners, or with liver/kidney disease.

1. Nicotinamide (Vitamin B3) ± riboflavin: 500–1000 mg/day (research doses higher under supervision). Function: Support ganglion cell energy. Mechanism: Boosts NAD+ pools and mitochondrial resilience.
2. Citicoline: 500–1000 mg/day. Function: Neuro‑support. Mechanism: Provides choline and cytidine for neuronal membranes and neurotransmission.
3. Coenzyme Q10: 100–200 mg/day. Function: Antioxidant for mitochondria. Mechanism: Electron transport support; reduces oxidative stress.
4. Ginkgo biloba extract (EGb 761): 60–120 mg/day. Function: Micro‑circulation/antioxidant. Mechanism: Improves blood flow; scavenges free radicals (caution with anticoagulants).
5. Omega‑3 fatty acids (EPA/DHA): 1–2 g/day combined. Function: Vascular and anti‑inflammatory support. Mechanism: Improves endothelial function and tear film.
6. Lutein + Zeaxanthin: 10 mg + 2 mg/day. Function: Retinal antioxidant support. Mechanism: Filters blue light; quenches oxidative stress.
7. Anthocyanins (bilberry/blackcurrant): per label (often 80–160 mg anthocyanins/day). Function: Antioxidant/vascular support. Mechanism: Polyphenols aiding micro‑vessels.
8. Resveratrol: 150–250 mg/day. Function: Antioxidant/mitochondrial signaling. Mechanism: Sirtuin pathways; anti‑oxidative effects.
9. Alpha‑lipoic acid: 300–600 mg/day. Function: Antioxidant recycling. Mechanism: Regenerates vitamins C and E, supports mitochondria.
10. Magnesium (glycinate/citrate): 200–400 mg elemental/day. Function: Vascular tone and sleep support (NTG). Mechanism: Vasodilation, neuronal stability.
11. Vitamin D3: 1000–2000 IU/day (or per level). Function: General neuro‑immune balance. Mechanism: Receptor‑mediated anti‑inflammatory actions.
12. Curcumin (enhanced bioavailability forms): 500–1000 mg/day. Function: Anti‑inflammatory/antioxidant. Mechanism: NF‑κB modulation.
13. N‑acetylcysteine (NAC): 600–1200 mg/day. Function: Glutathione support. Mechanism: Provides cysteine to make glutathione.
14. Taurine: 500–1000 mg/day. Function: Retinal cell support. Mechanism: Osmoregulation and mitochondrial protection (preclinical data).
15. Green tea catechins (EGCG standardized): per label (e.g., 200–300 mg/day). Function: Antioxidant. Mechanism: Reduces oxidative stress; supports vascular health.

Regenerative/Stem‑Cell” Drug Concepts

These are investigational or specialist‑guided. They are not replacements for pressure‑lowering therapy.

1. Nicotinamide riboside or nicotinamide + pyruvate “metabolic support” regimens (dosing individualized). Function: Boost retinal ganglion cell energy and survival. Mechanism: Enhances NAD+; supports mitochondria.
2. Citicoline (oral or eye drops) neuro‑support (500–1000 mg/day oral; drops per label where available). Function: Membrane and neurotransmitter support. Mechanism: Phospholipid precursor; neurotrophic signaling.
3. Ciliary neurotrophic factor (CNTF) delivery (intraocular implants in trials). Function: Direct neurotrophic protection. Mechanism: Trophic support pathways to ganglion cells.
4. Stem‑cell–derived retinal ganglion cell/optic‑nerve support (experimental). Function: Replace/support damaged cells. Mechanism: Cell replacement or trophic paracrine effects; currently research only.
5. Gene‑targeted therapy for specific mutations (e.g., MYOC) (experimental). Function: Correct causal gene dysfunction. Mechanism: Lowers misfolded protein stress in trabecular meshwork.
6. Rho‑kinase–mediated neuroregeneration strategies beyond IOP lowering (preclinical). Function: Promote axon growth and improve perfusion. Mechanism: Cytoskeleton/vascular modulation.

Surgical Options

1. Selective Laser Trabeculoplasty (SLT) (listed above as non‑drug because it’s an office laser; included here for context). Procedure: Outpatient laser to the trabecular meshwork. Why: First‑line or add‑on to lower IOP without drops; can be repeated.
2. Trabeculectomy. Procedure: Creates a controlled new drainage pathway (filter/bleb) under the upper eyelid. Why: Powerful and durable pressure lowering when drops/laser aren’t enough or disease is advanced.
3. Glaucoma drainage devices (tubes/shunts; e.g., Ahmed, Baerveldt). Procedure: A tiny tube shunts fluid from inside the eye to a plate reservoir. Why: For eyes at high risk of trabeculectomy failure or after prior surgeries.
4. Minimally invasive glaucoma surgery (MIGS; e.g., iStent, Hydrus, Kahook Dual Blade, OMNI, XEN gel stent). Procedure: Small internal devices or micro‑incisions that bypass or reshape the drain, often combined with cataract surgery. Why: Moderate pressure reduction with faster recovery and safety; good for mild‑to‑moderate disease.
5. Cyclophotocoagulation (transscleral or endoscopic). Procedure: Laser partially reduces the ciliary body’s fluid production. Why: For advanced/refractory cases where other surgeries failed or are unsuitable.

Choosing surgery depends on target IOP, disease stage, cornea/conjunctiva status, cataract presence, and your ability to use drops.

 Prevention & Protection Tips

1. Regular eye exams starting by age 40 (earlier with family history).
2. Know your numbers: IOP, corneal thickness, OCT baseline, and field results.
3. Use drops exactly as prescribed and don’t run out.
4. Tell every doctor you see that you have glaucoma—especially before steroids.
5. Exercise regularly (most days) and avoid long inverted yoga poses.
6. Treat sleep apnea and keep your head slightly elevated at night.
7. Don’t chug large amounts of water at once; sip through the day.
8. Moderate caffeine; avoid big single doses.
9. Stop smoking; limit alcohol binges.
10. Eat a colorful, nitrate‑rich diet (leafy greens, beets, berries, citrus, fish).

When to See a Doctor (or Go to the ER)

• Immediately (ER/urgent): Sudden severe eye pain, a very red eye, halos around lights, blurred vision with headache/nausea—possible acute angle closure.
• Soon (within days): New glare/halos, eye ache, or vision dips if you already have glaucoma.
• Routine (per plan): Regular checks every 3–12 months depending on stage. More often after medication changes or if OCT/fields are unstable.

What to Eat & What to Avoid

1. Eat leafy greens daily (spinach, kale, arugula): natural nitrates for blood‑flow support.
2. Add beets or beet juice a few times per week for nitric‑oxide support.
3. Choose fatty fish 2–3×/week (salmon, sardines, mackerel) for omega‑3s.
4. Snack on berries and citrus for vitamin C and polyphenols.
5. Use nuts/olive oil/avocado for healthy fats that help vessels.
6. Stay well hydrated but sip—avoid sudden large volumes at once.
7. Moderate caffeine (e.g., 1–2 coffees/day) and avoid mega‑shots.
8. Limit ultra‑processed foods, excess salt, and added sugars that harm vessels.
9. Avoid smoking and vaping—they hurt micro‑circulation.
10. If drinking alcohol, keep it light—binges can destabilize BP and sleep.

 Frequently Asked Questions

1. Can glaucoma be cured? No. Damage already done cannot be reversed, but lowering IOP prevents more loss.
2. If my pressure is “normal,” can I still have glaucoma? Yes—this is called normal‑tension glaucoma; treatment still aims to lower IOP further.
3. Do I need drops forever? Often yes. Some people switch to laser or surgery to reduce drops, but lifelong monitoring continues.
4. Is SLT as good as starting drops? Many patients do just as well starting with SLT; it avoids daily drops and systemic side effects.
5. Will glasses fix glaucoma vision loss? No. Glasses correct focus, not nerve damage. Low‑vision aids can help you use remaining vision better.
6. Do phone/TV screens cause glaucoma? No. They don’t raise glaucoma risk, though long screen time can cause dry eye.
7. Can I fly or travel at altitude? Yes for most people; check with your surgeon soon after eye surgery.
8. Are prostaglandin drops safe long‑term? Yes for most; they are first‑line and work 24 hours with 1 nightly dose.
9. What if one drop causes side effects? Tell your doctor—there are many alternatives and combinations.
10. Can diet or supplements replace drops? No. Diet helps overall nerve health, but pressure lowering is essential.
11. Is cannabis helpful? It can briefly lower IOP but is impractical and may have systemic effects; it’s not recommended as primary therapy.
12. Should I avoid all steroids? Not always. Sometimes they are needed, but your IOP must be monitored, and alternatives used when possible.
13. How do doctors set my “target pressure”? Based on your current damage, age, cornea thickness, and rate of change; targets often drop over time if progression is seen.
14. Can cataract surgery help glaucoma? It often lowers IOP a little and can widen the angle in angle‑closure eyes; MIGS can be added at the same time.
15. What happens if I do nothing? Glaucoma usually advances, silently shrinking side vision until central vision is threatened.