How long before symptoms appear?

Glaucoma is silent in its early stages. Central vision is preserved for a long time. The first signs appear in the peripheral visual field, but a large proportion of ganglion cell fibers can be lost before any defect is detected (Kerrigan-Baumrind, IOVS 2000).

Optic neuropathy

Glaucoma — protecting your optic nerve

Q: Can glaucoma cause blindness?

Glaucoma is one of the leading causes of irreversible blindness worldwide. But when it is detected early and treated appropriately, its progression can be significantly slowed, preserving functional vision over the long term. Hence the importance of screening.

Q: Normal eye pressure = no glaucoma?

No. There is a form called normal-tension glaucoma, in which IOP stays within the usual range despite genuine optic nerve damage. This is why a complete work-up (OCT, visual field) is still necessary, even when IOP appears normal.

Q: SLT or eye drops as first-line treatment?

Both are first-line options. The LiGHT trial (Gazzard, Lancet 2019, confirmed at 6 years in Ophthalmology 2023) showed that SLT is at least as effective as eye drops, better tolerated, and associated with better long-term control. The choice remains individualized.

Q: Can eye drops be stopped after surgery?

Sometimes yes, often partially. The goal is to reach the target IOP. Surgery provides a greater and more lasting IOP reduction, but some patients remain on one or two eye drops to secure the result.

Q: Should both eyes be operated on the same day?

Rarely. The more affected eye is operated on first, and we wait for the result before considering the second eye. This limits risk and allows a gradual adjustment.

Q: Is sport allowed with glaucoma?

Yes, for most activities, especially moderate aerobic exercise (walking, swimming, cycling). To avoid: sports with a risk of eye trauma (boxing), prolonged head-down positions (inverted yoga) and deep diving.

Q: Is glaucoma hereditary?

Partly, yes. Having an affected first-degree relative increases the risk (up to about ×4). Regular screening from age 40 is recommended for close relatives (parents, brothers, sisters).

Glaucoma is a progressive, silent optic neuropathy: there are no symptoms at an early stage, but the loss of nerve fibers is irreversible. It is one of the leading causes of irreversible blindness worldwide. Detected early and treated appropriately, its progression can be significantly slowed, which reduces the risk of disabling vision loss.

At the practice, I offer a comprehensive assessment based on the reference tests (Goldmann tonometry, RNFL and GCC OCT, automated visual field testing, gonioscopy) and stepwise care: eye drops, SLT laser, or filtering surgery — including new-generation techniques such as the Preserflo MicroShunt or the Paul implant for refractory glaucoma in previously operated eyes.

Tonometry RNFL OCT Visual field SLT laser Filtering surgery

Book a glaucoma screening ↗ When should you get screened?

Glaucomatous optic disc — deep cupping and thinning of the neuroretinal rim, seen at the slit lamp

Understanding

What is glaucoma?

Glaucoma is a progressive optic neuropathy characterized by damage to the optic nerve with loss of retinal ganglion cell fibers. It is often, but not always, associated with raised intraocular pressure (IOP).

The optic nerve: a fragile structure

Your optic nerve collects visual signals from the retina and carries them to the brain through about 1 million nerve fibers. Glaucoma gradually destroys these fibers, creating blind areas that first appear in the periphery and then slowly spread.

The optic disc cupping (the "cup" at the center of the optic nerve head) enlarges and the neuroretinal rim thins. This damage is irreversible.

The mechanism: hypoxia and mechanical stress

High IOP = compression of the optic nerve at the optic disc. This reduces microcirculation and causes progressive hypoxia of the axons. An inflammatory component adds to and amplifies the damage.

Epidemiology and what is at stake

76 million people affected worldwide in 2014 (Tham et al., Ophthalmology). Projection: 111 million by 2040.

One of the leading causes of irreversible blindness worldwide. Unlike cataract (which is curable), vision lost to glaucoma cannot be recovered.

Key point: 50% of patients are unaware they have glaucoma. Routine screening after age 40 = essential.

Classification

The main types of glaucoma

Primary open-angle glaucoma (POAG)

80% of cases

The most common form. Painless, with slow and insidious progression. The anterior chamber angle is open (normal gonioscopy). IOP is often, but not always, raised. Screening = key.

Angle-closure glaucoma

Acute or chronic

Pupillary block obstructs outflow. Acute attack: an emergency (pain, reduced vision, halos, nausea, IOP > 40). Chronic: gradual progression. Anatomy: bowed iris / anteriorly positioned lens.

Normal-tension glaucoma

IOP < 21 mmHg

Genuine optic nerve damage (cupping, visual field loss) despite "normal" IOP. Mechanism: increased sensitivity of the optic nerve to IOP and/or vascular dysregulation. About 30% of glaucoma cases in Asia.

Secondary glaucomas

Identified cause

Pseudoexfoliation, pigmentary, neovascular, steroid-induced, post-traumatic, uveitic. Management = treating the cause + controlling IOP.

Primary prevention

Risk factors & screening

Recognizing the risk factors helps determine who should be screened and how often.

Major risk factors

Age > 40 — 5% of the population at age 70
First-degree family history — risk ×4
African-Caribbean descent — 3–4× more glaucoma, and more severe
Ocular hypertension (IOP 22–30 mmHg without damage)
High myopia — a "more vulnerable" optic disc
Previous eye trauma
Long-term corticosteroid therapy (oral, inhaled)
Diabetes, sleep apnea

When should screening start?

From age 40 if there is no particular risk
From age 35–40 if there is a family history
From age 30 if of African-Caribbean descent or highly myopic
Every 2 years if IOP is normal and there is no risk factor
Every 1–2 years if there is ocular hypertension or one risk factor
Every year if glaucoma is suspected or at an early stage
Every 3–4 months if glaucoma is confirmed and treated

A silent disease: Symptoms appear only late (loss of the upper visual field, then of the whole field). Early diagnosis can only come from routine screening. Never wait for symptoms.

Clinical signs

Symptoms are rare and late

Chronic glaucoma — no symptoms

No pain
Vision remains good for a long time (the macula is relatively spared in the early phase)
The patient "feels nothing"
Late onset: loss of peripheral visual field, "bumping into furniture", hemianopia
Up to 25–50% of ganglion cell fibers can be lost before a defect becomes detectable on the visual field (Kerrigan-Baumrind, IOVS 2000)

Acute angle-closure attack — EMERGENCY

Severe eye pain (may radiate to the head)
Rapid drop in vision
Colored halos around lights (light scattered by corneal edema)
Nausea, vomiting
Conjunctival redness, mid-dilated pupil
IOP rises > 40–60 mmHg within a few hours
Immediate treatment: emergency eye care, eye drops, diuretics, YAG laser iridotomy

Explanatory diagram

Normal optic disc vs glaucomatous optic disc

At the practice

A complete glaucoma work-up

Screening and diagnosis rest on three pillars: tonometry, optic disc examination, and imaging (OCT, visual field). Here are the key screening figures and the essential tools.

≥40 yrs

Routine screening recommended

~5%

Prevalence at age 70

76M

Glaucoma patients worldwide (Tham 2014)

Major

Cause of irreversible blindness in the Western world

Pillar 1

Tonometry

Measurement of intraocular pressure. Goldmann tonometry remains the reference standard; iCare and air-puff (non-contact) tonometers are alternatives. The reading is interpreted in light of corneal pachymetry.

Pillar 2

Dilated fundus examination

Assessment of the optic nerve: size of the cup (cup/disc ratio), asymmetry between the two eyes, peripapillary hemorrhages. The ISNT rule (Inf ≥ Sup ≥ Nas ≥ Temp) helps identify abnormal thinning.

Pillar 3

RNFL & GCC OCT

Objective measurement of the thickness of the retinal nerve fiber layer (RNFL) and of the macular ganglion cell complex (GCC). Serial comparison over time is essential to detect change.

Pillar 4

Automated visual field testing

Functional assessment (often Humphrey 24-2). The MD, PSD and VFI indices track progression. Anderson's criteria help distinguish a glaucomatous defect from an artifact.

Pillar 5

Gonioscopy

An essential examination of the iridocorneal angle using a mirrored lens. It distinguishes open-angle from angle-closure glaucoma (Shaffer classification) and looks for secondary signs (pigment, exfoliation, synechiae).

Pillar 6

Optic disc photography

Annual photographic documentation. Qualitative comparison over time remains a valuable complement to OCT for spotting subtle changes in the optic nerve.

Pillar 7

Additional tests

Depending on the context: anterior segment OCT or UBM (suspected angle closure), 24-hour IOP curve, corneal hysteresis measurement (ORA) — useful in normal-tension glaucoma.

Follow-up and target

Treatment monitoring & the target IOP concept

Follow-up frequency adapted to the stage

Suspected glaucoma (isolated ocular hypertension): every 6–12 months. Early (abnormal OCT, normal visual field): 3–4 months. Moderate: 3–4 months. Advanced: 2–3 months (higher risk of progression ↑).

Tests at each visit and according to stage

At every visit: IOP measurement (Goldmann tonometry) and slit-lamp examination of the optic disc. RNFL and GCC OCT: at regular intervals depending on the stage and stability. Automated visual field: repeated every 6 to 12 months depending on the stage and rate of progression (more often in rapidly progressing or advanced glaucoma). Annual optic disc photography is useful for qualitative comparison over time.

Target IOP — a fundamental concept

The target IOP is the pressure level at which the disease is expected to be stabilized. It is expressed as a percentage reduction from the baseline IOP (measured before treatment) and depends on the stage of glaucoma (the more advanced the disease, the lower the target), the rate of progression and personal risk factors (age, family history, visual life expectancy). This target is individualized and reassessed regularly.

Criteria for progression

Visual field progression: MD decline ≥ 1 dB/year over 2 tests. OCT: RNFL thinning ≥ 1 μm/year. Optic disc: deepening of the cup or a new hemorrhage. If the disease progresses despite treatment → escalation (more eye drops, SLT, or surgery).

Medical treatment

Eye drops — 5 drug classes

Eye drops lower IOP by reducing aqueous humor production or by increasing its outflow.

Prostaglandin analogues (latanoprost, travoprost, bimatoprost, tafluprost)

Mechanism: increased uveoscleral outflow. Role: first-line medical treatment because of their IOP-lowering efficacy and good overall tolerability. Possible side effects: conjunctival hyperemia, lengthening and darkening of the eyelashes, hyperpigmentation of the iris and periorbital skin. Several preservative-free formulations are available (recommended when the ocular surface is fragile).

Beta-blockers (timolol, betaxolol)

Mechanism: reduced aqueous humor production. Role: effective, long-established drugs, often used second-line or in fixed combinations. Contraindications: asthma, COPD, bradycardia, atrioventricular block, uncontrolled heart failure. Betaxolol is cardioselective (fewer pulmonary contraindications but a weaker IOP-lowering effect).

Carbonic anhydrase inhibitors (dorzolamide, brinzolamide)

Mechanism: reduced aqueous humor secretion. Role: often in fixed combinations. Side effects: bitter taste, stinging, foreign body sensation. Caution in patients with a history of kidney stones.

Alpha-2 agonists (brimonidine)

Mechanism: dual action — reduced secretion and increased outflow. Side effects: conjunctival allergy is relatively common, drowsiness, dry mouth. A gradual loss of efficacy (tachyphylaxis) may occur.

Rho kinase inhibitors (netarsudil — available in France as the fixed combination Roclanda®)

Mechanism: increased trabecular outflow and reduced episcleral venous pressure — a mechanism complementary to the other classes. Availability in France: marketed as Roclanda® (netarsudil + latanoprost fixed combination). Side effects: frequent conjunctival hyperemia, reversible corneal deposits, possible small subconjunctival hemorrhages.

Common fixed combinations: Cosopt® (dorzolamide + timolol), Ganfort® (bimatoprost + timolol), DuoTrav® (travoprost + timolol), Combigan® (brimonidine + timolol), Simbrinza® (brinzolamide + brimonidine, without timolol), Roclanda® (netarsudil + latanoprost). Advantages: fewer drops per day, better adherence, less exposure to preservatives. Whenever possible, I favor preservative-free formulations (benzalkonium chloride can damage the ocular surface in the long term).

Laser treatment

Selective laser trabeculoplasty (SLT)

Since the LiGHT trial (Gazzard, Lancet 2019), SLT has been a valid first-line option, equivalent or even superior to eye drops for many patients. The 6-year extension (Gazzard, Ophthalmology 2023) confirms better long-term control and less need for surgery.

Mechanism of action

The laser selectively targets the pigmented cells of the trabecular meshwork without thermal damage to adjacent tissue (Latina, Exp Eye Res 1995). It stimulates phagocytosis and improves aqueous humor outflow. The IOP-lowering effect develops gradually (over a few weeks).

Clinical efficacy — LiGHT data

LiGHT at 3 years (Gazzard, Lancet 2019, 718 patients): SLT was non-inferior to eye drops for IOP lowering, with better tolerability. 6-year extension (Gazzard, Ophthalmology 2023): about 70% of SLT patients remained at target IOP without eye drops or surgery, with less incisional glaucoma surgery and less cataract surgery. SLT can be repeated and is cost-effective.

The procedure

An outpatient session under topical anesthesia (eye drops), using a gonioscopy lens. The laser is applied over 360° of the trabecular meshwork. Typical duration: 10 to 15 minutes per eye. Both eyes can be treated in the same session. Normal activities can be resumed immediately.

Recovery and follow-up

No particular restrictions. A transient inflammatory reaction (redness, discomfort) may occur for 24 to 48 hours. Anti-inflammatory eye drops are prescribed after the laser, with an IOP check after a few weeks (the time needed to reach the maximum effect), then check-ups at 3, 6 and 12 months.

Surgery

Filtering surgery & drainage devices

Surgery is considered when eye drops and laser are not enough to reach the target IOP, or from the outset in rapidly progressing or refractory glaucoma. The 6^th edition of the European Glaucoma Society guidelines (Pazos et al., 2024–2025) sets out a structured treatment escalation, placing surgery when a combination of two classes of eye drops proves insufficient.

Trabeculectomy — the historical reference procedure

Creation of a drainage pathway between the anterior chamber and the subconjunctival space, forming a "filtering bleb". Efficacy: large and lasting IOP reduction. Risks: hypotony (blurred vision, macular folds), bleb encapsulation, infection (blebitis, endophthalmitis — a lifelong risk with a filtering bleb), secondary cataract, transient induced astigmatism, and more rarely double vision. A long-proven technique that remains a reference in advanced glaucoma.

Non-penetrating deep sclerectomy (NPDS)

A non-penetrating variant: removal of the deep layers of the trabecular meshwork and Schlemm's canal, without fully opening into the anterior chamber. Advantage: a more favorable safety profile (less hypotony). Drawback: the IOP reduction is sometimes smaller than with trabeculectomy. A surgically demanding technique.

Preserflo MicroShunt — a minimally invasive implant

A SIBS implant (a biostable, biocompatible polymer), placed under the conjunctiva and connecting the anterior chamber to a posterior filtration pocket. Profile: a more standardized and less traumatic procedure than trabeculectomy. 12-month results (Cagini, J Ophthalmol 2024): IOP reduced by about one third and a clear reduction in the number of eye drops; complete success rate about 62%, with reoperation in about a quarter of cases. Compared with trabeculectomy (Khan meta-analysis, Acta Ophthalmol 2024), it offers a similar safety profile, slightly less IOP-lowering power, but fewer reoperations.

Paul implant — for refractory glaucoma after previous surgery

A new-generation tube implant (FDA 2019, European rollout 2020–2022): a very narrow lumen combined with a large posterior plate, providing good IOP control while limiting the risk of hypotony. Role in my practice: I use it for refractory glaucoma in patients who have already had surgery (failed trabeculectomy, sclerectomy or Preserflo). A 2025 prospective multicenter study (251 eyes): large and lasting IOP reduction at 1 year. Not to be confused with older tube implants (Molteno).

Other tube implants and MIGS

Ahmed (valved tube, anti-reflux mechanism) and Baerveldt (non-valved tube, large-surface posterior plate): indicated in highly refractory or special glaucomas (neovascular, post-traumatic, uveitic). MIGS (minimally invasive glaucoma surgery): iStent, Hydrus, XEN, ab interno goniotomy. Less invasive, mainly indicated in mild to moderate glaucoma, often combined with cataract surgery.

Dr HAGE's research

Preserflo MicroShunt — refractory glaucoma

During my time as an Assistant Spécialiste at the Hôpital National des Quinze-Vingts (Paris), in Prof. Christophe Baudouin's department, I contributed to a study evaluating the Preserflo MicroShunt in refractory glaucoma.

Co-author · 2022

Safety and Efficacy of the Preserflo Microshunt in Refractory Glaucoma

Journal of Clinical Medicine · 2022;11(23):7086

This 12-month prospective study of 30 eyes with refractory glaucoma reports a significant reduction in intraocular pressure with a favorable safety profile and no serious complications. This work helps document a less invasive surgical option than trabeculectomy for patients in whom medical and laser treatment has failed.

DOI ↗ PubMed ↗

Eye emergency

Acute glaucoma — the angle-closure attack

Recognizing an acute attack

Sudden symptoms: severe eye pain (may be mistaken for migraine or toothache), rapid drop in vision, colored halos around lights, nausea/vomiting. Objective signs: red eye, mid-dilated non-reactive pupil, hazy cornea (edema), shallow anterior chamber, IOP > 40–60 mmHg.

Pathophysiology

A bowed (anteriorly displaced) iris blocks the trabecular meshwork and the angle. Aqueous humor can no longer drain → IOP rises very quickly. It mainly affects hyperopic patients (anteriorly positioned lens) and presbyopic patients (thickened lens). Sometimes triggered by pupil dilation (mydriasis) or exertion.

Immediate treatment

An absolute emergency: urgent ophthalmic consultation. Immediate medical treatment: a combination of pilocarpine (iris constriction), a topical beta-blocker, a carbonic anhydrase inhibitor (topical and/or systemic) and, if needed, a hyperosmotic agent. Goal: rapidly lower the IOP and clear the cornea so that a YAG laser iridotomy can be performed.

YAG iridotomy — the definitive treatment

Once the IOP has been lowered sufficiently and the cornea is clear, a YAG laser iridotomy is performed in both eyes (the fellow eye carries a comparable risk). The opening in the iris restores direct communication between the posterior and anterior chambers, which reopens the angle. High success rate. If there are extensive synechiae, additional surgery may be needed.

Lifestyle

Living with glaucoma

Recommended activities

Moderate exercise: walking, swimming, cycling, jogging — benefit circulation
Regular sleep: > 7 h/night. Head slightly raised at night
Diet: rich in antioxidants (fruit, vegetables, omega-3), reduces inflammation

To avoid

Inverted yoga: head-down positions → raise IOP
Deep diving: rapid pressure changes → IOP fluctuations
Smoking: affects microcirculation
Excessive caffeine: > 2 cups of coffee/day may raise IOP
Eye trauma: contact sports (boxing)
Extreme heat: saunas (IOP may rise transiently)

Your care pathway

Managing glaucoma

Screening & Diagnosis

IOP, RNFL OCT, visual field, gonioscopy. Classification: suspected, early, moderate, advanced.

Starting treatment

Eye drops first-line (or SLT depending on the profile). Individual target IOP set. Patient education.

Regular follow-up & adjustment

A visit every 3–4 months. The trio: IOP, OCT, visual field. If progressing → escalation (+ eye drops, SLT, or surgery).

Long-term stabilization

Stabilized vision, reassured patients. Lifelong annual follow-up. Adherence = the key to success.

Frequently asked questions

FAQ — Glaucoma

Can glaucoma cause blindness? +

Normal eye pressure = no glaucoma? +

How long before improvement? +

SLT or eye drops as first-line treatment? +

Can eye drops be stopped after surgery? +

Should both eyes be operated on the same day? +

Is sport allowed with glaucoma? +

Is glaucoma hereditary? +

Next step

Protect your vision

Glaucoma is silent. Regular screening (tonometry, OCT, visual field) is the only way to detect it in time and protect your optic nerve.

Book an appointment with Dr HAGE ↗ 01 84 19 11 66

Cabinet OPHTALIFE — Boulogne-Billancourt (Paris area)

Former Assistant Spécialiste, Hôpital des Quinze-Vingts

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Learn more

Related eye care pages

Lens

Cataract

Glaucoma and cataract together: combined or staged surgical approach.

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Ocular surface

Dry eye disease

Eye symptoms: dark circles or dryness during glaucoma treatment?

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Research

Scientific publications

Dr HAGE's work in ophthalmology, including studies on glaucoma and filtering surgery.

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Bibliography

Scientific references

This page is based on international guidelines and key publications. All sources can be verified.

The content of this website is for information only and is not a substitute for a medical consultation. Any treatment decision should be made together with your ophthalmologist.