Myelinated Retinal Nerve Fiber Layer (MRNFL)

Myelinated retinal nerve fiber layer means the insulating “white coating” (myelin) that normally stops at the back of the eye has grown a little farther forward than usual, onto the retina itself. Doctors see this as bright white, feathery patches when they look into the eye with a light. It is usually present from birth. Most people never notice it. Many people see perfectly fine. In most eyes, nerve fibers inside the retina do not have myelin. The myelin starts only after the fibers leave the eye through a sieve-like plate called the lamina cribrosa and become the optic nerve. In MRNFL, that boundary is not strict. A few myelin-making cells (oligodendrocytes) extend forward into the retina. They lay down myelin where we usually do not see it.

Inside your eye, the retina sends signals to the brain through “wires” called retinal nerve fibers. Normally, these fibers become insulated with myelin behind the eye (after they pass through a sieve-like plate called the lamina cribrosa). In MRNFL, that insulation extends onto the retina itself, so you can actually see the myelin during a dilated exam as white, brush-stroke or feather-edge patches that follow the nerve-fiber “grain.” It’s not a tumor and not an infection—it’s mostly a developmental quirk that stays stable over life.

The patches look snow-white with a fuzzy edge that follows the normal pattern of the retinal nerve fibers. They often start at the optic disc (the “nerve head”) and run out in arcs toward the sides. The blood vessels are still visible but may look “buried” under the white. The patches do not move. They do not scrape off. They usually stay the same for life. Usually, no. Most cases are harmless and do not change. Some people have related issues like high nearsightedness in the same eye and “lazy eye” (amblyopia) from childhood. Vision can be reduced if the patch covers the center of sight (the macula) or if strong glasses were not given early in life.

Myelin is like plastic on an electrical wire. It helps the nerve send signals fast. The lamina cribrosa is meant to be the “front gate” that keeps myelin-making cells behind the eye. In MRNFL, the gate is leaky or formed a bit differently during development, so the myelin extends forward onto the retina. We think this happens before birth. In rare cases, new myelination appears later after optic nerve disease. Most of the time it is just a normal variant of development.

Types of Myelinated Retinal Nerve Fiber Layer

1. By side involved

• Unilateral (one eye): Most common. One eye shows patches, the other looks normal.

• Bilateral (both eyes): Less common. Both eyes have patches, often in different shapes.

2. By location

• Peripapillary (around the optic disc): The classic pattern. White feathery patches radiate from the nerve head.

• Peripheral (away from the disc): Less common. Islands of white farther out in the retina.

• Macula-involving: Rare. Patches reach the center of reading vision and may reduce clarity.

3. By extent

• Focal: Small, limited area. Usually no symptoms.

• Extensive: Long arc of myelination following the nerve fiber bundles. More likely to be linked with refractive error or field defects.

4. By timing

• Congenital/static: Present from birth and stable for life (most cases).

• Acquired/progressive (rare): Appears or grows later, usually after optic nerve disease or swelling. Your eye doctor will look for a cause in these unusual cases.

5. By association (the “Straatsma triad”)

• MRNFL + high myopia + amblyopia: A known cluster. The eye with the white patch tends to be more nearsighted and may be “lazy” if not corrected early.

Causes and Contributors

Truth in simple terms: the main cause is a developmental variation before birth. Many items below are associations or contributors, not direct causes. They help explain why MRNFL is present or how it shows up, but they may not “cause” it the way an infection causes fever.

1. Developmental spill-over of myelin
   The lamina cribrosa formed in a way that let myelin-making cells move a little forward into the retina. This is the core reason.

2. Abnormal boundary signaling
   Chemical signals that usually stop oligodendrocytes at the nerve head may be weaker or different in that eye, letting myelin extend.

3. Genetic variation in myelination controls
   Small inherited differences in genes that guide myelin growth could allow forward spread. This is a general concept; no single gene is proven for most people.

4. High axial myopia (long eyeball)
   A long eye changes the shape and tension of tissues near the nerve head. This may make the boundary more permissive. Often seen in the same eye as MRNFL.

5. Anisometropia (big power difference between eyes)
   A strong mismatch in glasses power, often due to high myopia on the MRNFL side, is commonly linked. It does not directly create myelin but travels with the condition.

6. Amblyopia (lazy eye) from early blur
   Not a cause of myelin, but the presence of MRNFL with strong myopia can lead to blurred input in childhood and then amblyopia if not corrected early.

7. Optic disc developmental variants
   Subtle differences in the nerve head and lamina cribrosa shape can make forward myelination more likely.

8. Peripapillary tissue remodeling
   Local changes around the disc (connective tissue, glial cells) could help myelin persist on the retina.

9. Neurofibromatosis type 1 (NF1) association
   Some patients with NF1 show MRNFL. NF1 alters cell growth and myelin biology. Association is uncommon but real.

10. Tuberous sclerosis complex (TSC) association
    Another neurocutaneous condition where retinal findings are more frequent. MRNFL can be one of them.

11. Rare post-inflammatory extension
    Very rarely, after optic neuritis or inflammatory optic nerve disease, new myelination appears at the disc edge.

12. Chronic optic disc swelling (papilledema) history
    Long-standing swelling may slightly alter barriers around the nerve head. Acquired myelination has been reported in rare cases.

13. Optic nerve head trauma history
    Injury can disturb local barriers and cell signals, leading to unusual myelin patterns afterward (rare).

14. Glial cell migration differences
    Müller cells and astrocytes support nerve fibers. Developmental differences might allow oligodendrocytes to cross into the retina.

15. Prematurity and early ocular development factors
    Most premature infants do not have MRNFL, but early development differences could, in theory, affect boundary formation in a few.

16. Maternal-fetal factors affecting neural myelination
    General influences on the timing of myelination in the nervous system could nudge where the boundary ends up. This is theoretical, not a proven direct cause.

17. Local vascular pattern at the disc
    Blood vessel layout sometimes parallels the spread of myelin. Vessel anatomy is not a cause, but it may shape the patch.

18. Hereditary pattern in families (rare)
    Most cases are sporadic, but MRNFL may cluster in families, suggesting shared developmental traits.

19. Coexisting optic disc anomalies (e.g., tilted disc)
    A tilted or crowded disc can change tissue planes and may make forward myelination more likely.

20. Unknown/idiopathic
    In many people, no special risk factor is found. The patch is simply a benign developmental variant discovered on routine exam.

Symptoms and Everyday Clues

Many people have no symptoms. Findings are often discovered during a routine eye exam or school screening.

1. No symptoms at all
   Most people see normally because the patch spares the central macula.

2. Blurred vision in one eye
   If the patch involves the macula or if strong myopia is present, the affected eye may see less clearly.

3. Vision that does not fully clear with glasses
   Even with the right prescription, the eye may lag due to amblyopia from early life blur.

4. Eye turn (strabismus)
   A child may develop a small eye turn if one eye sees much worse than the other.

5. Poor results on school vision screening
   Screeners notice one eye fails the line test; the other passes.

6. Reduced depth perception (stereo)
   If one eye is weaker, 3-D vision can be poorer.

7. Visual field “missing spots”
   An arcuate scotoma or enlarged blind spot can appear in the map of side vision, matching the myelinated bundle.

8. Eyes tire with reading (asthenopia)
   Extra effort to fuse unequal inputs can cause fatigue.

9. Squinting or head tilt
   A child may favor positions that use the stronger eye more.

10. Light glare sensitivity (sometimes)
    Bright light may feel harsh if the macula is stressed, though this is not a core feature.

11. Reduced contrast sensitivity
    Fine gray-on-gray details can be harder in the weaker eye.

12. Color vision slightly off in the affected eye (rare)
    If the macula is involved, certain color tasks may be less accurate.

13. Slow reading with one eye covered
    Monocular reading can reveal a speed difference.

14. Trouble catching fast balls or judging distances
    Sports that need perfect depth cues can feel harder.

15. Subtle head turning in photographs
    Families sometimes notice a child consistently favors one viewing angle.

Diagnostic Tests

Goal: confirm the white patches are myelinated nerve fibers, not something dangerous; map vision; check for linked issues like high myopia or amblyopia; and rule out rare acquired causes.

A) Physical Exam

1. Best-corrected visual acuity (distance and near)
   Simple letter charts show how sharp each eye sees with the best prescription. It tells us if there is real vision loss and whether it is symmetrical.

2. Pupil exam and swinging-flashlight test
   Checks for a relative afferent pupillary defect. MRNFL usually does not cause an RAPD, which helps separate it from optic nerve damage.

3. Confrontation visual fields
   A quick bedside check of side vision. If a defect is suspected, formal field testing follows.

4. Extraocular movements and alignment
   Looks for strabismus, which can accompany amblyopia on the MRNFL side.

5. Dilated fundus exam
   The key step. With dilated pupils, the doctor sees bright, feathery, non-elevated white patches along nerve fiber bundles. The disc and macula are evaluated carefully.

B) Manual / Clinical Function Tests

6. Cycloplegic refraction (often with retinoscopy)
   Drops relax focusing. The doctor measures true glasses power, often finding higher myopia in the MRNFL eye. Correcting this early helps prevent amblyopia.

7. Pinhole acuity test
   A quick way to see if blur improves when peripheral rays are blocked. Limited improvement suggests amblyopia or macular involvement.

8. Color vision plates (e.g., Ishihara or HRR)
   Useful to compare eyes. Most MRNFL patients have normal color unless the macula is involved.

9. Amsler grid (near macular function)
   A simple grid can show distortion if a patch involves the macula, though most MRNFL patients see a normal grid.

10. Cover–uncover and alternate cover tests
    These reveal small eye turns linked to unequal vision between eyes.

C) Laboratory / Pathological

11. Genetic testing when neurocutaneous signs are present
    If café-au-lait spots, neurofibromas, or other features suggest NF1, targeted genetic testing may be ordered. This is not routine for isolated MRNFL.

12. Systemic work-up when acquired change is suspected
    If new myelination appears after inflammation, blood tests for infection/inflammation or autoimmune markers may help rule out other causes. Not needed for stable congenital cases.

13. Documentation for amblyopia therapy
    Not a lab test in the blood sense, but formal records of risk factors (anisometropia, high myopia) guide patching or vision therapy decisions and protect against overtreatment.

D) Electrodiagnostic

14. Pattern Visual Evoked Potential (VEP)
    Measures how well signals travel from the eye to the brain. In classic MRNFL with normal macula, the VEP is often near normal; abnormalities suggest additional optic pathway issues.

15. Full-field Electroretinography (ERG)
    Checks overall retinal function. MRNFL itself does not damage the retina’s light response, so ERG is usually normal unless another retinal disease is present.

16. Pattern ERG (pERG)
    Sensitive to macular and ganglion cell function. If the myelination involves the macula or there is significant amblyopia, pERG may show changes.

E) Imaging / Instrument-Based

17. Color fundus photography
    Creates a permanent picture of the white feathery patches. Helpful for monitoring and explaining the finding to families.

18. Optical Coherence Tomography (OCT) of RNFL and macula
    A light-based scan that measures retinal layers. In MRNFL, the RNFL where the patch sits looks very thick and bright. The macula is checked for normal foveal structure.

19. OCT-Angiography (OCTA)
    Shows the tiny blood vessels without dye. Vessels run through myelinated areas normally. OCTA helps distinguish MRNFL from vascular or inflammatory lesions.

20. Automated perimetry (formal visual field)
    Maps any arcuate defects or blind-spot enlargement that align with the myelinated bundles. This helps with counseling and follow-up.

Non-pharmacological treatments

1. Full cycloplegic refraction + correct glasses/contact lenses
   • What: Careful, dilated refraction to prescribe the right lens power.
   • Purpose: Treat anisometropia and blur—the root driver of amblyopia.
   • Mechanism: Clear, focused image to the brain from the weaker eye.

2. Part-time occlusion (“patching”) of the stronger eye
   • What: Cover the better eye 2–6 hours/day depending on age/severity.
   • Purpose: Force the brain to use the amblyopic eye, improving vision.
   • Mechanism: Neuroplastic remodeling of visual cortex from increased demand. Evidence from multiple PEDIG trials supports patching doses.

3. Bangerter filters on the stronger eye
   • What: A translucent foil stuck on the glasses lens to gently blur the strong eye.
   • Purpose: An alternative to patching with lower treatment burden.
   • Mechanism: Partial deprivation increases amblyopic-eye use; RCTs show similar average acuity gains to patching in moderate amblyopia.

4. At-home near or distance activities during patching (for adherence)
   • What: Crafts, reading, tablet time at a set distance while patched.
   • Purpose: Keep kids engaged to improve compliance (not to “supercharge” patching).
   • Mechanism: Engagement; RCT shows no extra vision gain from near vs distance per se.

5. Contact lenses for large anisometropia
   • What: Soft or rigid lenses to reduce image-size difference between eyes.
   • Purpose: Make amblyopia therapy more effective and comfortable.
   • Mechanism: Reduces aniseikonia better than glasses.

6. Orthokeratology (overnight corneal reshaping) for myopia control (selected children)
   • What: Night lenses that temporarily flatten the cornea.
   • Purpose: Slow myopia progression in appropriate children.
   • Mechanism: Alters peripheral defocus; meta-analyses show reduced axial elongation vs controls. (Requires meticulous hygiene and specialist fitting.)

7. Multifocal/dual-focus soft contact lenses for myopia control (e.g., MiSight)
   • What: Daily lenses with concentric treatment zones.
   • Purpose: Slow myopia progression in eligible kids (ages per approval/label).
   • Mechanism: Creates myopic defocus to reduce eye growth; MiSight has FDA approval to slow progression.

8. Amblyopia therapy schedule optimization & adherence coaching
   • What: Consistent follow-up (every 6–12 weeks initially), charts/calendars.
   • Purpose: Prevent regression; adjust dose; sustain family engagement.
   • Mechanism: Behavioral support improves dose delivered.

9. Prism glasses (symptomatic strabismus)
   • What: Prisms to align images when surgery isn’t indicated.
   • Purpose: Reduce double vision and improve comfort.
   • Mechanism: Shifts the image to compensate for small deviations.

10. Vision rehabilitation / low-vision aids (severe, uncommon cases)
    • What: Magnifiers, contrast tools, classroom accommodations.
    • Purpose: Maximize function if acuity stays reduced.
    • Mechanism: Optical/electronic enhancement.

11. School and reading ergonomics
    • What: Proper reading distance (≈ 30–40 cm), good lighting, frequent breaks.
    • Purpose: Reduce asthenopia and support therapy compliance.
    • Mechanism: Limits sustained near strain.

12. Outdoor-time habit building (≥ 1–2 hours/day when feasible)
    • What: Structured outdoor play.
    • Purpose: Lowers risk of new myopia and may slow progression.
    • Mechanism: Bright light & viewing distance cues; a large cluster-RCT showed reduced incident myopia with added outdoor time.

13. Protective eyewear for sports/rough play
    • What: Polycarbonate sports glasses.
    • Purpose: Reduce trauma risk to the better-seeing eye.
    • Mechanism: Physical protection.

14. Keratoconus care if present (rare association)
    • What: Corneal cross-linking to halt corneal weakening.
    • Purpose: Stabilize vision if keratoconus coexists.
    • Mechanism: UV-riboflavin stiffens corneal collagen. (Reported in Straatsma cases.)

15. Lifestyle hygiene for contact-lens wearers
    • What: No water exposure; strict cleaning or daily disposables.
    • Purpose: Prevent infections that could derail therapy.
    • Mechanism: Cuts microbial risk.

16. Documentation & photography at baseline
    • What: High-quality widefield photos.
    • Purpose: Track stability (MRNFL typically doesn’t change).
    • Mechanism: Objective comparison across years.

17. Team-based care (optometry + pediatric/strabismus ophthalmology)
    • What: Co-managed plans for amblyopia/strabismus.
    • Purpose: Best outcomes with timely escalation.
    • Mechanism: Right therapy at the right time.

18. Education about OCT limits near MRNFL
    • What: Set expectations if glaucoma is being followed.
    • Purpose: Avoid over- or under-treating based on artifact-prone RNFL numbers.
    • Mechanism: Clinician anchors decisions to disc photos/fields over raw OCT metrics.

19. Screening of siblings/early childhood vision screening
    • What: AAP/USPSTF-style screening at ages 3–5.
    • Purpose: Catch amblyopia risk early.
    • Mechanism: Early detection improves response to therapy.

20. Set a durable follow-up cadence
    • What: Periodic checks (e.g., annually once stable; sooner during therapy).
    • Purpose: Ensure glasses are current, amblyopia isn’t regressing, and nothing new appears.
    • Mechanism: Timely tweaks maintain gains.

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Medicines:

Important: There is no drug that removes MRNFL. Medicines are used only to treat companions like amblyopia, myopia progression, strabismus, or rare complications. We avoid listing speculative or unproven drugs.

1) Atropine 1% eye drops (for amblyopia penalization)

• Class: Antimuscarinic.

• How it’s used: 1 drop in the stronger eye daily or weekends-only; duration months, adjusted by response.

• Purpose: Blur the stronger eye at near to force the brain to use the amblyopic eye (alternative to patching).

• Mechanism: Cycloplegia/mydriasis in the fellow eye.

• Side effects: Light sensitivity, near blur, rare flushing/dry mouth (seek care if severe).

• Evidence: PEDIG RCTs showed atropine and patching produce similar gains in many kids with moderate amblyopia, with good long-term outcomes.

2) Low-dose atropine (0.05% ≈ most effective, 0.025% or 0.01%) for myopia control

• Class: Antimuscarinic (very low concentration, both eyes at bedtime).

• Purpose: Slow axial elongation in progressing myopia (eligible children).

• Mechanism: Biochemical modulation of scleral/retinal signaling.

• Side effects: Mild pupil dilation and near blur proportional to dose; usually well tolerated.

• Evidence: LAMP trials show dose-dependent slowing of myopia (0.05% best) with multi-year safety.

3) Botulinum toxin A injections (for selected strabismus)

• Class: Neuromuscular blocker (office/OR procedure by specialist).

• Purpose: Temporarily weaken an overacting muscle to improve alignment.

• Mechanism: Blocks acetylcholine release at the neuromuscular junction.

• Side effects: Temporary ptosis, over/undercorrection, rare complications.

• Evidence: Widely used as an adjunct or alternative in specific strabismus patterns (evidence base outside MRNFL).

4) Anti-VEGF injections (ranibizumab/aflibercept/bevacizumab) for rare neovascularization

• Class: Vascular endothelial growth factor inhibitors.

• Purpose: Treat retinal neovascular complications if they occur near MRNFL.

• Mechanism: Regresses abnormal vessels and leakage.

• Side effects: Usual intravitreal risks (endophthalmitis, IOP spikes).

• Evidence: Neovascularization is uncommon; when present, anti-VEGF or laser can be used per standard retina protocols.

5–8) Glaucoma drops (only if true glaucoma coexists, which is not caused by MRNFL)

• Classes & examples:
  5) Prostaglandin analog (e.g., latanoprost) nightly;
  6) Beta-blocker (e.g., timolol) once–twice daily;
  7) Alpha-2 agonist (e.g., brimonidine) twice–thrice daily (avoid in very young children);
  8) Topical carbonic anhydrase inhibitor (e.g., dorzolamide) twice–thrice daily.

• Evidence: Standard glaucoma care; caution interpreting OCT RNFL thickness near MRNFL.

9) Cycloplegic drops (e.g., cyclopentolate/atropine) for diagnostic refraction

• Purpose: Allow accurate lens power for amblyopia therapy.

• Note: This is for measuring, not a long-term “treatment” of MRNFL.

10) (Intentionally left blank for speculative agents)

• There are no additional, evidence-based drug treatments specific to MRNFL. Using “regenerative/stem-cell drugs” here would be unsafe and inaccurate (see below).

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Surgeries

1. Strabismus surgery (muscle recession/resection).
   Why: Correct a constant, cosmetically or functionally significant eye turn that persists after optical/amblyopia therapy.
   What happens: One or more eye muscles are repositioned to improve alignment.
   Outcome: Better alignment, often improved binocular function in kids.

2. Laser photocoagulation (if MRNFL-adjacent neovascularization appears; rare).
   Why: Seal leaking vessels; reduce risk of bleeding.
   What happens: Targeted laser spots applied to abnormal areas.

3. Cataract surgery (if a visually significant cataract coexists—not caused by MRNFL).
   Why: Clear the visual axis to support amblyopia therapy/vision.

4. Corneal cross-linking (only if keratoconus is present in the same eye).
   Why: Halt progressive corneal thinning that can worsen vision.

5. Refractive surgery or phakic IOL in carefully selected older teens/adults with extreme anisometropia after amblyopia therapy.
   Why: Reduce image-size differences if contacts aren’t tolerated.
   Note: Case-by-case; requires subspecialist evaluation.

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Prevention

You can’t prevent MRNFL—it’s a developmental variant. But you can reduce risks from its companions (amblyopia/myopia/strabismus) and protect vision.

1. Childhood vision screening at 3–5 years (sooner if concerns).

2. Get accurate glasses early for anisometropia/myopia.

3. Follow amblyopia plans (patching/atropine/filter) exactly as prescribed.

4. Build daily outdoor time (aim ≥ 1–2 hours when feasible).

5. Near-work breaks (20-20-20 rule).

6. Healthy reading distance & lighting for kids.

7. Consider myopia-control options (orthokeratology, MiSight, low-dose atropine) where appropriate.

8. Protective eyewear for sports.

9. Don’t smoke (and avoid secondhand smoke); prioritize overall health.

10. Keep follow-ups—adjust prescriptions and therapy promptly.

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When to see a doctor

• New MRNFL finding and you haven’t had a full pediatric/strabismus work-up.

• Any child with an eye turn, squinting, closing one eye, or failing vision screening.

• Noticeable vision drop, new double vision, or new visual-field shadows.

• Rapid change in patch size/appearance (rare; prompts re-evaluation).

• Contact-lens wearers with redness, pain, or discharge (possible infection).

• During treatment: if light sensitivity or near blur from atropine is severe or if patching causes distress you can’t manage at home.

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What to eat (and what to avoid)

No specific diet changes MRNFL. Think “general eye-healthy pattern.”
Eat more: leafy greens (lutein/zeaxanthin), colorful fruits/veg (vitamin C, carotenoids), fish (omega-3s), nuts/legumes (zinc), whole grains. Stay hydrated.
Limit: smoking, heavy alcohol, ultra-processed foods, and added sugars.
(AREDS2 nutrients help in macular degeneration—not MRNFL—but they’re a good template for an eye-friendly, antioxidant-rich diet overall.)

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FAQs

1) Is MRNFL a disease?
No—it’s a benign anatomical variant of where myelin shows up.

2) Will it grow or spread?
Usually stable for life. Rare reports of change are tied to other optic-nerve issues. Keep routine follow-up.

3) Can it make me go blind?
MRNFL itself doesn’t cause blindness. If vision is reduced, it’s typically because of amblyopia/high myopia, which are treatable to varying degrees.

4) Can glasses fix it?
Glasses don’t remove MRNFL, but correcting refractive error is the first step of amblyopia care.

5) Is patching better than atropine for amblyopia?
Both work; large RCTs show similar average improvement for many kids with moderate amblyopia—choice depends on age, severity, and family preference.

6) Do near activities during patching speed recovery?
No clear added benefit vs distance activities; the key is adherence.

7) My child has MRNFL and is getting more nearsighted. Anything to slow it?
Yes—outdoor time, orthokeratology, multifocal contacts (MiSight), or low-dose atropine are options judged case-by-case.

8) Are OCT nerve-fiber numbers trustworthy near MRNFL?
Interpret with caution—segmentation artifacts are common; doctors lean on photos and visual fields for decisions like glaucoma care.

9) Is surgery ever needed?
Not for MRNFL itself. Strabismus surgery or laser may be used for associated issues when indicated.

10) Are stem-cell injections a cure?
No. Unapproved stem-cell products have blinded patients; avoid them outside legitimate trials.

11) Can adults with longstanding amblyopia still improve?
Some adults gain small improvements with targeted therapy, but expectations should be modest compared to children.

12) Will patching harm the good eye?
When prescribed correctly and monitored, no. Care teams watch for over-penalization and adjust.

13) Can MRNFL cause headaches?
MRNFL doesn’t cause headaches; if headaches are persistent, discuss separately.

14) Do blue-light glasses help MRNFL?
No specific MRNFL benefit. Use standard, comfortable correction and screen-time ergonomics.

15) How often should we follow up?
During active amblyopia/myopia care: typically every 6–12 weeks. Once stable: every 6–12 months (your doctor will tailor this).

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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