Myopic Traction Maculopathy (MTM)

Myopic traction maculopathy (MTM) is a problem that happens in some people with high (pathologic) myopia. The very back of the eye (the macula, which you use for sharp central vision) gets pulled and stretched by tiny forces inside the eye. That pulling makes the macula look split or thickened on scans (called “foveoschisis” or “retinoschisis”), and it can also lead to small or large macular holes or a shallow detachment under the fovea. In short, MTM is a traction (pulling) disease of the macula in highly myopic eyes. Dove Medical PressEyeWiki

Myopic traction maculopathy (MTM) happens in eyes with high/pathologic myopia when the retina at the center of vision (the macula) is pulled and gradually splits and/or lifts because the eyeball is too long and the wall is bowed (posterior staphyloma). That traction can come from microscopic “glues” and membranes on the retina’s surface and from the retina being stretched over the bulged back wall. Over time this can blur and distort central vision and—if it progresses—lead to a foveal detachment or a macular hole. OCT scans (the “retinal ultrasound made of light”) are key to diagnose and follow it. Surgery is the main treatment when vision is threatened; medicines mainly treat associated problems (like myopic choroidal neovascularization). EyeWikiRetina Today

People with high myopia (often −6.00 D or more, or axial length ≥26–26.5 mm) have long, stretched eyes. Many also have a posterior staphyloma—a bulging of the back wall of the eye—that changes the eye’s shape and makes traction more likely. MTM is part of the tractional side of pathologic myopia, which modern systems group together with atrophic and neovascular changes (the ATN classification). Dove Medical PressPMC

Reports suggest about 9% to 34% of highly myopic eyes show MTM changes at some point. Symptoms can be mild at first (or none at all), and later include blurred central vision, distortion, or a gray spot. Retina TodayEyeWiki

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Why it happens

Myopic traction maculopathy—also called myopic foveoschisis—is a problem that happens in eyes with high myopia (very strong near-sightedness). The central retina (the macula, which you use for reading and recognizing faces) gets pulled and stretched by several forces inside the eye. Those forces can create split-like spaces in the retina (schisis), tiny detachments under the fovea, and sometimes macular holes. The eye is usually longer than normal and may bulge backward (posterior staphyloma), which adds more pull on the macula. On scans (OCT), doctors see thickened, split layers of the retina with or without shallow detachment; on exam they also look for membranes on the retinal surface that tug on it. EyeWikiPMC

MTM is caused by several kinds of traction (pulling forces) acting on a macula that’s already under stress from a long, stretched eye:

• Front-to-back (perpendicular) pull caused by the eye’s shape (especially a posterior staphyloma) tends to split the retina into layers (schisis) or lift it (foveal/macular detachment).

• Side-to-side (tangential) pull from sticky gel (vitreous), a thin internal limiting membrane (ILM) that behaves like a tight film, or a surface membrane (epiretinal membrane) can open lamellar or full-thickness macular holes.

• The retina’s own “glue” (Müller cells, external limiting membrane, ILM) tries to hold things together. When traction wins, problems appear on OCT. Dove Medical PressEyeWiki

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Types

Doctors now use an OCT-based staging table called the MTM Staging System (MSS). Think of two tracks that can run at the same time:

1. Retinal (layer-splitting) track — driven mostly by front-to-back pulling

   • Stage 1: Early inner/inner+outer layer splits (retinoschisis).

   • Stage 2: Mostly outer-layer schisis.

   • Stage 3: Schisis plus shallow macular detachment.

   • Stage 4: Macular detachment dominates.

2. Foveal (hole) track — driven mostly by side-to-side pulling

   • a: Fovea looks normal.

   • b: Inner lamellar macular hole appears.

   • c: Full-thickness macular hole forms (sometimes with detachment).

Notes in the system use “O” to mark outer lamellar holes and “+” to mark extra surface traction (like epiretinal membranes). As stages rise, vision tends to fall, and changes can accelerate (late stages progress faster than early ones). Dove Medical Press

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Causes

Below are 20 plain-English “causes”—things that create or increase pulling forces on the macula, or reduce macular support, making MTM more likely or worse.

1. High (pathologic) myopia – a long eye stretches tissues and makes traction more likely. Dove Medical Press

2. Posterior staphyloma – the back wall bulges, changing curvature and adding front-to-back pull. Dove Medical Press

3. Vitreomacular traction – the eye gel (vitreous) doesn’t separate cleanly and tugs on the fovea. EyeWiki

4. Residual cortical vitreous – thin sheets of leftover gel keep sticking and pulling. EyeWiki

5. Epiretinal membrane (ERM) – a thin film grows on the macula and contracts sideways. EyeWiki

6. Stiff or tight internal limiting membrane (ILM) – the eye’s inner “skin” can transmit tangential traction. EyeWiki

7. Retinal vessel traction – firm attachments along vessels can create local tethers. EyeWiki

8. Long axial length – the longer the eye, the more mechanical stress across the macula. PMC

9. Thinning of sclera and choroid – less outside support means the macula deforms more easily. Dove Medical Press

10. Age-related vitreous changes in myopes – the gel liquefies but stays partly attached, increasing traction. Dove Medical Press

11. Asymmetric eye shape – complex curves in a staphyloma focus stress on the macula. Dove Medical Press

12. Weakening of “retinal glue” (Müller cells/ELM) – less ability to resist tractional forces. Dove Medical Press

13. Pre-existing lamellar macular hole – an opening can enlarge as traction continues. Dove Medical Press

14. Outer lamellar macular hole – a companion change that signals outer-layer weakness. Dove Medical Press

15. Premacular membranes or proliferations – any extra tissue on the surface can contract. EyeWiki

16. Paravascular schisis/adhesions – traction concentrates near vessels, splitting nearby retina. EyeWiki

17. Lack of “protective” geometry (e.g., no dome-shaped macula) – some shapes resist detachment better; without them, traction wins more easily. Dove Medical Press

18. Rapid stage progression once detachment starts – later stages evolve quicker as forces add up. Dove Medical Press

19. Coexisting pathologic myopia changes (atrophy/lacquer cracks) – reduce structural support around the fovea. PMC

20. History in the fellow eye – similar axial length and staphyloma shape can mean similar risks in both eyes (clinical pattern noted in series and staging work). Dove Medical Press

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Symptoms

1. Blurry central vision—words or faces are not sharp.

2. Metamorphopsia—straight lines look bent or wavy. Retina Today

3. Micropsia—letters look smaller than normal.

4. A dim or gray spot in the center (central scotoma). Retina Today

5. Slow reading—you lose your place or need more light.

6. Poor contrast—faded or washed-out look.

7. Color looks off—especially for fine shades.

8. Glare sensitivity—bright light makes it worse.

9. Trouble recognizing faces from a distance.

10. Needing to move text closer/farther to find a sweet spot.

11. Double or shadowed central image (from macular split/hole effects).

12. Fluctuating vision—better some days, worse on others.

13. No symptoms at first—many cases are silent until they advance. Dove Medical Press

14. Sudden drop in vision if a full-thickness macular hole or detachment develops. Dove Medical Press

15. Symptoms in one eye first—you may notice when covering the better eye.

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Diagnostic tests

A) Physical exam

1. Best-corrected visual acuity (BCVA).
   Reading a standardized chart tells how sharp your central vision is and helps track change over time.

2. Refraction and pinhole check.
   This separates blur from glasses power (refractive) versus macular disease. Big differences after refraction may point away from macular damage; small changes suggest a retinal cause.

3. Slit-lamp biomicroscopy with a macular lens.
   The doctor looks directly at the macula. In high myopia, atrophy and a posterior staphyloma can make the view tricky; that is why scans are essential. EyeWiki

4. Dilated fundus exam (indirect ophthalmoscopy).
   This wide view checks for myopic degeneration around the macula and vitreous traction signs, and it helps rule out other causes of fluid under the macula.

B) Manual/bedside functional tests

5. Amsler grid.
   A simple square grid to detect waviness (metamorphopsia) or missing spots at home or in clinic.

6. Near-vision reading assessment.
   Measures how macular changes affect real-world tasks like reading.

7. Contrast sensitivity test.
   Letters in low contrast show functional losses that acuity alone can miss.

8. Color vision testing (e.g., Ishihara or arrangement tests).
   Subtle macular problems can reduce color discrimination.

C) Lab & pathological tests

9. HbA1c or fasting glucose (to exclude diabetic macular edema if the picture is unclear).

10. Inflammation/infection screens when history suggests uveitis (e.g., syphilis serology, TB testing, ESR/CRP).

11. Autoimmune/vasculitis panels if the doctor suspects an inflammatory maculopathy.
    Note: These are not routine when the OCT clearly shows typical MTM.

D) Electrodiagnostic tests

12. Multifocal ERG (mfERG).
    Maps macular function; can document central depression from long-standing MTM.

13. Full-field ERG.
    Confirms the rest of the retina is functioning if the picture is mixed.

14. Visual evoked potentials (VEP).
    Helps when there’s confusion between macular and optic-nerve problems.

E) Imaging tests

15. Optical coherence tomography (OCT).
    This is the gold standard. OCT shows layer splitting (schisis), foveal detachment, lamellar or full-thickness macular holes, and epiretinal membranes in detail. It also shows how deep the split is (inner vs outer layers) and whether detachment is present. The MSS staging system is based on OCT. Dove Medical Press

16. Swept-source OCT (SS-OCT) or enhanced-depth imaging.
    Penetrates deeper in myopic eyes and better displays the shape of a posterior staphyloma and outer layers.

17. OCT-Angiography (OCT-A).
    Looks at macular blood flow to rule in/out myopic choroidal neovascularization (mCNV) when vision drops quickly or fluid patterns change. (This matters because ATN recognizes tractional and neovascular components together.) PMC

18. Fluorescein angiography (FA).
    Uses dye to confirm or exclude CNV if OCT-A is unclear and to map leakage patterns.

19. Color fundus photography (including ultra-widefield).
    Documents atrophy, lacquer cracks, and overall macular context for follow-up in high myopia.

20. Axial length biometry ± B-scan ultrasound/3D MRI (selected cases).
    Biometry quantifies eye length (a key risk metric). Ultrasound or even 3D MRI can map complex staphyloma shapes when the view is poor, explaining unusual traction directions. Dove Medical Press

Non-pharmacological treatments

(Each item = what it is, purpose, how it helps)

1. Observation with scheduled OCT
   Purpose: Safely watch early/stable MTM.
   Mechanism: Traction can plateau; surgery is timed when progression shows. (Clinicians follow OCT stage changes like T1→T3.) PMC

2. Patient education + home Amsler grid
   Purpose: Catch early distortion/blur changes; seek care quickly if they appear.
   Mechanism: Self-monitoring reduces delay to treatment.

3. Activity modifications
   Purpose: Avoid sudden big spikes of vitreoretinal traction.
   Mechanism: Reasonable caution with forceful Valsalva, eye rubbing, and high-impact trauma; wear eye protection for sports.

4. Low-vision rehabilitation
   Purpose: Make everyday tasks easier if central vision is down.
   Mechanism: Specialists train magnification, lighting, contrast enhancement strategies.

5. High-quality task lighting and contrast boosting
   Purpose: Improve reading/near work.
   Mechanism: Better signal-to-noise compensates for macular defects.

6. Optical aids (magnifiers, electronic video magnifiers, large-print, high-DPI screens)
   Purpose: Make print bigger and clearer.
   Mechanism: Increased letter size/contrast counters reduced macular resolution.

7. Digital ergonomics
   Purpose: Reduce asthenopia and make reading easier.
   Mechanism: Adjust font size, line spacing, high-contrast modes, regular breaks (20-20-20 rule).

8. Optimal refractive correction
   Purpose: Best possible focus.
   Mechanism: Up-to-date glasses/contacts (including high-index lenses) reduce blur that adds to macular distortion.

9. Dry-eye care (if present)
   Purpose: Stabilize the tear film for clearer vision.
   Mechanism: Preservative-free lubricants, blinking habits, lid hygiene.

10. UV and blue-light control outdoors
    Purpose: Reduce light-related retinal stress and glare.
    Mechanism: Sunglasses with UV blocking and hats help comfort and function.

11. Monocular precautions if one eye is worse
    Purpose: Protect the better eye.
    Mechanism: Polycarbonate safety lenses; avoid unnecessary risk.

12. Smoking cessation
    Purpose: Reduce oxidative stress that harms macula generally.
    Mechanism: Stopping smoking benefits overall ocular health; smokers must avoid beta-carotene supplements.

13. Cardio-metabolic health (BP, lipids, exercise)
    Purpose: Support retinal microcirculation.
    Mechanism: Systemic health supports ocular perfusion.

14. Healthy weight and sleep
    Purpose: General vascular/oxidative benefits; avoid apnea-related spikes.

15. Myopia-control counseling for family/younger relatives
    Purpose: Lower lifetime risk of pathologic myopia that predisposes to MTM.
    Mechanism: More outdoor time lowers myopia onset/progression risk in children; clinicians use optical and pharmacologic tools when appropriate. PMCAAO Journal

16. Outdoor-time habit (if the patient is still young)
    Purpose: Part of myopia prevention/slowdown.
    Mechanism: Daily 40–80 minutes of additional outdoor light exposure in trials lowered incident myopia. Myopia Institute –

17. Orthokeratology / myopia-control spectacle or contact lenses (younger patients)
    Purpose: Slow axial elongation in developing myopia.
    Mechanism: Peripheral myopic defocus signaling. (This doesn’t treat existing MTM but can reduce future high-myopia risk profile.) Myopia Institute –

18. Falls-risk/home safety review
    Purpose: Protect vision by reducing trauma risk in those with low vision.
    Mechanism: Better lighting, remove trip hazards.

19. Counseling on unregulated procedures
    Purpose: Avoid harm.
    Mechanism: Do not pursue unapproved “stem-cell” injections—documented cases of severe, permanent vision loss occurred. PMC

20. Shared decision-making aids
    Purpose: Choose timing of surgery confidently.
    Mechanism: Use OCT trends, symptoms, and visual needs to decide “observe vs operate.” (Modern staging helps.) PMC

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Medication treatments

Important: There is no medicine that directly releases the traction of MTM. Drugs are adjuncts—mainly for myopic choroidal neovascularization (mCNV) or for co-existing macular edema/inflammation. Surgery treats traction.

1. Ranibizumab (anti-VEGF, intravitreal) — for mCNV
   Dose/Timing: 0.5 mg injection; often 1 + PRN (one injection, then as-needed by activity).
   Purpose/Mechanism: Blocks VEGF to stop/leak less from abnormal new vessels.
   Side effects: Eye pain, floaters, rare endophthalmitis, IOP spikes. Strong evidence supports anti-VEGF as first-line in mCNV. PMCNature

2. Aflibercept (anti-VEGF) — for mCNV
   Dose/Timing: 2 mg intravitreal; 1 + PRN dosing common.
   Evidence: Effective for mCNV (e.g., MYRROR study); broadly first-line. EyeWiki

3. Bevacizumab (anti-VEGF, off-label) — for mCNV
   Dose/Timing: 1.25 mg intravitreal; PRN.
   Evidence: Widely used off-label with good results and low cost; real-world series support monotherapy. JKMS

4. Conbercept (anti-VEGF) — for mCNV
   Dose/Timing: 0.5 mg intravitreal; used in some regions (e.g., China) with PRN retreatment.
   Evidence: Comparative studies/meta-analyses include conbercept among effective agents. PMC

5. Verteporfin photodynamic therapy (PDT) — sometimes combined with anti-VEGF for mCNV
   Dose/Timing: IV verteporfin with reduced-fluence laser per protocol.
   Purpose: Can decrease injection burden in selected cases.
   Evidence: Combination PDT + anti-VEGF may improve thickness/BCVA and reduce injections in some analyses; now tailored to lesion type. Molina Healthcare

6. Dorzolamide 2% (topical carbonic anhydrase inhibitor)
   Dose/Timing: 1 drop TID.
   Purpose: Off-label to reduce cystoid macular edema if present (e.g., post-surgery or coexisting conditions); can lower intra-retinal fluid in some macular disorders.
   Evidence: CAIs improve CME in retinal dystrophies; used empirically when edema co-exists. Side effects: stinging, rare allergy. PMCFrontiers

7. Acetazolamide (oral CAI)
   Dose/Timing: 250–500 mg/day short courses.
   Purpose: Similar rationale to dorzolamide for edema; monitor electrolytes, paresthesias, fatigue, kidney stones. Frontiers

8. Topical corticosteroids (e.g., prednisolone acetate 1%)
   Dose/Timing: QID, tapered; typically peri-operative or for inflammatory edema—not for traction.
   Cautions: IOP rise, cataract.

9. Intravitreal dexamethasone implant (0.7 mg)
   Purpose: Off-label for refractory macular edema (not traction).
   Cautions: IOP rise, cataract acceleration; PRN retreatment.

10. Ocriplasmin (protease for VMA)—generally avoid in high myopia
    Dose/Timing: 0.125 mg intravitreal, single dose.
    Note: Approved for symptomatic focal VMA, but reports link it to worsening macular hole/retinal detachment in highly myopic eyes; efficacy is limited and safety concerns exist—not a standard MTM therapy. PMCCanada’s Drug Agency

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Dietary & supportive supplements

Key honesty note: Supplements do not fix traction and do not replace surgery. Evidence mainly comes from macular aging studies (AMD) or eye-strain research—not MTM. Use them, if at all, as general macular-health support after discussing safety with your clinician.

1. Lutein 10–20 mg/day
   Function: Builds macular pigment; may improve contrast/glare.
   Mechanism: Antioxidant carotenoid concentrated in the macula. MPOD increases at doses >10 mg/day in trials. PMC

2. Zeaxanthin 2–4 mg/day
   Function/Mechanism: Works with lutein; macular pigment support; similar benefits. PMC

3. Meso-zeaxanthin 10 mg/day
   Function: Complements L+Z; some analyses suggest better contrast outcomes when combined. ScienceDirect

4. AREDS2-style antioxidant base
   Vitamin C 500 mg + Vitamin E 400 IU + Zinc 80 mg + Copper 2 mg + Lutein/Zeaxanthin (instead of beta-carotene).
   Function: Proven to slow AMD progression; not MTM.
   Mechanism: Antioxidant/trace mineral support. Smokers should avoid beta-carotene; use AREDS2. National Eye Institute

5. Omega-3 (DHA/EPA ~1 g/day)
   Function: General retinal support; evidence mixed for AMD prevention.
   Mechanism: Anti-inflammatory membranes; safe dietary inclusion (fatty fish). National Eye Institute

6. Saffron (Crocus sativus) 20 mg/day
   Function: Small RCTs in AMD show modest visual function improvements; mechanism may be neuroprotective/antioxidant. Evidence not MTM-specific. PMCPubMed

7. Astaxanthin 6–12 mg/day
   Function: May reduce digital eye strain and improve certain visual tasks in trials; mechanism antioxidant. Not MTM-specific. PMCMDPI

8. Bilberry anthocyanins 80–160 mg/day
   Function: Mixed evidence for contrast/eye-fatigue; mechanism antioxidative; use cautiously due to limited high-quality data. PubMedPMC

9. Zinc (part of AREDS2) 80 mg/day with copper 2 mg/day
   Function: Antioxidant enzymes; prevent copper deficiency anemia with copper co-supplementation. National Eye Institute

10. Vitamin C 500 mg/day (if not already counted in AREDS2)
    Function: Antioxidant support. National Eye Institute

11. Vitamin E 400 IU/day (if not already counted in AREDS2)
    Function: Antioxidant; watch interactions with anticoagulants. National Eye Institute

12. Copper 2 mg/day (AREDS2 pairing)
    Function: Prevents copper deficiency when using high-dose zinc. National Eye Institute

13. Dietary lutein/zeaxanthin from food (spinach, kale, eggs)
    Function: Food-based intake; supplements raise MPOD more predictably at >10 mg/day. PMC

14. Mediterranean-style diet pattern
    Function: Overall retinal health support (best evidence in AMD). Mechanism: High fruits/veg/fish/nuts; low processed foods. National Eye Institute

15. General multivitamin within RDA
    Function: Baseline nutrition only; avoid megadoses. Avoid beta-carotene if you smoke. National Eye Institute

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Regenerative / stem-cell” topics

There are no approved regenerative or stem-cell drugs for MTM. The items below are experimental, mainly for macular degeneration models—not traction. They must only be accessed in regulated clinical trials.

1. iPSC-derived RPE cell sheets (subretinal)
   Status: Early human studies suggest feasibility/safety, but this targets RPE loss (AMD), not MTM traction. New England Journal of MedicineScienceDirect

2. hESC-derived RPE transplantation
   Status: Small trials show safety signals and some functional hints; still investigational. PMC

3. Photoreceptor precursor cell therapy
   Status: Pre-clinical/early translation; not MTM-specific. Annals of Translational Medicine

4. Mesenchymal stem-cell intravitreal injections
   Warning: Unregulated clinics have caused blinding complications; do not pursue outside bona fide trials. PMCAmerican Academy of Ophthalmology

5. Bioengineered scaffolds/hydrogels for RPE delivery
   Status: Pre-clinical development; not for traction relief. ScienceDirect

6. Gene-modulated “anti-fibrotic” biologics
   Status: Conceptual/pre-clinical; no approved therapy for MTM.

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Surgeries

1. Pars plana vitrectomy (PPV) with ILM peeling
   What: Removes the vitreous gel and peels the ILM to release traction; may add a short-acting gas bubble.
   Why: Relieves the pull causing schisis/detachment and helps the retina re-adhere. Evidence supports favorable anatomy and vision outcomes. PMC

2. Fovea-sparing ILM peeling (FS-ILM)
   What: Peel the ILM around the fovea but leave a central island to reduce risk of creating a macular hole.
   Why: Studies show good structural recovery and vision gains, with lower postoperative macular-hole risk compared with total ILM peel in myopic foveoschisis. PMCOphthalmology RetinaNature

3. Gas tamponade (SF6/C3F8) with PPV
   What: A temporary bubble supports the macula as schisis/detachment resolves.
   Why: Helps appose layers post-traction release; face-down positioning may be advised case-by-case.

4. Macular buckling
   What: A small custom buckle is placed on the outside of the eye under the macula to counter-curve the staphyloma and physically support the macula.
   Why: Particularly useful when posterior staphyloma dominates. Systematic reviews and series show high reattachment and hole-closure rates and vision gains. PubMedPMC

5. Combined PPV + macular buckling
   What/Why: Uses both internal (vitrectomy/ILM work) and external (buckle) approaches in advanced or recurrent cases. oftalmoloji.org

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Prevention & protection tips

1. Regular retina check-ups with OCT if you have high myopia or staphyloma.

2. Know warning signs (new distortion, sudden blur, curtain, many floaters/flashes).

3. Protect eyes from trauma (sports eyewear).

4. Don’t rub eyes; avoid pressure on the globe.

5. Stop smoking.

6. Control BP, lipids, diabetes.

7. Outdoor time for kids/teens in the family (40–80 extra minutes/day) to reduce myopia risk. Myopia Institute

8. Ergonomic near work: larger fonts, breaks.

9. Healthy diet pattern (Mediterranean-like). National Eye Institute

10. Avoid unregulated “stem-cell” clinics. PMC

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When to see a doctor—immediately

• A sudden dark curtain, shower of floaters, or flashes

• Sudden central blur or a new central grey spot

• Rapid worsening of distortion

• Pain, redness, or vision drop after an injection or surgery (possible infection)

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What to eat & what to avoid

1. Eat leafy greens (spinach, kale), eggs, and orange/yellow veg for natural lutein/zeaxanthin. PMC

2. Eat fatty fish (salmon, sardines) 1–2×/week for omega-3s. National Eye Institute

3. Eat nuts/legumes/whole grains for antioxidants and zinc. National Eye Institute

4. Drink water; keep the ocular surface comfortable during long reading sessions.

5. Avoid smoking; if you ever use an AREDS-type vitamin, use AREDS2 (no beta-carotene) if you smoke or used to smoke. National Eye Institute

6. Avoid ultra-processed, very salty foods (can worsen general vascular health).

7. Avoid mega-dose, unproven supplements that claim to “cure myopia/MTM.”

8. Avoid unregulated stem-cell “treatments” advertised online. PMC

9. Limit alcohol; protect sleep.

10. Aim for a Mediterranean-style pattern most days. National Eye Institute

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Frequently asked questions

1. Does MTM always need surgery?
   No. Early or stable traction can be observed closely. Surgery is considered when vision declines or OCT shows progression toward detachment/hole. PMC

2. Which operation is “best”—vitrectomy or macular buckle?
   They solve different problems. Vitrectomy/ILM work relieves internal traction; macular buckling counteracts a deep staphyloma. Some advanced cases do best with both. Choice depends on OCT, staphyloma shape, and surgeon expertise. oftalmoloji.org

3. What is fovea-sparing ILM peeling, and why do surgeons like it for MTM?
   It peels the ILM around the fovea but spares the center, lowering the risk of a postoperative macular hole while still releasing traction—good visual and anatomic outcomes are reported. PMCOphthalmology Retina

4. How successful is macular buckling?
   Modern series/meta-analyses report high reattachment and encouraging vision gains; longer, standardized studies are still needed. PubMedPMC

5. Can eye drops fix the traction?
   No. Drops can help edema or post-op inflammation, but traction needs surgical release.

6. If I also have myopic CNV, what is the drug of choice?
   Anti-VEGF injections are first-line; many patients do well with a single injection followed by PRN retreatment guided by activity. PMCNature

7. Will supplements reverse MTM?
   No. Supplements may support overall macular health (best evidence in AMD), but they don’t undo traction. National Eye Institute

8. Is ocriplasmin helpful?
   Generally no for high myopes; case reports link it to worse macular hole/detachment—it isn’t standard for MTM. PMC

9. What happens if I delay needed surgery?
   Progression can lead to foveal detachment, macular hole, or retinal detachment, which may reduce the chance of full visual recovery. Timely intervention matters. ScienceDirect

10. How long is recovery after vitrectomy?
    Vision often improves over weeks to months as fluid clears and layers re-settle; positioning instructions vary by case.

11. Will I need face-down positioning?
    Sometimes, especially when a gas bubble is used; your surgeon tailors this.

12. Is MTM likely to come back?
    Recurrence is uncommon after successful traction release, but other myopic maculopathy issues (e.g., CNV, atrophy) can still occur over time—hence ongoing follow-up. PMC

13. Can glasses or LASIK fix MTM?
    They correct focus at the front of the eye, not traction at the macula. They don’t treat MTM.

14. Can children get MTM?
    It’s mainly an adult complication of long-standing high myopia. For kids, the priority is myopia control (outdoor time, optical options). PMC

15. Bottom line for my daily life?
    Keep appointments and OCT checks, monitor with Amsler, use good lighting and magnification, protect your eyes, and seek care fast for sudden changes.

Disclaimer: Each person’s journey is unique, treatment plan, life style, food habit, hormonal condition, immune system, chronic disease condition, geological location, weather and previous medical  history is also unique. So always seek the best advice from a qualified medical professional or health care provider before trying any treatments to ensure to find out the best plan for you. This guide is for general information and educational purposes only. Regular check-ups and awareness can help to manage and prevent complications associated with these diseases conditions. If you or someone are suffering from this disease condition bookmark this website or share with someone who might find it useful! Boost your knowledge and stay ahead in your health journey. We always try to ensure that the content is regularly updated to reflect the latest medical research and treatment options. Thank you for giving your valuable time to read the article.

The article is written by Team RxHarun and reviewed by the Rx Editorial Board Members

Last Updated: August 13, 2025.

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