Inverse Bell’s Phenomenon

Inverse Bell’s Phenomenon is a rare eye movement problem that happens when you try to close your eyes.
Normally, when we close our eyes — especially tightly — the eyeballs automatically roll upward and outward (this is called the Bell’s phenomenon). This movement protects the cornea (the clear front window of the eye) from injury by moving it under the eyelid.

But in inverse Bell’s phenomenon, instead of moving upward, the eyeballs move downward or sometimes downward and inward when you try to close your eyes. This unusual movement can expose the cornea and make it more likely to get dry, irritated, or scratched.

This condition is not a disease by itself — it is often a sign of another eye, nerve, or facial muscle problem. It may happen after eyelid surgery, facial nerve injury, trauma, or certain neurological diseases.

Inverse Bell’s Phenomenon is a rare and unusual eye movement pattern. Normally, when you close your eyes tightly, your eyeballs roll slightly upward and outward. This natural reflex is called the Bell’s phenomenon and it helps protect the eyes from injury by hiding the sensitive cornea under the upper eyelid.

In Inverse Bell’s Phenomenon, the exact opposite happens. Instead of moving upward, the eyeballs move downward when you try to close your eyes. This downward rolling is not normal and can make the eyes more exposed to dust, dryness, or injury.

This condition is usually noticed by doctors during an eye examination when they ask a person to close their eyes and observe the movement of the eyeballs. It can happen in one eye (unilateral) or both eyes (bilateral), and it can be temporary or permanent depending on the cause.

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Types of Inverse Bell’s Phenomenon

Doctors classify it in a few ways depending on how it appears and why it happens.

1. Based on Eye Movement Direction

1. Pure Downward Type – Eye moves straight down on attempted closure.

2. Downward and Inward Type – Eye moves diagonally down toward the nose.

3. Downward and Outward Type – Eye moves diagonally down toward the temple.

2. Based on Cause

4. Post-Surgical Type – Seen after eyelid surgery, such as ptosis correction.

5. Post-Trauma Type – Seen after head or facial injury.

6. Neurological Type – Caused by brain or nerve disorders.

7. Post-Infectious Type – After certain infections like Bell’s palsy due to viruses.

3. Based on Duration

8. Transient (Temporary) Type – Improves on its own over weeks or months.

9. Persistent (Permanent) Type – Does not recover without treatment.

Even though it is rare, doctors classify Inverse Bell’s Phenomenon into types based on how it appears and what causes it.

1. Unilateral Inverse Bell’s Phenomenon

   • Only one eye moves downward during eyelid closure.

   • May be due to injury, nerve damage, or surgery on one side of the face.

2. Bilateral Inverse Bell’s Phenomenon

   • Both eyes roll downward when closing.

   • Often linked to neurological disorders or muscle problems affecting both sides.

3. Temporary (Transient) Inverse Bell’s Phenomenon

   • Happens for a short time, often after surgery (such as eyelid surgery or facial nerve repair).

   • Usually recovers when swelling or nerve irritation heals.

4. Permanent Inverse Bell’s Phenomenon

   • The downward movement remains for life if the underlying cause cannot be treated.

5. Congenital Inverse Bell’s Phenomenon

   • Present from birth due to abnormal nerve or muscle development.

6. Acquired Inverse Bell’s Phenomenon

   • Develops later in life due to injury, disease, or surgery.

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Causes of Inverse Bell’s Phenomenon

1. Facial Nerve Palsy – Damage to the nerve that controls eyelid closure can cause abnormal eye movement patterns.

2. Lagophthalmos – Inability to fully close the eyelids, often linked to nerve or muscle weakness.

3. Eyelid Surgery Complications – Swelling or nerve irritation after blepharoplasty or ptosis repair.

4. Bell’s Palsy Recovery – Sometimes as nerves heal, abnormal patterns like inverse movement appear.

5. Trauma to the Eye Area – Direct injury can affect eye muscles or nerves.

6. Neurological Disorders – Brain lesions or multiple sclerosis can disturb normal reflex pathways.

7. Stroke – Can damage brain areas controlling eye movement reflexes.

8. Orbital Fractures – Broken bones around the eye can affect how it moves.

9. Guillain-Barré Syndrome – Rare nerve disease affecting movement control.

10. Tumors near the Eye or Brainstem – Pressure on nerve pathways can cause unusual movements.

11. Eye Muscle Disorders – Such as myasthenia gravis or thyroid eye disease.

12. Post-LASIK or Corneal Surgery – Changes in corneal sensation can affect eye closure reflexes.

13. Facial Muscle Spasm Disorders – Like hemifacial spasm interfering with normal eyelid closure.

14. Brainstem Injury – Since the brainstem coordinates eye movement, damage here can reverse the Bell’s reflex.

15. Miller Fisher Syndrome – A rare neurological condition affecting eye movement.

16. Infections near the Eye or Brain – Such as herpes zoster ophthalmicus or meningitis.

17. Paralysis after Acoustic Neuroma Surgery – Facial nerve damage during tumor removal.

18. Congenital Facial Nerve Weakness – Present at birth and causing unusual eye movement patterns.

19. Post-anesthesia Effects – Temporary nerve disturbance after certain surgeries.

20. Idiopathic (Unknown Cause) – Sometimes no exact cause is found.

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Symptoms of Inverse Bell’s Phenomenon

1. Downward Eye Movement on Closing – Main sign noticed during examination.

2. Eye Redness – From exposure to air.

3. Dryness – Due to less protection during blinking.

4. Foreign Body Sensation – Feeling like grit in the eye.

5. Excess Tearing – Eye tries to compensate for dryness.

6. Blurred Vision – From dryness or corneal changes.

7. Light Sensitivity – Eyes feel more sensitive to bright light.

8. Incomplete Eye Closure – May accompany the condition.

9. Eye Irritation in Windy Conditions – Due to more exposure.

10. Recurrent Eye Infections – Like conjunctivitis from reduced protection.

11. Corneal Ulcers – Severe cases may lead to open sores on the cornea.

12. Difficulty Sleeping Comfortably – Eyes may remain partly open.

13. Facial Weakness – If caused by nerve problems.

14. Drooping Eyelid – May occur in some cases.

15. Eye Pain – Especially if the cornea becomes damaged.

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Diagnostic Tests

Physical Examination

1. Direct Observation of Eye Closure – Doctor watches the eye movement when you close your eyes.

2. Eyelid Strength Test – Checks how strongly you can shut your eyes.

3. Corneal Reflex Test – Touching the cornea lightly to see reflex movement.

4. Facial Symmetry Check – Looks for nerve weakness signs.

Manual Tests

5. Forced Eye Closure Test – Asking the patient to close eyes tightly while the doctor observes movement.

6. Blink Reflex Observation – Checking how eyes move during quick blinks.

7. Tear Break-up Time – Manual method to assess dryness.

Lab and Pathological Tests

8. Blood Sugar Levels – To check for diabetes-related nerve damage.

9. Thyroid Function Tests – For thyroid eye disease.

10. Autoimmune Panel – For immune-related nerve or muscle disease.

11. Infection Screening – For herpes or bacterial infections affecting nerves.

Electrodiagnostic Tests

12. Electromyography (EMG) – Measures muscle activity around the eye.

13. Nerve Conduction Studies – Checks speed of nerve signals to eyelid muscles.

14. Electro-oculography (EOG) – Tracks eye movement patterns electronically.

Imaging Tests

15. MRI Brain and Orbits – To find tumors, inflammation, or structural damage.

16. CT Scan of Orbit – Detects fractures or bone changes.

17. Ultrasound of Eye (B-scan) – Shows structural eye changes.

18. High-resolution MRI of Brainstem – For subtle nerve pathway damage.

19. Orbital X-rays – For fractures in suspected trauma.

20. Optical Coherence Tomography (OCT) – To check corneal health and nerve fiber layer.

Non-pharmacological treatments

1. Scheduled blinking and “soft close” drills: Gentle, frequent complete blinks keep the tear film even; avoids harsh squeezing that exaggerates IBP. Purpose: smoother tear spread. Mechanism: mechanical resurfacing of tears.

2. Humidifier and draft control: Raise room humidity, avoid fans/AC aimed at eyes. Purpose: reduce evaporation. Mechanism: higher ambient moisture slows tear loss.

3. Moisture chamber at night: Simple wrap-around shield or plastic film over petrolatum on skin to trap humidity. Purpose: overnight protection. Mechanism: creates a sealed micro-environment. Best evidence for moisture chambers in exposure care. EyeWiki

4. Eyelid taping for sleep: Micropore tape to gently close lids at night if lagophthalmos. Purpose: keep cornea covered. Mechanism: physical lid apposition—works as well as frequent lubrication in some ICU data. EyeWiki

5. Eye patch (short stints): Protects from airflow during naps/travel. Mechanism: barrier to evaporation. EyeWiki

6. Warm compresses (10 minutes): Thins oil from meibomian glands to stabilize the tear film. Mechanism: improves lipid layer to slow evaporation.

7. Lid hygiene/massage: Clears blocked glands; supports tear quality. Mechanism: better meibum flow → more stable surface.

8. Blink reminders (phone timer): Behavioral nudge to avoid prolonged stare time (screens).

9. Protective eyewear outdoors: Wrap-around glasses block wind/UV. Mechanism: reduces desiccating stress.

10. Bandage contact lens (by clinician): A soft lens shields the cornea while epithelium heals. Mechanism: mechanical barrier; needs close follow-up to prevent infection. EyeWiki

11. Scleral lens (e.g., PROSE): A large rigid lens holds a liquid reservoir over the cornea all day. Mechanism: continuous lubrication and protection; highly effective in severe exposure. EyeWiki

12. Punctal occlusion with plugs (office procedure): Keeps natural tears on the eye longer. Mechanism: slows drainage. EyeWiki

13. Schedule-based lubrication routine (non-drop): See Drug section for products; the “therapy” here is adherence—hourly PRN daytime tears + ointment at night when needed. EyeWiki

14. Workstation ergonomics: Screen a bit lower so gaze is slightly downward (reduces palpebral fissure area and evaporation).

15. Sleep position hacks: Avoid sleeping with direct AC to the face; consider side sleeping that allows the upper lid to rest more fully.

16. Short “eye breaks” during reading/screening: 20-20-20 rule (every 20 minutes, 20 seconds looking 20 feet away) to normalize blinking.

17. Avoid smoke/irritants: Cuts reflex tearing/irritation spiral.

18. Cool compress for inflamed lids (when warm makes worse): Reduces swelling that prevents full closure.

19. Frequent follow-up while acute: Early detection of abrasions/ulcers prevents complications. Mechanism: step-up therapy at first sign of epithelial defects. EyeWiki

20. Treat the root cause: Coordinate with neuro/ENT/oculoplastics for facial palsy, thyroid eye disease, or post-surgical edema—this is the most important “non-drug” step. EyeWiki

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Drug treatments

(Doses are typical adult ranges; prescribers individualize care. Always use preservative-free tears/ointments for frequent use.) EyeWiki

1. Artificial tears – carboxymethylcellulose 0.5% / hydroxypropyl methylcellulose (lubricant drops)
   Class: ocular lubricant. Dose/time: 1–2 drops q1–2h PRN (PF vials if frequent).
   Purpose: first-line surface protection. Mechanism: replaces aqueous layer; reduces friction.
   Side effects: brief blur/sting.

2. Sodium hyaluronate 0.1–0.3% (PF hyaluronic acid tears)
   Class: viscoelastic lubricant. Dose: 1 drop q4–6h or PRN.
   Purpose: longer retention on cornea. Mechanism: water-binding polymer mimics mucin/ECM.
   Side effects: minimal.

3. Carbomer gel / hydroxypropyl guar gel (lubricating gels)
   Class: gel lubricant. Dose: 1 drop q6–8h; often bedtime.
   Purpose: thicker, night protection when ointment is too smeary.
   Side effects: transient blur.

4. Petrolatum–mineral oil ointment (PF)
   Class: occlusive lubricant. Dose: 0.5–1 cm qHS (at bedtime) ± naps.
   Purpose: seals moisture overnight; cornerstone in exposure.
   Mechanism: reduces evaporation dramatically.
   Side effects: blur, stickiness.

5. Topical antibiotic ointment (e.g., erythromycin 0.5% ointment)
   Class: macrolide antibiotic. Dose: thin strip qHS–QID if epithelial defect/bandage lens.
   Purpose: infection prophylaxis when surface is broken or with bandage lens.
   Side effects: local irritation; rare allergy. EyeWiki

6. Topical fluoroquinolone (e.g., moxifloxacin 0.5% drops)
   Class: broad-spectrum antibiotic. Dose: QID if abrasion/ulcer risk per clinician.
   Purpose: treat/prophylax bacterial keratitis risk in significant defects.
   Side effects: irritation; rare hypersensitivity. EyeWiki

7. Short course topical steroid (e.g., loteprednol 0.2–0.5%)
   Class: corticosteroid. Dose: QID → taper for 1–2 weeks if inflammation prominent (doctor-supervised).
   Purpose: calm post-op inflammation/fornix hyperemia that worsens IBP.
   Risks: ↑IOP, cataract with prolonged use; infection masking—close follow-up essential.

8. Topical cyclosporine (0.05% or 0.1%)
   Class: calcineurin inhibitor, immunomodulator. Dose: BID; effect in weeks.
   Purpose: improves chronic dry eye component (better baseline surface).
   Side effects: burning; rare infection reactivation in immunosuppressed. EyeWiki

9. Topical lifitegrast 5%
   Class: LFA-1 antagonist (anti-inflammatory). Dose: BID.
   Purpose: similar to cyclosporine—reduces inflammation in evaporative/aqueous-deficient dry eye contributing to exposure symptoms.
   Side effects: dysgeusia, irritation.

10. Botulinum toxin A to levator (office injection)
    Class: neuromuscular blocker (chemical ptosis). Dose: tiny units targeted; effect ~3 months.
    Purpose: temporarily lower the upper lid so the cornea is covered while IBP/lagophthalmos settles—useful in facial palsy or severe exposure.
    Side effects: asymmetry, temporary droop; rare dry eye worsened if lower lid. EyeWiki Medscape

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Dietary / molecular / other supplements (supportive—not cures)

Evidence for supplements is supportive and mainly targets dry-eye/ocular-surface health while IBP runs its course. Always discuss with a clinician if pregnant, anticoagulated, or on multiple meds.

1. Omega-3 fatty acids (EPA/DHA, 1000–2000 mg/day): Supports meibomian oil quality → slower evaporation.

2. Flaxseed oil (ALA 1000–2000 mg/day): Plant omega-3; milder effect on tear film.

3. Gamma-linolenic acid (GLA 240–480 mg/day): Anti-inflammatory lipids; may improve symptoms.

4. Vitamin D (check level; often 1000–2000 IU/day): Low D correlates with dry-eye symptoms in some studies.

5. Vitamin A (dietary; avoid high-dose pills without doctor): Epithelial nutrition; deficiency harms cornea.

6. L-carnitine (500–1000 mg/day): Osmoprotective support in some dry-eye formulas.

7. Taurine (500 mg/day): Antioxidant/osmoprotective in experimental tear support blends.

8. N-acetylcysteine (oral 600 mg/day or low-dose topical by Rx): Mucolytic/antioxidant; can help filamentary irritation.

9. Curcumin (500–1000 mg/day with food): Systemic anti-inflammatory adjunct.

10. Astaxanthin (6–12 mg/day): Antioxidant; small studies suggest symptom improvement.

11. Hyaluronic acid (oral 120–240 mg/day): Skin/ocular surface hydration adjunct; main benefit is topical.

12. Lactoferrin (100–300 mg/day): Tear protein mimic; limited but plausible surface support.

13. Bilberry extract (per label): Antioxidant visual comfort; modest.

14. Zinc (up to 15 mg/day with copper balance): Epithelial/immune health; avoid excess.

15. Adequate hydration & balanced electrolytes: The cheapest “supplement”—supports tear production.

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Regenerative / stem-cell–type” and advanced biologic options

1. Autologous serum tears (20–50%)
   What: Your own diluted serum as eye drops.
   Why: Contains growth factors/vitamins similar to natural tears; helps heal persistent epithelial defects.
   Mechanism: Bioactive trophic support to corneal epithelium.

2. Platelet-rich plasma (PRP) eye drops
   What: Platelet concentrate drops.
   Why/Mechanism: Platelet-derived growth factors promote epithelial healing.

3. Cenegermin (recombinant human nerve growth factor) 0.002%
   Use: Approved for neurotrophic keratitis; can be relevant when poor corneal nerve function worsens exposure damage.
   Mechanism: Stimulates corneal nerve/epithelial regeneration.

4. Amniotic membrane (in-office self-retained or sutured in OR)
   Use: Biologic bandage for non-healing defects.
   Mechanism: Anti-inflammatory, anti-scarring matrix; fosters epithelial regrowth. EyeWiki

5. Matrix-regenerating agents (RGTA, e.g., Cacicol—availability varies)
   Use: Mimics heparan-sulfate binding to protect growth factors on the corneal surface.
   Mechanism: Enhances epithelial repair in recalcitrant defects.

6. Topical cyclosporine/lifitegrast (immune-modulating, already listed under Drugs)
   Why here: They’re not “regenerative,” but they normalize immune tone on the surface so the cornea can heal and stay stable.

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Surgeries / procedures

1. Temporary tarsorrhaphy
   What: A few stitches to partially close the eyelids for days–weeks.
   Why: Immediate corneal coverage during severe exposure/ulcer risk.
   Outcome: Strong corneal protection; fully reversible. EyeWiki

2. Permanent (partial) lateral tarsorrhaphy
   What: A small permanent narrowing of the eyelid opening.
   Why: For chronic exposure when other options fail.
   Outcome: Durable protection, minor cosmetic trade-off. EyeWiki

3. Upper-lid gold/platinum weight implantation
   What: A tiny weight in the upper lid.
   Why: In facial palsy, gravity helps the lid close, protecting the cornea even with weak muscles.
   Outcome: Highly effective; weight can be adjusted/removed. EyeWiki

4. Canthoplasty/lid tightening or ectropion repair
   What: Repositions or tightens the lid.
   Why: Fixes mechanical malpositions that prevent closure.
   Outcome: Restores lid seal; reduces exposure. EyeWiki

5. Amniotic membrane transplantation (surgical)
   What: Biological graft sewn or glued onto cornea if there’s a persistent defect/ulcer.
   Why: Promotes healing; reduces scarring/inflammation.
   Outcome: Often speeds re-epithelialization with fewer complications. EyeWiki

(Separately, if IBP started after ptosis surgery and persists alongside problematic lid position, your oculoplastic surgeon may consider revision once swelling fully resolves.) EyeWiki

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Prevention tips

1. Pre-op Bell’s check before eyelid surgery (baseline documentation and risk counseling). ResearchGate

2. Gentle post-op care: Cold then warm compresses as advised; don’t rub eyes.

3. Night protection early after eyelid surgery (ointment + moisture chamber) until the surgeon says you’re in the clear. EyeWiki

4. Manage dry eye proactively (blinks, humidifier, PF tears).

5. Shield eyes from wind/AC (wrap-arounds outside, avoid sleeping under vents).

6. Screen ergonomics to reduce wide-eyed staring.

7. Treat lid malpositions early—don’t wait for chronic exposure. EyeWiki

8. Address thyroid eye disease promptly with your specialist. EyeWiki

9. If facial palsy develops, seek early care—there’s a short window where systemic therapy helps and eye protection is critical. Medscape

10. Keep follow-up appointments—exposure damage can sneak up fast. EyeWiki

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When to see a doctor—urgent vs routine

• Urgent (same day or ER): Severe pain, light sensitivity, sudden blurry vision, a white spot on the cornea, pus, trauma, or you can’t close your eye—these suggest abrasion/ulcer/infection. EyeWiki

• Soon (within a few days): New IBP after surgery, any incomplete lid closure, persistent redness/tearing not relieved by lubrication. EyeWiki

• Routine: Dry-eye-type symptoms that aren’t improving with OTC lubrication and lifestyle changes.

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What to eat and what to avoid

What to eat:

• Omega-3–rich foods (fatty fish like sardines/salmon, walnuts, flax) for healthier tear oils.

• Colorful vegetables/fruit (vitamin A precursors, antioxidants) for epithelial health.

• Hydrating foods and fluids (water, soups, citrus) to keep tears flowing.

• Lean proteins (amino acids for repair).

What to avoid (or limit):

• Very dry, salty, ultra-processed foods (worsen dehydration).

• Excess alcohol (dehydrates mucous membranes).

• Cigarette smoke exposure (ocular surface irritant).

• Mega-dose vitamin A supplements without medical oversight (risk of toxicity).

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Frequently Asked Questions

1) Is IBP dangerous by itself?
Usually no—it’s a sign, not a disease. The danger is exposure of the cornea if the eyelids don’t close well. Protect the surface and it’s typically fine while the reflex normalizes. EyeWiki

2) How long does post-surgical IBP last?
Commonly days to weeks, sometimes a few months, improving as swelling settles. EyeWiki

3) Can IBP be “fixed” with a pill or eye exercise?
There’s no specific pill. The mainstay is lubrication + protection and addressing the cause. Exercises won’t rewire the reflex, but blink hygiene helps the surface. EyeWiki

4) Will it affect my vision permanently?
Not if managed early. Neglected exposure can scar the cornea; that’s why we’re aggressive with lubrication and protection. EyeWiki

5) I only notice symptoms at night—what should I do?
Use PF ointment at bedtime and a moisture chamber or taping to keep the eye fully closed while sleeping. EyeWiki

6) Do I need antibiotics?
Only if there’s a surface defect, bandage lens, or infection risk—your doctor will decide. Routine dryness alone doesn’t need antibiotics. EyeWiki

7) Are preservative-free drops really necessary?
If you’re using drops frequently, PF is kinder to the surface and tear film. EyeWiki

8) What if I have facial palsy?
Protect the eye immediately (tape, ointment, moisture chamber) and see a clinician. Early systemic therapy for Bell’s palsy and oculoplastic support can help recovery and protect the cornea. Medscape

9) Will a bandage or scleral lens help me?
Often yes when exposure is moderate–severe; they act like a shield and liquid reservoir. Needs close follow-up. EyeWiki

10) When is surgery considered?
If conservative care fails or exposure is dangerous (ulcer risk), tarsorrhaphy or gold weight can be vision-saving. EyeWiki

11) Is IBP ever “normal”?
A small percentage of people naturally roll down/in on forceful closure and never have trouble; we still protect the surface if symptomatic. EyeWiki

12) Can thyroid eye disease cause issues with IBP?
Yes—proptosis and lid retraction make closure harder; surface protection and thyroid management both matter. EyeWiki

13) Could this be permanent?
It can persist in some neuro/cicatricial cases, but post-surgical IBP usually resolves. Your plan focuses on eye safety in the meantime. EyeWiki

14) Do screens make it worse?
They reduce blink rate, so exposure feels worse. Use the 20-20-20 rule and blink reminders.

15) What’s the single most important thing I can do today?
Start a strict lubrication + night-protection routine and book a check if you have any pain, light sensitivity, or blur—that’s how we prevent complications. EyeWiki

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 08, 2025.

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