Pathologic Myopia

Pathologic myopia is short-sightedness that has gone beyond just needing stronger glasses. In this condition, the back part of the eye (the retina, the layer that sees; the choroid, the blood layer; and the white coat called the sclera) becomes stretched and damaged. Doctors look for specific damage at the back of the eye, such as posterior staphyloma (an outward bulging of the eye wall) or myopic maculopathy (wear and tear in the center of vision). If they see these changes, they call it “pathologic” even if the glasses power is not extremely high. In other words, it is defined by the damage, not just by the number on your glasses. Myopia Institute –+1IOVS

“High myopia” vs “pathologic myopia

• High myopia means very strong short-sightedness (many experts use −6.00 diopters or more, or an eye length over ~26 mm).

• Pathologic myopia means the eye shows degenerative changes like staphyloma or myopic maculopathy. These changes can happen in high myopia, but can also appear in some eyes that are not extremely myopic. So, high myopia talks about the glass power; pathologic myopia talks about damage inside the eye. PMCMyopia Institute –

Pathologic myopia is a major cause of vision loss worldwide. It raises the risk of serious problems such as retinal detachment, myopic choroidal neovascularization (new, fragile blood vessels under the retina), traction problems at the macula, glaucoma, and cataract. The risk of retinal detachment is much higher in very myopic eyes because the eye is longer and the retina is more stretched and fragile. PMCIOVSAAO

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Types and simple classifications you may hear

Doctors often use two friendly systems to describe what they see.

1) The META-PM maculopathy scale (an atrophy-focused ladder)

This scale describes how worn the central retina looks:

• Category 0: no myopic retinal lesions.

• Category 1: “tessellated” fundus (a mottled look).

• Category 2: diffuse atrophy (widespread thinning).

• Category 3: patchy atrophy (islands of bare areas).

• Category 4: macular atrophy (central area severely thinned).
  “Plus” signs can be added for lacquer cracks (fine breaks), myopic CNV, or Fuchs spots (scars after CNV). Pathologic myopia usually means category 2 or worse, or any plus sign, or a posterior staphyloma. ScienceDirect

2) The ATN system (Atrophic–Tractional–Neovascular)

• A (Atrophic) describes the degree of thinning and atrophy at the macula.

• T (Tractional) captures pulling problems such as myopic traction maculopathy and foveoschisis (retinal layers splitting).

• N (Neovascular) marks myopic CNV.
  This system helps doctors show all three damage paths in one label. PubMed

A staphyloma is a bulge of the back wall of the eye. It is a hallmark change in pathologic myopia and can drive many of the macular problems listed above. Modern wide-field OCT imaging shows its shape and depth clearly. PMC

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20 causes and contributors (written as simple, short explanations)

Pathologic myopia does not come from one single cause. It grows from many factors that make the eye grow too long and the back wall too thin and weak. Below are 20 known contributors. Some are risks rather than direct causes, but each can push the eye toward damage.

1. Family history (genes). If parents are myopic, children have a higher risk of myopia and later high or pathologic myopia. Many genes interact with environment. MDPI

2. Early start of myopia. If myopia begins in the early primary school years, there is more time to progress to high or pathologic levels. Myopia Institute –

3. Long eye length (axial elongation). A longer eyeball stretches the retina and choroid and raises the chance of atrophy, tearing, and detachment. PMC

4. Near work overload. Long hours of reading or screens at close distance are linked to myopia onset and progression. PubMed

5. Low outdoor time. Spending less time outdoors is linked to more myopia; extra outdoor time can reduce new myopia in children. Bright light and dopamine signaling are possible explanations. JAMA Network

6. Higher education intensity. Heavy academic load and long schooling are associated with more myopia. MDPI

7. Urban living. City life is linked with more near work and less outdoor time, which together raise myopia risk. IOVS

8. Peripheral hyperopic defocus. When the peripheral retina receives “behind-the-retina” blur, the eye may lengthen to chase the focus, encouraging axial growth. PMCIOVS

9. Accommodation lag. A delay or mismatch in focusing at near may add to retinal blur signals that promote eye growth. (Accommodation and binocular vision are part of IMI risk factors.) Myopia Institute –

10. Ethnic background. East Asian populations have higher rates of high and pathologic myopia, likely from gene-environment interaction. IOVS

11. Female sex (population trend). Several population datasets show slightly higher myopia (and sometimes high myopia) in females, especially in adolescence, likely due to a mix of biology and behavior. PMC

12. Prematurity and Retinopathy of Prematurity (ROP). Premature birth, especially with ROP, is linked to early high myopia and later myopic degeneration. PMC

13. Connective tissue disorders (e.g., Marfan syndrome). Weak zonules and long eyes can lead to high myopia and pathologic changes. EyeWiki

14. Stickler syndrome (collagen disorder). Strongly linked to early high myopia and retinal detachment risk. NCBI

15. Ehlers-Danlos spectrum. Collagen problems can thin the sclera, increase myopia, and favor degenerative myopia. PMC

16. Myopic traction forces. Vitreous pulling, tight internal limiting membrane, and staphyloma curvature can cause foveoschisis and macular holes. PMC

17. Choroidal thinning. The blood-rich layer under the retina becomes thin in long eyes, reducing support to the photoreceptors and RPE and promoting atrophy. (Seen clearly on enhanced-depth OCT in pathologic myopia.) Retina Today

18. Posterior staphyloma geometry. The bulge itself alters stress on the macula and optic nerve and drives tractional and atrophic change. PMC

19. Lacquer cracks. Tiny breaks in Bruch’s membrane from stretching can trigger bleeding and myopic CNV and later scarring. PMC

20. Systemic metabolic disorders that move the lens (e.g., homocystinuria). Lens subluxation increases myopic power and can speed high myopia in youth. PMC

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15 common symptoms (each explained simply)

1. Blurry distance vision that keeps getting worse over years.

2. Needing frequent prescription changes because the eye is still elongating.

3. Distortion of straight lines (wavy or bent lines), which suggests macular damage or CNV.

4. A gray or dark central spot when reading, which points to macular atrophy or scarring.

5. Sudden drop in vision with a new central blur, which may mean bleeding or new CNV. AAO

6. Flashes of light (photopsia), often from vitreous pulling on the retina.

7. New floaters or a “shower of black spots,” which can signal a posterior vitreous detachment or a retinal tear.

8. Curtain or shadow in the side vision, which can mean a retinal detachment.

9. Poor contrast sensitivity (letters look washed out), common in macular disease.

10. Trouble in dim light because a thin choroid and macular damage reduce low-light performance.

11. Eye strain and headaches after long near work due to high focusing demand.

12. Peripheral vision defects, sometimes from staphyloma shape or from detachment.

13. Double or shifted images if the macular surface is split (foveoschisis) or a macular hole changes fixation. NCBI

14. Color vision not as rich when the macula is damaged.

15. Slow visual recovery after light due to photoreceptor/RPE stress in long, thinned eyes.

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20 diagnostic tests (grouped and explained)

Doctors will tailor these tests to the person. Not all are needed for every patient. Some tests confirm pathologic changes; others check complications or risk.

A) Physical examination (at the slit lamp and with lenses)

1. Best-corrected visual acuity (distance and near). This shows how well you see with the right prescription and tracks change over time.

2. Pupil checks and RAPD test. Healthy light responses help rule out nerve damage.

3. External and eye movement exam. Looks for eye alignment problems and any outward signs of connective tissue disorders.

4. Anterior segment slit-lamp exam. Checks for lens tilt/subluxation, early cataract, or narrow angles (all sometimes seen with high myopia or syndromes). EyeWiki

5. Dilated fundus examination (indirect ophthalmoscopy). This is the core step. The doctor looks for tessellation, lacquer cracks, areas of atrophy, CNV scars (Fuchs spots), lattice degeneration, or a posterior staphyloma. ScienceDirectPMC

B) Manual and functional clinic tests

6. Pinhole test. A quick way to tell if blur is from refractive error or macular disease.

7. Retinoscopy and subjective refraction. These measure the true focusing power and pick up rapid progression.

8. Goldmann applanation tonometry. Checks eye pressure, because myopes have higher glaucoma risk and thin corneas can hide high pressure.

9. Confrontation visual fields. A bedside screen for gross peripheral field loss.

10. Standard automated perimetry (Humphrey or similar). Maps subtle field loss from glaucoma or macular disease in long eyes.

11. Amsler grid. A simple paper or screen test to pick up new central distortion from CNV or macular traction.

C) Laboratory and pathological context (used selectively)

12. Genetic testing when syndromes are suspected (e.g., COL2A1/COL11A1 for Stickler; FBN1 for Marfan). This helps explain very early high myopia, frequent detachments, or systemic signs. NCBIAAO

13. Plasma homocysteine when homocystinuria is suspected (child with lens subluxation, developmental clues). Treating the metabolic cause can limit lens-induced high myopia. PMC

14. Vitamin D level or other systemic markers in research or special cases, as low outdoor time and biology interact; not routine for diagnosis but sometimes part of a broader myopia assessment. MDPI

D) Electrodiagnostic tests (when the structure looks worse than vision—or vice versa)

15. Full-field ERG (electroretinography). Tests whole-retina function when atrophy seems widespread.

16. Multifocal ERG. Focuses on macular function to match OCT changes in foveoschisis or CNV scars.

17. Pattern ERG and VEP (visual evoked potentials). Differentiate macular vs optic-nerve dysfunction when vision is poor but the view is unclear.

E) Imaging and biometry (the heart of modern diagnosis)

18. Optical coherence tomography (OCT) of the macula (including enhanced-depth imaging). This shows myopic traction maculopathy (foveoschisis, shallow detachments), lamellar or full-thickness macular holes, ellipsoid-zone damage, and choroidal thinning in exquisite detail. NCBI

19. OCT-Angiography (OCT-A). Non-invasive flow maps help detect myopic CNV early, guide treatment, and monitor for recurrence. Retina Today

20. Color fundus photography and ultra-widefield imaging. These record tessellation, atrophy, lacquer cracks, and staphyloma outlines and are great for tracking change over years. Fluorescein angiography and indocyanine green angiography are added when leakage or CNV is suspected. B-scan ultrasound helps when the view is cloudy, and optical/ultrasound biometry measures axial length to track eye growth. AAORetina Today

Non-pharmacological treatments (therapies and “other” measures)

Below are practical, drug-free actions. Some protect children from getting worse. Some help adults live better with the condition. For each item you’ll see: Description, Purpose, Mechanism (how it helps).

1. Regular dilated eye exams with OCT and wide-field imaging
   Description: Visit your ophthalmologist as advised (often every 6–12 months; sooner if symptoms).
   Purpose: Early detection of mCNV, macular traction, holes, or retinal tears.
   Mechanism: Careful imaging finds small leaks, splits, or tears before they cause permanent vision loss.

2. Fast attention to new warning symptoms
   Description: Treat any new floaters, flashes, a curtain/shadow, sudden blur, or metamorphopsia (wavy lines) as urgent.
   Purpose: Quick care can save sight in mCNV or retinal detachment.
   Mechanism: Early laser/surgery/injections before damage spreads.

3. Outdoor time for children and teens (≈2 hours/day)
   Description: Daily daylight exposure during school years.
   Purpose: Slow myopia progression when young (reduces future risk of pathologic changes).
   Mechanism: Bright light increases retinal dopamine, which slows axial elongation.

4. Near-work ergonomics
   Description: Keep reading screens/books ≥30–40 cm away; sit upright.
   Purpose: Reduce eye strain and accommodative stress.
   Mechanism: Less “pull” on focus systems may curb signals that encourage eye growth in youth.

5. 20-20-20 breaks
   Description: Every 20 minutes, look at something ≥20 feet away for 20 seconds.
   Purpose: Relax focusing muscles and reduce fatigue.
   Mechanism: Frequent relaxation limits sustained accommodative demand.

6. Good lighting and glare control
   Description: Use bright, even room light and reduce glare.
   Purpose: Clearer vision and less strain.
   Mechanism: Better contrast lowers accommodative effort.

7. Correct and update your spectacle prescription
   Description: Wear accurate glasses (or contacts).
   Purpose: Prevent constant squinting and strain; protect mobility and safety.
   Mechanism: Clear focus reduces unnecessary effort and improves quality of life.

8. Myopia-control spectacles (e.g., DIMS-type lenses) for kids
   Description: Special spectacle designs create peripheral myopic defocus.
   Purpose: Slow progression in children at risk of high/pathologic myopia.
   Mechanism: Peripheral image focus sends “slow down” signals to eye growth systems.

9. Multifocal soft contact lenses for kids/teens
   Description: Daily wear with center-distance optics and peripheral defocus.
   Purpose: Slow axial elongation.
   Mechanism: Similar myopic defocus effect to #8.

10. Orthokeratology (Ortho-K) for carefully selected youth
    Description: Overnight rigid lenses temporarily flatten the cornea.
    Purpose: Slows progression and offers daytime unaided vision.
    Mechanism: Changes peripheral focus profile; requires strict hygiene to reduce infection risk.

11. Rigid gas-permeable (RGP) lenses for high prescriptions
    Description: Hard lenses that give sharp optics in very high myopia or irregular corneas.
    Purpose: Improve image quality when glasses are heavy or distorted.
    Mechanism: Stable optical surface can reduce aberrations.

12. UV-blocking sunglasses and brimmed hats outdoors
    Description: Quality sunglasses with UV-A/UV-B blocking.
    Purpose: Protect fragile macula and lens from light stress.
    Mechanism: Lower cumulative light damage on thin tissues.

13. Healthy sleep (7–9 hours for adults; age-appropriate for kids)
    Description: Regular sleep schedule, dark room, limited late-night screens.
    Purpose: Supports hormonal balance and visual comfort.
    Mechanism: Good circadian rhythm may stabilize visual function and behavior.

14. Exercise and cardiovascular health
    Description: Moderate exercise most days.
    Purpose: Support retinal and optic nerve blood flow and overall resilience.
    Mechanism: Better vascular health benefits delicate ocular microcirculation.

15. Stop smoking and avoid secondhand smoke
    Description: Tobacco damages blood vessels and raises many eye risks.
    Purpose: Protect macula and optic nerve.
    Mechanism: Less oxidative stress and vascular injury.

16. Control blood pressure and blood sugar
    Description: Treat hypertension and diabetes as advised.
    Purpose: Reduce microvascular damage in already thin choroids/retina.
    Mechanism: Stable perfusion protects fragile macula.

17. Low-vision rehabilitation when needed
    Description: Magnifiers, electronic readers, contrast enhancement, training.
    Purpose: Maximize remaining vision if macular atrophy or scars develop.
    Mechanism: Optical and training strategies improve function despite damage.

18. Safe home and work lighting, contrast, and layout
    Description: Bright task lights, high-contrast labels, decluttered pathways.
    Purpose: Prevent falls and improve reading/work accuracy.
    Mechanism: Better visibility reduces accidents and strain.

19. Protective eyewear for sports and risky tasks
    Description: Polycarbonate sports goggles or safety glasses.
    Purpose: Prevent eye trauma that could cause retinal tears/detachment.
    Mechanism: Physical barrier blocks impact.

20. Education and symptom diary
    Description: Learn warning signs; keep a simple log if vision fluctuates.
    Purpose: Recognize changes early and communicate clearly with your doctor.
    Mechanism: Earlier presentation → earlier intervention → better outcomes.

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Drug treatments

Important: Doses and timing below are typical. Your ophthalmologist may adjust based on your eye, imaging, and response. Many medicines below treat complications of pathologic myopia (especially myopic CNV). They do not make the eye shorter; they stop leakage, bleeding, or swelling and protect the macula.

1. Ranibizumab (anti-VEGF intravitreal injection)
   Class: Anti-VEGF antibody fragment.
   Dosage & Time: 0.5 mg/0.05 mL injected into the eye. Often one injection, then monitor monthly with OCT and re-inject as needed. Many patients need 1–3 injections in the first year for mCNV.
   Purpose: Stop abnormal vessel growth and leakage under the macula.
   Mechanism: Blocks VEGF, the signal that drives new leaky vessels.
   Side effects: Temporary irritation/floaters; rare infection (endophthalmitis), inflammation, pressure spikes, very rare retinal tear/detachment.

2. Aflibercept (anti-VEGF intravitreal)
   Class: VEGF-trap fusion protein.
   Dosage & Time: 2 mg/0.05 mL intravitreal. Often one injection followed by as-needed re-treatment with close OCT checks.
   Purpose/Mechanism: Same goal as ranibizumab—shut down leakiness and bleeding by binding VEGF.
   Side effects: Similar to ranibizumab.

3. Bevacizumab (anti-VEGF, off-label intravitreal)
   Class: Anti-VEGF monoclonal antibody.
   Dosage & Time: 1.25 mg/0.05 mL intravitreal, as needed based on OCT/vision.
   Purpose/Mechanism: Same VEGF blockade; used off-label in many countries.
   Side effects: As above; discuss off-label use and quality control with your doctor.

4. Verteporfin photodynamic therapy (PDT)
   Class: Light-activated photosensitizer (systemic, then laser activation to the lesion).
   Dosage & Time: 6 mg/m² IV over ~10 minutes, then a 689-nm laser dose to the CNV spot. Some patients need repeat PDT if leakage recurs.
   Purpose: Close abnormal vessels if anti-VEGF is unsuitable or as an adjunct in select cases.
   Mechanism: Drug accumulates in CNV; light activation damages abnormal vessels while sparing most surrounding tissue.
   Side effects: Photosensitivity (avoid bright light/sun for ~48 hours), infusion reactions; rare vision changes.

5. Low-dose atropine eye drops (for children/teens at high risk)
   Class: Muscarinic antagonist (cycloplegic).
   Dosage & Time: 0.01%–0.05%, 1 drop nightly in each eye, typically for years under supervision.
   Purpose: Slow myopia progression in youth, lowering future risk of pathologic changes.
   Mechanism: Alters retinal/scleral signals that drive eye growth.
   Side effects: Light sensitivity, mild near blur, dry mouth/skin if absorbed; advise sunglasses and good drop technique.

6. Topical dorzolamide (select cases with macular edema/schisis; off-label)
   Class: Carbonic anhydrase inhibitor.
   Dosage & Time: 2%, 3 times daily, limited trial if your retina specialist recommends.
   Purpose: Try to reduce retinal fluid when surgery is not yet indicated.
   Mechanism: Promotes fluid movement out of the retina.
   Side effects: Stinging, bitter taste, rare allergic reactions.

7. Oral acetazolamide (short course; off-label for select macular fluid)
   Class: Carbonic anhydrase inhibitor.
   Dosage & Time: 250 mg 1–2 times daily for days–weeks if your specialist thinks a trial is reasonable.
   Purpose/Mechanism: Similar to dorzolamide but systemic; may reduce fluid in certain macular conditions.
   Side effects: Tingling in fingers/toes, frequent urination, taste change, fatigue, kidney stone risk, metabolic acidosis—not for everyone.

8. Latanoprost (if glaucoma co-exists)
   Class: Prostaglandin analogue (IOP-lowering).
   Dosage & Time: 0.005%, 1 drop nightly.
   Purpose: Protect the optic nerve if you also have open-angle glaucoma risk with high myopia.
   Mechanism: Increases eye fluid outflow to lower pressure.
   Side effects: Redness, eyelash growth, iris darkening, periocular skin darkening.

9. Brimonidine (if glaucoma co-exists or as adjunct)
   Class: Alpha-2 agonist (IOP-lowering; possible neuroprotective effects).
   Dosage & Time: 0.2%, 2–3 times daily.
   Purpose: Additional pressure control.
   Mechanism: Lowers aqueous production and increases uveoscleral outflow.
   Side effects: Allergic conjunctivitis, dry mouth, fatigue.

10. Topical steroids/NSAIDs around eye surgery (peri-operative care)
    Class: Anti-inflammatory drops (e.g., prednisolone acetate; ketorolac).
    Dosage & Time: As directed around cataract or retinal surgery.
    Purpose: Control inflammation and reduce cystoid macular edema risk after surgery.
    Mechanism: Block inflammatory pathways that can blur vision post-op.
    Side effects: Pressure rise with steroids, surface irritation with NSAIDs; follow taper exactly.

Note: Newer anti-VEGF or dual-pathway agents and some regional drugs (e.g., faricimab, conbercept) may be used in certain countries or as off-label options; your specialist will guide this based on local approvals and evidence.

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Dietary molecular supplements (adjuncts)

Supplements do not cure pathologic myopia. They may support retina metabolism and antioxidant defenses, especially if your diet is low in these nutrients. Discuss each with your doctor, especially if you are pregnant, on blood thinners, or have kidney issues.

1. Lutein 10 mg/day + Zeaxanthin 2 mg/day
   Function: Build macular pigment, improving light filtering and antioxidant capacity.
   Mechanism: Concentrate in the macula and neutralize free radicals from light.

2. Omega-3 (EPA + DHA ≈ 1,000 mg/day combined)
   Function: Support retinal cell membranes and anti-inflammatory balance.
   Mechanism: Incorporate into photoreceptor membranes; produce less-inflammatory mediators.

3. Vitamin C 500 mg/day
   Function: Antioxidant recycling and collagen support.
   Mechanism: Reduces oxidative stress; aids connective tissue health.

4. Vitamin E 200 IU/day
   Function: Fat-soluble antioxidant for photoreceptor and RPE protection.
   Mechanism: Stabilizes cell membranes against oxidative damage.

5. Zinc 25–40 mg/day + Copper 2 mg/day
   Function: Enzyme co-factors for retinal metabolism; balance copper to prevent deficiency.
   Mechanism: Support antioxidant enzymes (e.g., superoxide dismutase).

6. Astaxanthin 6 mg/day
   Function: Potent antioxidant; may reduce asthenopia symptoms.
   Mechanism: Quenches singlet oxygen and lipid peroxidation.

7. Taurine 500–1,000 mg/day
   Function: Amino acid abundant in retina; supports photoreceptor function.
   Mechanism: Osmoregulation and membrane stabilization in retinal cells.

8. Coenzyme Q10 (Ubiquinone) 100–200 mg/day
   Function: Mitochondrial energy support and antioxidant action.
   Mechanism: Electron transport chain co-factor; reduces oxidative stress.

9. Bilberry extract 80–160 mg/day (standardized)
   Function: Anthocyanins for night-vision comfort and antioxidant effects.
   Mechanism: Scavenges free radicals; may improve microcirculation.

10. Saffron extract 20–30 mg/day (standardized to crocins)
    Function: Antioxidant/neuromodulatory support for macular function.
    Mechanism: Modulates retinal neurotransmission and oxidative balance.

Caution: Evidence is stronger for general macular support than for preventing pathologic myopia complications. Use as add-ons, not replacements for medical care.

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Regenerative / Stem-cell” drug concepts

It is important to be clear and safe: there are no approved “hard immunity booster” drugs that treat pathologic myopia or stop the eye from being long. Likewise, stem-cell and regenerative therapies for myopic maculopathy are investigational. You should not receive stem-cell injections or “regenerative” shots outside regulated clinical trials, because unapproved treatments have caused severe, permanent vision loss.

Here are six research/experimental directions to be aware of (for understanding only; no dosing because these are not approved for routine care):

1. iPSC-derived retinal pigment epithelium (RPE) sheets
   Goal: Replace damaged RPE in macular atrophy.
   Mechanism: Lab-grown cells support photoreceptors. Status: clinical trials only.

2. Photoreceptor precursor transplantation (iPSC/ESC-derived)
   Goal: Restore lost light-sensing cells.
   Mechanism: Cell replacement/integration. Status: early research.

3. Mesenchymal stem-cell–derived exosomes
   Goal: Deliver growth factors/anti-inflammatory signals without whole-cell risks.
   Mechanism: Nanovesicle signaling. Status: preclinical/early trials.

4. Ciliary neurotrophic factor (CNTF) implants
   Goal: Neuroprotection for degenerative retina.
   Mechanism: Slow photoreceptor loss. Status: limited trial data in other retinal diseases.

5. Gene-targeted anti-fibrosis / scleral remodeling approaches
   Goal: Strengthen sclera or reduce damaging scarring.
   Mechanism: Modulate TGF-β/ECM pathways. Status: experimental.

6. Cross-linking concepts for posterior sclera
   Goal: Stiffen the back of the eye to resist stretching.
   Mechanism: Photo/chemical cross-linking of scleral collagen. Status: investigational; not standard.

Bottom line: If you are interested in regenerative options, ask your retina specialist about legitimate clinical trials. Avoid any clinic offering high-priced “stem-cell cures” outside a registered trial.

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Surgeries

1. Pars plana vitrectomy (PPV) with internal limiting membrane (ILM) peel ± gas/oil
   Procedure: The surgeon removes the vitreous gel, peels a thin retinal membrane, and may place a gas bubble or silicone oil.
   Why: Treat myopic traction maculopathy, foveoschisis, or macular hole (with or without detachment) to flatten the retina and improve/restore central vision.

2. Macular buckling
   Procedure: A custom support (buckle) is placed outside the eye behind the macula.
   Why: Counteracts posterior staphyloma and traction, reducing stress on the macula when PPV alone may not be enough.

3. Retinal detachment repair (PPV, scleral buckle, or pneumatic retinopexy)
   Procedure: Reattach the retina using internal surgery, an external buckle, and/or a gas bubble; laser seals the breaks.
   Why: Emergency sight-saving treatment if the retina peels off, which is more common in long eyes.

4. Posterior scleral reinforcement (PSR) (select centers)
   Procedure: A graft/band is anchored on the back of the eye.
   Why: Attempt to slow progression of extreme axial elongation in youth/young adults with fast worsening. It is specialized and not widely available.

5. Cataract extraction with intraocular lens (IOL) in high myopia
   Procedure: Remove cloudy lens and implant an IOL; calculations are customized for long eyes.
   Why: Cataracts often start earlier in high myopia and can seriously blur vision. Careful planning reduces refractive surprises.

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Prevention tips

1. Get kids outside daily (target ~2 hours of daylight).

2. Keep reading distance ≥30–40 cm and use the 20-20-20 rule.

3. Bright, even task lighting; avoid long hours in dim rooms.

4. Update glasses/contacts regularly.

5. Do not smoke; avoid secondhand smoke.

6. Control blood pressure and blood sugar.

7. Wear UV-blocking sunglasses outdoors.

8. Use protective eyewear during sports or risky tasks.

9. Sleep enough and limit late-night screen glare.

10. Attend scheduled eye exams; never ignore new floaters, flashes, or a shadow.

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When should you see a doctor urgently?

• Sudden new floaters, flashes of light, or a dark curtain from any side (possible tear/detachment).

• Sudden central blur, distortion, or wavy lines (possible myopic CNV or macular traction).

• Pain, redness, light sensitivity, or vision drop after an injection or surgery.

• Any rapid change in vision you can’t explain.

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What to eat” and “what to avoid/limit

1. Eat: Dark leafy greens (spinach, kale) for lutein/zeaxanthin. Limit: Deep-fried/processed foods that raise oxidative stress.

2. Eat: Oily fish (salmon, sardines) 2–3×/week for omega-3s. Limit: Trans fats and excess omega-6 oils.

3. Eat: Eggs, corn, orange/yellow veggies for macular pigments. Limit: High-glycemic snacks that spike sugar.

4. Eat: Citrus/berries for vitamin C. Limit: Sugary drinks and desserts.

5. Eat: Nuts/seeds for vitamin E and minerals. Limit: Excess salt if you have blood pressure issues.

6. Eat: Beans/lean proteins for overall tissue repair. Limit: Heavy alcohol (damages nutrition and sleep).

7. Eat: Whole grains for steady energy. Limit: Highly refined carbs that may worsen vascular health.

8. Eat: Hydrate with water; keep eyes and body well hydrated. Limit: Energy drinks late at night (sleep disruption).

9. Eat: Colorful fruits/veg daily “rainbow.” Limit: Smoking (not food, but top “avoid”).

10. Consider: Evidence-based supplements (see list) after medical advice. Avoid: Mega-doses without supervision.

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Frequently asked questions

1) Is pathologic myopia the same as “high myopia”?
High myopia means a strong prescription or long eye. Pathologic myopia means the eye is long and has tissue damage (maculopathy, staphyloma, etc.). Not everyone with high myopia has pathology, but risk rises with eye length.

2) Can glasses or LASIK cure pathologic myopia?
No. Glasses, contacts, and laser surgery focus light better but do not shorten the eye or repair thin tissues. They help clarity but not the underlying stretching.

3) Can anti-VEGF injections cure the disease?
They treat myopic CNV, stopping leakage and bleeding and often improving vision. They do not reverse staphyloma or make the eye shorter. Many patients need few injections compared with AMD, but careful follow-up is vital.

4) Will I need injections forever?
Many mCNV cases respond to 1–3 injections in year one, then monitor only. Some need more. Your OCT scans guide timing.

5) Is low-dose atropine only for kids?
Yes, it’s mainly to slow eye growth in children/teens. It does not treat adult degenerative changes.

6) Are supplements required?
No. A healthy diet is the base. Supplements are adjuncts, helpful if your diet is low in specific nutrients. They do not replace medical treatment.

7) Can pathologic myopia cause blindness?
It can cause serious vision loss if complications are untreated (CNV, detachment, macular atrophy). Early detection and treatment greatly improve outcomes.

8) How often should I be checked?
Your doctor decides based on risk. Many adults go every 6–12 months; sooner after a recent CNV, surgery, or new symptoms.

9) I see straight lines as wavy. What does that mean?
That is metamorphopsia, often from macular swelling or traction. It needs prompt retina evaluation.

10) Can pregnancy affect myopic eyes?
Most do well. Rarely, fluid changes may influence the retina. Report new symptoms at once; keep scheduled checks.

11) Is screen time dangerous for pathologic myopia?
Screens don’t directly cause degeneration, but long, close viewing strains the system. Use good distance, bright light, and breaks.

12) Can I exercise normally?
Yes, most people can. Avoid high-impact or contact sports without eye protection. Ask your surgeon about post-op restrictions if you’ve had retinal surgery.

13) Does sleeping position matter?
Not usually. After certain surgeries, your doctor may ask for face-down or other positioning for a short time.

14) Are “stem-cell” eye injections available?
Only in clinical trials. Avoid commercial “stem-cell cures.” Unapproved injections have caused blindness.

15) What is my long-term outlook?
With regular monitoring, fast treatment of complications, and healthy habits, many people keep useful vision for life. The key is early detection and consistent follow-up.

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 20, 2025.