10 Normal Tension Glaucoma

What is normal tension glaucoma (NTG), and how does it relate to primary open-angle glaucoma (POAG)?

NTG is a form of open-angle glaucoma with glaucomatous optic neuropathy despite IOP measurements that are consistently in the statistically normal range, typically <21 mmHg.
NTG is considered part of the POAG spectrum, not a completely separate disease.

Why is the cutoff of 21 mmHg imperfect when defining “normal” IOP?

21 mmHg is an arbitrary statistical marker, not a biologic cutoff for safety.
Some patients develop glaucomatous optic nerve damage at pressures below this level, while others may tolerate higher pressures without damage.

What are the key clinical findings required to diagnose NTG?

NTG requires:

• Open angle

• Progressive optic nerve damage

• Visual field loss

• Statistically normal IOP

• No other obvious cause of optic neuropathy

What do population studies show about the prevalence of NTG among glaucoma patients?

A substantial proportion of glaucoma patients have normal-range IOP:

• Baltimore Eye Study: glaucoma prevalence 2.4%, and 24% of glaucoma patients had NTG

• Beaver Dam Eye Study: glaucoma prevalence 2.1%, and 32% of glaucoma cases had IOP <22 mmHg

Why is NTG clinically important even though IOP is “normal”?

NTG shows that glaucoma is not only an “eye pressure disease.”
A large number of patients develop optic nerve damage and visual field loss despite statistically normal IOP, meaning other mechanisms such as vascular insufficiency may contribute.

How do NTG and typical POAG compare in outcome?

NTG and POAG may have different associated clinical findings, but both can lead to the same final outcome: progressive retinal ganglion cell/optic nerve death → visual field loss.

What major etiologic theories explain glaucomatous optic neuropathy, especially in NTG?

• Mechanical: IOP-related stress on the optic nerve head

• Vascular: reduced ocular blood flow causes ischemia/hypoxia

• Biochemical: cellular or molecular injury pathways contribute to nerve damage

In NTG, the vascular theory becomes especially important because high IOP is not the main explanation.

How can reduced ocular blood flow contribute to NTG?

If IOP is not high enough to explain mechanical optic nerve stress, then reduced ocular blood flow may create a hypoxic stimulus at the optic nerve head, leading to glaucomatous optic neuropathy.

What is the formula for ocular perfusion pressure (OPP), and why is it important in NTG?

OPP = diastolic blood pressure (DBP) − intraocular pressure (IOP)

OPP matters because the optic nerve head depends on adequate perfusion. A drop in diastolic BP or an increase in IOP can reduce perfusion and potentially harm the optic nerve.

Why is low diastolic blood pressure a concern in patients with NTG?

Low diastolic BP can reduce ocular perfusion pressure, which may decrease blood flow to the optic nerve head.
This can worsen optic nerve hypoxia and contribute to glaucomatous damage even when IOP is normal.

What vascular mechanisms can increase risk for normal tension glaucoma by reducing optic nerve head perfusion?

NTG risk increases when ocular perfusion pressure decreases or optic nerve head blood flow becomes unstable.
Accepted vascular risk factors include:

• Nocturnal hypotension

• Sleep apnea

• Vasospastic disease, especially migraine and Raynaud’s phenomenon

• Hemodynamic crisis

• Primary vascular dysfunction (PVD)

Why are nocturnal hypotension and sleep apnea important in NTG?

Both can reduce oxygen delivery to the optic nerve head.

• Nocturnal hypotension: lowers diastolic BP during sleep → ↓ ocular perfusion pressure

• Sleep apnea: intermittent hypoxia → reduced oxygen delivery and vascular stress

What systemic vascular or blood disorders are suspected risk factors for NTG?

Suspected vascular risk factors include:

• Carotid artery disease

• High cholesterol

• Hypercoagulation disorders

• Severe anemia

• Cardiac arrhythmia

• Blood dyscrasias

What is the classic vasospastic disease association with NTG?

NTG is associated with vasospastic disease, especially:

• Migraine

• Raynaud’s phenomenon

These suggest abnormal vascular regulation, which may cause unstable or reduced optic nerve head perfusion.

What is translaminar pressure difference (TPD), and what is the formula?

TPD = IOP − intracranial pressure (ICP)

TPD represents the pressure gradient across the lamina cribrosa between the eye and the retrobulbar cerebrospinal fluid space.

How can abnormal translaminar pressure difference contribute to glaucomatous optic nerve damage?

If IOP is high relative to ICP, the increased pressure gradient across the lamina cribrosa can promote posterior deformation and optic nerve cupping.

What optic nerve findings occur when IOP is greater than ICP versus when ICP is greater than IOP?

• IOP > ICP: increased posterior force across lamina cribrosa → glaucomatous cupping

• ICP > IOP: anterior pressure effect → disc swelling, as seen in conditions like elevated ICP or ocular hypotony

Basically:
Cupping = IOP relatively higher than ICP
Swelling = ICP relatively higher than IOP

How does IOP have opposite effects in the OPP and TPD equations?

• In OPP = DBP − IOP, higher IOP decreases ocular perfusion pressure

• In TPD = IOP − ICP, higher IOP increases translaminar pressure difference

Why can IOP still matter in normal tension glaucoma even when IOP is statistically normal?

Because IOP is part of multiple risk pathways:

1. Perfusion pathway: higher IOP lowers OPP

   • OPP = DBP − IOP

2. Mechanical gradient pathway: higher IOP raises TPD

   • TPD = IOP − ICP

Thus, a “normal” IOP may still be too high for a specific patient’s optic nerve, especially if DBP is low or ICP is low.

What optic nerve and visual field findings are characteristic of normal tension glaucoma?

NTG commonly shows:

• Saucer-like cupping with temporal rim thinning

• Deep, localized visual field defects

• Visual field defects often located near fixation

• Increased frequency of Drance hemorrhages

How do visual field defects in NTG typically differ from those in classic POAG?

NTG visual field defects are often:

• Deeper

• More localized

• Closer to fixation

What is a Drance hemorrhage, and why is it clinically important in NTG?

A Drance hemorrhage is an optic disc hemorrhage, often flame-shaped or splinter-like near the disc margin.

It is more common in NTG than POAG:

• 25% in NTG

• 8% in POAG

What is saucerization of the optic nerve head?

Saucerization is an optic nerve head appearance with an ill-defined, shallow cup rather than a steep, deep glaucomatous cup.

It is more characteristic of normal tension glaucoma than classic POAG.

How is saucerization associated with visual function?

Saucerization is associated with an overall decrease in visual field sensitivity.

Why can saucerization be easy to miss clinically?

Saucerization may be subtle because the optic nerve head has a broad, shallow, ill-defined cup rather than obvious deep excavation.

How does saucerization change the cup-to-disc relationship compared with a healthy optic nerve?

In a healthy nerve, the cup is smaller and more clearly contained within the optic nerve head.

In saucerization, the cup becomes broad and shallow, occupying a greater proportion of the optic nerve head with less distinct borders.

What is the key structural difference between saucerization and classic glaucomatous cupping?

• Saucerization: broad, shallow, ill-defined excavation

• Classic glaucomatous cupping: deeper, more obvious excavation

Why does temporal rim thinning in NTG often produce visual field defects near fixation?

Temporal neuroretinal rim thinning affects retinal ganglion cell axons that correspond to the macular/paracentral visual field, so NTG commonly produces defects close to fixation.

How can NTG cause mechanical damage even when IOP is relatively low?

A structurally or genetically weak lamina cribrosa may make retinal ganglion cell axons more susceptible to mechanical stress, even at “normal” or relatively low IOP.

What is the macular vulnerability zone, and why is it important in NTG?

The macular vulnerability zone refers to retinal ganglion cell axons serving the macula that are especially susceptible to glaucomatous damage.

In NTG, damage here can cause paracentral visual field defects, which may threaten fixation earlier than more peripheral defects.

What imaging should be included in the work-up of NTG suspects, and why?

Ganglion cell layer / ganglion cell complex imaging should be included at baseline or shortly afterward.

Reason: NTG often affects the macular ganglion cell region, and macular damage may be missed if evaluation relies only on optic nerve appearance or standard visual field testing.

What structural OCT finding corresponds to paracentral visual field defects in NTG?

Ganglion cell analysis thinning, especially in the macular region, corresponds to paracentral visual field defects.

Why can paracentral defects be easy to miss with standard 24-2 visual field testing?

The 24-2 visual field samples central points relatively sparsely, so small defects near fixation can be underdetected or underestimated.

This is especially important in NTG because defects often occur close to fixation.

How does 10-2 visual field testing complement 24-2 testing in NTG?

The 10-2 visual field tests the central field more densely, making it better for detecting and quantifying paracentral defects.

Use both when NTG or macular involvement is suspected:

• 24-2: broader glaucomatous field assessment

• 10-2: detailed central/paracentral assessment

What clinical workflow helps avoid missing NTG-related paracentral damage?

In NTG suspects, evaluate both structure and function near fixation:

1. Macular ganglion cell analysis/GCC OCT

2. Optic nerve/RNFL OCT

3. 24-2 visual field

4. Add 10-2 visual field if paracentral damage is suspected or if GCA thinning is present

What risk factors are associated with presenting with a paracentral glaucomatous defect in NTG?

Risk factors for paracentral glaucomatous defects include:

• Migraine

• Low blood pressure

• Sleep apnea

• Drance hemorrhage

Why are migraine, low blood pressure, and sleep apnea important clues in an NTG patient with paracentral field loss?

These conditions can reduce or destabilize optic nerve head oxygen delivery:

• Migraine: vasospastic tendency

• Low blood pressure: decreased ocular perfusion pressure

• Sleep apnea: intermittent hypoxia

• Drance hemorrhage: marker of optic nerve stress and progression risk

What is a Drance hemorrhage, and what does it suggest clinically?

A Drance hemorrhage, also called a disc hemorrhage, is a hemorrhage at or near the optic nerve head.

It suggests the optic nerve is under stress and is one of the most significant predictors of glaucoma progression.

Is a Drance hemorrhage the cause or result of glaucomatous axonal damage?

It is unclear whether axonal damage occurs before or after the hemorrhage.

The slide frames this as an “ocular chicken and egg” situation.
High-yield takeaway: Regardless of timing, a Drance hemorrhage is a major warning sign for active or future progression.

How does the frequency of Drance hemorrhage differ between NTG and POAG?

Drance hemorrhages are more common in NTG than in POAG.

Earlier slide association:

• NTG: about 25%

• POAG: about 8%

Why is physiologic cupping an important differential diagnosis for NTG?

Because NTG has statistically normal IOP, the initial concern often comes from the optic nerve head appearance rather than elevated pressure.

Clinicians must distinguish true glaucomatous cupping from physiologic cupping.

What features favor physiologic cupping rather than glaucomatous NTG damage?

Physiologic cupping is more likely when:

• The optic disc is large, because large discs often have large cups

• The cupping is stable over time

• There is no associated functional vision loss

• Visual fields are normal or non-progressive

What findings favor NTG over physiologic cupping?

Findings favoring NTG include:

• Progressive optic nerve/rim thinning

• Corresponding RNFL or GCC/GCA loss

• Reproducible visual field defects

• Paracentral defects near fixation

• Drance hemorrhage

• Structural or functional progression over time

What is “red disease,” and why is it an important differential diagnosis for NTG?

Red disease refers to false-positive OCT abnormalities where RNFL or GCC/GCA sectors appear “red” or abnormal on OCT printouts, leading clinicians to overdiagnose glaucoma.

How can OCT misinterpretation lead to overdiagnosis of normal tension glaucoma?

OCT can falsely flag abnormal thinning due to artifacts or normal anatomic variation. This can make a physiologic or nonglaucomatous optic nerve look glaucomatous.

Common reasons include:

• Segmentation errors

• Poor scan quality

• High myopia or tilted discs

• Large or small disc anatomy

• Database mismatch

• Media opacity or poor centration

What should you do before labeling a normal-IOP patient as NTG based on OCT abnormalities?

Confirm true structure-function correlation:

1. Inspect the raw OCT B-scans for artifact

2. Compare OCT thinning with optic nerve/rim appearance

3. Check for corresponding visual field loss

4. Repeat testing if results are questionable

5. Look for progression over time

How can primary open-angle glaucoma be mistaken for NTG?

POAG can be mistaken for NTG if the patient has “normal” IOP during office visits but has masked high IOP at other times.

Possible reasons include:

• IOP spikes outside office hours

• Nocturnal or early morning IOP elevation

• Thin central corneal thickness causing underestimated IOP

• Systemic beta-blocker use lowering office IOP measurements

Why does thin central corneal thickness matter in the NTG differential?

A thin CCT can cause applanation tonometry to underestimate true IOP.

Clinical consequence:
A patient may appear to have normal IOP, but the true pressure may be higher, making the diagnosis more consistent with POAG rather than NTG.

Why can systemic beta-blocker treatment mask elevated IOP?

Systemic beta-blockers can lower aqueous humor production and reduce IOP.

If a patient is taking systemic beta-blockers, office IOP measurements may appear normal even if the patient has an underlying tendency toward higher IOP.

What is the purpose of diurnal IOP measurement in suspected NTG?

Diurnal IOP measurement checks IOP at multiple times of day to identify pressure peaks that may be missed during a single office visit.

Why must intermittent angle closure be ruled out before diagnosing NTG?

Intermittent angle closure can cause episodic IOP spikes, but IOP may be normal between attacks.

This can mimic NTG if the clinician only sees normal IOP during routine visits.

What test does every glaucoma suspect need to rule out angle closure?

Gonioscopy

How can post-dilation IOP help in the work-up of suspected intermittent angle closure?

Measuring post-dilation IOP can help reveal patients who experience pressure elevation after dilation due to narrow or occludable angles.

What findings suggest intermittent angle closure rather than true NTG?

Findings suggesting intermittent angle closure include:

• Narrow or occludable angles on gonioscopy

• Episodic IOP spikes

• Elevated post-dilation IOP

• Symptoms during attacks, if present

• Glaucomatous damage despite normal IOP between episodes

Why must secondary glaucomas be ruled out before diagnosing normal tension glaucoma?

Secondary glaucomas can cause glaucomatous optic nerve damage with IOP that may appear normal at a single visit.

Important secondary causes to rule out include:

• Pseudoexfoliative glaucoma

• Pigment dispersion syndrome

• Previous uveitic glaucoma

What anterior segment findings suggest pseudoexfoliative glaucoma rather than true NTG?

Pseudoexfoliative glaucoma is suggested by pseudoexfoliative material on anterior segment structures, especially the lens capsule or pupillary margin.

Clinical importance: Pseudoexfoliation can cause intermittent or fluctuating IOP elevation, so a normal office IOP does not fully exclude prior pressure-related damage.

What findings suggest pigment dispersion syndrome as a masquerader of NTG?

Pigment dispersion syndrome may show:

• Pigment release from the iris pigment epithelium

• Pigmented trabecular meshwork on gonioscopy

• Iris transillumination defects

• Possible IOP spikes

How can prior uveitic glaucoma mimic NTG?

Prior uveitis can damage the trabecular meshwork or cause inflammatory IOP spikes.

Even if current IOP is normal, past episodes of elevated IOP may have caused glaucomatous optic neuropathy.

What non-glaucomatous optic neuropathies can mimic NTG?

Important mimics include:

• Ischemic optic neuropathy

• Compressive optic neuropathy

• Optic neuritis

• Prior traumatic optic neuropathy

Why can ischemic optic neuropathy be confused with NTG?

Ischemic optic neuropathy can leave optic nerve pallor and visual field defects that may resemble glaucomatous damage.

However, ischemic optic neuropathy often has a more acute history and may show pallor disproportionate to cupping.

What clinical features suggest non-glaucomatous optic neuropathy rather than NTG?

Features suggesting non-glaucomatous optic neuropathy include:

• Unilateral presentation

• Pallor greater than cupping

• Decreased visual acuity

• Dyschromatopsia

• Visual field loss respecting the vertical midline

• Visual field damage worse than disc appearance

• Rapidly progressing visual field or visual acuity loss

Why is “pallor greater than cupping” a red flag against NTG?

In glaucoma, optic nerve damage is typically characterized by cupping and rim thinning.

If optic nerve pallor is more prominent than cupping, the cause may be non-glaucomatous optic neuropathy, such as ischemic, compressive, inflammatory, or traumatic optic neuropathy.

What visual field pattern should make you suspicious for compressive or neurologic optic neuropathy instead of NTG?

Visual field loss that respects the vertical midline is suspicious for a neurologic or compressive process.

Glaucomatous visual field loss more often respects the horizontal meridian due to retinal nerve fiber layer anatomy.

What mismatch between visual field loss and optic disc appearance suggests a non-glaucomatous optic neuropathy?

If the visual field damage is worse than the disc appearance, consider a non-glaucomatous optic neuropathy.

High-yield red flag: Severe or rapidly progressive functional loss with only mild glaucomatous-appearing cupping should prompt reconsideration of the diagnosis.

What ancillary tests are useful in the workup of suspected normal tension glaucoma?

Useful NTG workup tests include:

• 10-2 threshold visual fields

• Ganglion cell layer analysis

• Fundus photos

• Color vision testing

• Corneal hysteresis

Why are 10-2 visual fields and ganglion cell layer analysis especially useful in NTG?

NTG often causes paracentral defects near fixation and macular ganglion cell loss.

• 10-2 VF: better samples central/paracentral visual field

• Ganglion cell layer analysis: detects macular RGC damage

Why should fundus photos be included in NTG workup?

Fundus photos provide a baseline to monitor:

• Optic nerve cupping

• Rim thinning

• Disc hemorrhages

• Structural progression over time

Why is color vision testing useful in a suspected NTG patient?

Color vision testing helps screen for non-glaucomatous optic neuropathy.

Abnormal color vision, especially with decreased visual acuity or pallor greater than cupping, should raise concern for optic neuritis, compressive optic neuropathy, ischemic optic neuropathy, or other nonglaucomatous causes.

What is corneal hysteresis, and why does it matter in glaucoma risk assessment?

Corneal hysteresis reflects the cornea’s biomechanical ability to absorb and dissipate pressure-related energy.

Lower corneal hysteresis suggests a more deformable or less resilient ocular tissue response and is associated with higher risk of glaucoma conversion or progression.

What corneal hysteresis values are considered normal, suspicious, risky, or potentially protective?

Corneal hysteresis reference values:

• <9 mmHg: risk factor for conversion or progression

• 9 to 9.5 mmHg: suspicious for conversion or progression

• 10 mmHg: normal/average

• >11 mmHg: potentially protective against conversion or progression

How should low corneal hysteresis affect management thinking in NTG?

Low corneal hysteresis suggests greater susceptibility to glaucoma progression even when IOP is statistically normal.

Clinical implication: A patient with NTG and low corneal hysteresis may need closer monitoring and possibly a lower target IOP.

What were the key inclusion criteria for the Collaborative Normal Tension Glaucoma Study?

Inclusion criteria included:

• Average IOP ≤20 mmHg

• No history of documented IOP >24 mmHg

• Open angles

• No systemic beta blocker use

• No other apparent cause for optic neuropathy or visual field loss

Why did the CNTGS exclude patients with systemic beta blocker use?

Systemic beta blockers can lower IOP and potentially mask elevated pressure.

Excluding these patients helped ensure that study participants had true normal-tension glaucoma rather than POAG with medication-masked high IOP.

Why did the CNTGS require open angles and no other cause of optic neuropathy or visual field loss?

These criteria ensured that patients had true NTG rather than another condition mimicking NTG.

The study excluded:

• Angle closure mechanisms

• Secondary glaucomas

• Nonglaucomatous optic neuropathies

• Other causes of visual field loss

What did the Collaborative Normal Tension Glaucoma Study show about untreated NTG progression?

Not all untreated NTG progresses.

In CNTGS:

• 65% of randomized, untreated eyes did not show progression

• 35% of untreated eyes did progress

How did treatment affect progression in the Collaborative Normal Tension Glaucoma Study?

IOP-lowering treatment reduced progression risk.

• 35% of untreated eyes progressed

• Only 12% of treated eyes progressed

Why does IOP reduction still help in NTG if IOP is already normal?

“Normal” IOP may still be too high for a vulnerable optic nerve.

Lowering IOP may:

• Reduce mechanical stress at the lamina cribrosa

• Improve ocular perfusion pressure indirectly

• Reduce risk of further retinal ganglion cell/optic nerve damage

What were the major CNTGS risk factors for NTG progression?

CNTGS risk factors for progression included:

• Disc hemorrhage: 2.72 times greater risk

• Migraine: 2.58 times greater risk

• Female sex: 1.85 times greater risk

• African ancestry: possible risk factor, but based on a small sample

What is the strongest risk factor for NTG progression listed in the CNTGS slides?

Disc hemorrhage was the strongest listed risk factor, with a 2.72 times greater risk of progression.

Clinical meaning: A Drance/disc hemorrhage is not just a finding, it is a major warning sign for future glaucomatous progression.

Why is migraine associated with higher risk of NTG progression?

Migraine suggests vascular dysregulation or vasospasm, which may reduce or destabilize optic nerve head perfusion.

CNTGS finding:

• Migraine = 2.58 times greater risk of progression

Which factors were confirmed non-risk factors for NTG progression in CNTGS?

Confirmed non-risk factors for progression included:

• Baseline IOP

• Age

• Family history

• Hypertension

How should you interpret baseline IOP not being a confirmed CNTGS risk factor for progression?

In CNTGS patients, baseline IOP did not predict progression as strongly as factors like disc hemorrhage or migraine.

This does not mean IOP is irrelevant. Lowering IOP still reduced progression from 35% untreated to 12% treated.

Key distinction:

• Baseline IOP did not predict who progressed

• IOP reduction still lowered progression risk

What clinical profile suggests an NTG patient is at higher risk for progression and may deserve more aggressive treatment?

Higher-risk NTG features include:

• Disc/Drance hemorrhage

• Migraine

• Documented structural or visual field progression

• Paracentral defects near fixation

• Low corneal hysteresis

• Other vascular risk factors, such as low BP or sleep apnea

Why should clinicians avoid rushing to treat every patient with normal tension glaucoma?

Many NTG patients do not progress without treatment, and progression is often slow.

How should progression be monitored in suspected or confirmed NTG?

Monitor progression over time using:

• OCT

• Optic disc photos

• Visual fields

Why should IOP be checked multiple times at different times of day in NTG management?

Multiple IOP measurements help detect missed IOP peaks or fluctuations.

This helps distinguish:

• True NTG
  from

• POAG with masked high IOP or diurnal/nocturnal pressure spikes

What additional testing may be considered in NTG patients, and why?

Additional testing may include:

• Sleep study: if sleep apnea or nocturnal hypoxia is suspected

• MRI: if findings suggest nonglaucomatous optic neuropathy

Clinical clue: Consider MRI when there is pallor > cupping, decreased visual acuity, dyschromatopsia, vertical midline VF loss, unilateral findings, or rapid progression.

What IOP reduction target is suggested for treatment of NTG?

Aim for about a 30% reduction in IOP.

Why can achieving target IOP in NTG be difficult with medications alone?

Because baseline IOP is already low, achieving an additional 30% reduction can be challenging.

In the CNTGS, about 43% of eyes required trabeculectomy to achieve a 30% IOP reduction.

What medications are generally first-line for NTG treatment, and which should be used cautiously?

Prostaglandin analogs (PGAs) are typically first-line because they lower IOP effectively.

Beta blockers should be avoided or used cautiously because they may decrease ocular perfusion, especially if they lower systemic blood pressure or worsen nocturnal hypotension.

Why might beta blockers be less desirable in NTG compared with other glaucoma medications?

NTG is often linked to reduced optic nerve perfusion. Beta blockers may worsen perfusion by lowering systemic blood pressure or reducing ocular blood flow.

What possible non-IOP benefit has been suggested for brimonidine in NTG?

Brimonidine may have neuroprotective capability, meaning it may reduce visual field progression beyond its IOP-lowering effect.

This is suggested by studies where brimonidine and timolol lowered IOP similarly, but brimonidine-treated patients had less visual field progression.

What question did the Low Tension Glaucoma Treatment Study ask about brimonidine?

The study asked whether brimonidine is neuroprotective in low/normal tension glaucoma.

It compared:

• 0.2% brimonidine

• 0.5% timolol

over a 4-year period.

How did brimonidine and timolol compare in IOP lowering in the Low Tension Glaucoma Treatment Study?

Brimonidine and timolol produced equal drops in IOP.

This is important because differences in visual field progression were not simply explained by different levels of IOP reduction.

What were the visual field progression results for brimonidine versus timolol?

Visual field progression occurred in:

• 9.1% of brimonidine-treated patients

• 39.2% of timolol-treated patients

What is the clinical implication of the brimonidine versus timolol study for NTG treatment?

In NTG, medication choice may matter beyond IOP lowering.

Brimonidine may be favored because it may:

• Lower IOP

• Avoid beta-blocker-related perfusion concerns

• Possibly provide neuroprotection

But the main confirmed treatment principle remains: lower IOP, especially in progressing or high-risk NTG.

What limitation complicates interpretation of the Low Tension Glaucoma Treatment Study’s brimonidine results?

A large proportion of brimonidine-treated patients discontinued the study, mainly due to adverse effects from the drop.

Discontinuation rates:

• 28.3% of brimonidine-treated patients discontinued

• 11.4% of timolol-treated patients discontinued

Why should brimonidine’s neuroprotective effect in NTG be interpreted cautiously?

Although brimonidine-treated patients had less visual field progression than timolol-treated patients in one study, the evidence is not definitive because:

• Brimonidine had a higher discontinuation rate

• Adverse effects caused many patients to stop treatment

• A Cochrane review did not support a proven neuroprotective effect of brimonidine