Vitreopapillary Traction Syndrome

Vitreopapillary Traction Syndrome is a condition where the vitreous—the clear gel that fills the back of the eye—pulls abnormally on the optic nerve head, also called the optic disc or papilla. The optic disc is the “entry port” where the optic nerve leaves the eye and carries visual information to the brain. Normally, the vitreous is gently attached to the optic disc in youth and separates with age. In VPTS, that separation is incomplete, tight, or distorted, so the gel or the thin posterior vitreous membrane keeps tugging on the disc. This traction can distort the disc shape, elevate the papilla, crease the surrounding retina, and disturb vision. Importantly, this can mimic true optic nerve swelling (papilledema) even though the problem is mechanical pulling rather than pressure in the brain.

Vitreopapillary Traction Syndrome (VPTS) means the clear gel inside the eye (the vitreous) has not fully let go of the optic nerve head (the “disc,” where the nerve exits the eye). Instead of separating cleanly, a thin layer of this gel stays stuck around the edge of the optic disc and pulls on it. This pulling (traction) can lift the nerve head a little, disturb nearby tissues, and sometimes affect vision or visual fields. Eye scans (OCT) can show the sticky attachment and the pulling forces very clearly. VPTS is part of a family of conditions that happen when the vitreous separates in an abnormal way (an “anomalous posterior vitreous detachment”). EyeWikiPMCJAMA Network

Why this matters: that persistent pull can cause optic nerve head elevation, small hemorrhages, visual field defects, or symptoms like “cloudy patches,” brief dimming with eye movement, and distorted central vision if the pull spreads toward the macula. In some patients the traction can function like a front-of-the-nerve (anterior optic) neuropathy; in others it can mimic optic disc edema from other causes, which is why OCT and a careful eye exam are important. PMCLippincott JournalsBMJ Case Reports

How does VPTS happen?

In early life, the vitreous is a firm, transparent gel attached to the retina at several natural “adhesion points,” especially the optic disc, macula, retinal vessels, and vitreous base near the front of the eye. With age or disease, the gel liquefies (syneresis) and typically peels off the retina in a process called posterior vitreous detachment (PVD). If that peeling is uneven or the adhesion is unusually strong at the optic disc, the vitreous can stay stuck and pull. This pulling force may be static (always present) or dynamic (worse with eye movements). The traction can alter the contour of the optic disc, cause peripapillary retinal folds, produce small hemorrhages, disturb nerve fiber alignment, and sometimes create visual field defects. When the traction also involves the nearby macula, it can coexist with vitreomacular traction or epiretinal membranes.

Types of Vitreopapillary Traction Syndrome

1) Focal vs. Broad adhesion

• Focal adhesion means a small, tight point of vitreous attachment right on the optic disc edge, like a tiny string pulling one spot.

• Broad adhesion means a wider sheet of posterior vitreous or epiretinal tissue is stuck across the disc and surrounding retina, causing more extensive distortion.

2) Static vs. Dynamic traction

• Static traction is constant pulling present even when eyes are still.

• Dynamic traction worsens with eye movements, blinking, or changes in gaze, when the vitreous shifts and tugs more.

3) Primary (Idiopathic) vs. Secondary (Disease-related)

• Primary/Idiopathic VPTS occurs without a known eye disease, often due to an anomalous or incomplete PVD.

• Secondary VPTS occurs because of another condition, such as diabetic retinopathy, inflammation, trauma, or previous eye surgery, which alters the vitreoretinal interface and makes adhesions stronger.

4) Acute vs. Chronic

• Acute VPTS develops suddenly, often with new floaters, flashes, or a noticeable visual change.

• Chronic VPTS is slow and persistent, with long-standing subtle traction and gradual structural changes at the disc.

5) Predominantly anterior vs. tangential vector

• Anterior traction pulls forward toward the vitreous cavity, tending to elevate the papilla.

• Tangential traction pulls sideways along the retinal surface, creating creases or folds around the disc.

6) Isolated vitreopapillary traction vs. combined traction

• Isolated traction involves only the disc region.

• Combined traction involves the disc and macula (e.g., vitreomacular traction or an epiretinal membrane bridging both areas).

Causes

1. Incomplete Posterior Vitreous Detachment (PVD)
   When the vitreous partially peels off but stays stuck at the optic disc, residual attachment keeps pulling on the papilla.

2. Anomalous PVD
   The vitreous liquefies without clean separation, leaving areas of strong adhesion at the disc that generate abnormal traction.

3. Epiretinal Membrane (ERM) extending to the disc
   A thin scar-like membrane on the retinal surface can shrink and tug on both the disc and peripapillary retina.

4. Vitreoschisis
   A split within the vitreous cortex leaves a sticky layer on the retinal surface, creating unexpected traction at the disc.

5. Proliferative Diabetic Retinopathy (PDR)
   New fibrovascular tissue grows and anchors to the posterior hyaloid, producing firm traction across the disc and vessels.

6. Non-proliferative diabetic interface changes
   Even without frank PDR, diabetes can alter collagen and adhesion strength, making the posterior hyaloid stickier at the disc.

7. High Myopia
   Elongated eyeballs in high myopia change retinal curvature and vitreous behavior, sometimes producing abnormal adhesions near the disc.

8. Inflammatory uveitis
   Inflammation makes tissues edematous and sticky, encouraging the vitreous to adhere more tightly to the disc.

9. Post-traumatic changes
   Blunt trauma can redistribute vitreous forces, create micro-tears or microscarring, and fix the posterior hyaloid to the disc.

10. Post-operative changes
    After retinal or cataract surgery, healing membranes or altered vitreous dynamics can strengthen adhesions at the optic disc.

11. Vascular occlusions near the disc
    Local vein or artery blockages can change tissue oxygen and healing responses, encouraging adhesive fibroglial tissue.

12. Optic disc anomalies
    Unusual disc structures, such as tilted discs or peripapillary atrophy, can change mechanical anchoring of the vitreous.

13. Retinal vascular disease (non-diabetic)
    Inflammation or ischemia from other vascular conditions can remodel the vitreoretinal interface and increase stickiness.

14. Age-related vitreous syneresis with strong residual adhesion
    The vitreous liquefies with age, but if adhesion at the disc remains strong, traction develops during eye movements.

15. Peripapillary chorioretinal scars
    Old scars around the disc bind membranes and guide traction vectors toward the papilla.

16. Proliferative vitreoretinopathy (PVR)
    Following retinal tears or detachment, contractile membranes form and pull on the disc and surrounding retina.

17. Infectious retinochoroiditis
    Infections that scar near the disc (e.g., toxoplasmosis) can leave adhesive planes where vitreous traction persists.

18. Radiation retinopathy
    After ocular or orbital radiation, vascular injury and scarring can make the vitreoretinal interface abnormally sticky.

19. Sickle cell or other hemoglobinopathies
    Ischemia and neovascularization may create fibrovascular bridges that tether vitreous to the disc.

20. Connective tissue disorders
    Systemic collagen conditions can alter vitreous collagen and adhesion strength, increasing risk of traction at the disc.

Symptoms and Signs

1. Blurred vision
   Vision may look smudged or soft because traction distorts the optic disc and nearby retina.

2. Intermittent blur with eye movement
   When you move your eyes, the vitreous shifts and pulls, so blur changes moment to moment.

3. Metamorphopsia (distortion)
   Straight lines may look wavy or bent due to retinal folds near the disc.

4. Paracentral smudges or scotomas
   Small dim or blank spots can appear near the center, reflecting nerve fiber layer stress or traction-related microchanges.

5. Reduced contrast sensitivity
   Fine shades of gray become harder to tell apart because the retinal layers are mechanically stressed.

6. Transient obscurations of vision
   Brief fading or graying of vision can happen with rapid gaze, when traction peaks.

7. Photopsias (flashes)
   Pulling on the retina can trigger light sensations, especially during onset of PVD or vigorous eye movement.

8. New floaters
   Small moving specks may appear as the vitreous rearranges and liquefies.

9. Perceived eye strain
   The eye can feel tired because vision is unstable and work is required to maintain clarity.

10. Headache from visual effort
    Not caused by the disc itself, but trying to see clearly through distortion may provoke headaches.

11. Color desaturation
    Colors can look less vivid if traction subtly affects nerve fiber transmission near the disc.

12. Visual field notching or arcuate defects
    Some patients notice missing slices of side vision, echoing nerve fiber layer stress.

13. Amsler grid distortion
    When checked, small boxes near the center may look curved or uneven, reflecting peripapillary folds.

14. Pseudo-disc swelling appearance (exam sign)
    Clinicians may see an elevated, blurred disc rim on exam that mimics papilledema, but it is traction-related.

15. Peripapillary hemorrhages or vessel kinks (exam sign)
    Tiny hemorrhages or curved vessels can be seen where traction is strongest.

Diagnostic Tests

Below are 20 tests grouped into Physical Exam (4), Manual Tests (4), Lab & Pathological (3), Electrodiagnostic (4), and Imaging (5). Each paragraph explains what the test is, what it looks for, and why it helps.

A) Physical Exam

1. Best-corrected visual acuity (BCVA)
   Measuring line-by-line vision with the best glasses or pinhole shows the baseline impact of VPTS on sharpness and helps monitor change over time.

2. Pupillary light reflex
   Checking pupils for relative afferent pupillary defect (RAPD) screens for asymmetric optic nerve function; marked RAPD is unusual in pure traction and may point to other optic neuropathies.

3. Color vision testing (Ishihara or similar)
   Simple color plates detect subtle optic nerve dysfunction. Mild color desaturation can accompany traction near the disc, while severe loss suggests alternative diagnoses.

4. Confrontation visual fields at the slit lamp
   A quick bedside map of side vision can identify gross field defects and guide the need for formal perimetry.

B) Manual Tests

5. Slit-lamp biomicroscopy with a high-power fundus lens (e.g., 90D/78D)
   The clinician directly inspects the disc for traction signs—elevated papilla, peripapillary retinal folds, tiny hemorrhages, and vessel kinking.

6. Indirect ophthalmoscopy
   A wide-angle view allows assessment of the vitreous face, peripheral retina, and whether traction connections extend from the disc to other regions.

7. Dynamic observation with eye movements
   Guided saccades and blinks during exam can accentuate subtle traction, letting the examiner see movement-dependent changes in the posterior hyaloid and disc contour.

8. Scleral depression (careful, selected cases)
   Gentle external pressure on the eye periphery (performed by a specialist when appropriate) can reveal vitreous mobility and the anatomic extent of adhesions; it is not routine if traction is obvious on imaging.

C) Lab & Pathological Tests

9. Glycemic panel (fasting glucose, HbA1c)
   Because diabetes can thicken and stick the vitreoretinal interface, documenting glycemic control is crucial when VPTS coexists with diabetic retinopathy.

10. Inflammation markers (ESR, CRP) ± targeted infectious/autoimmune tests
    When exam suggests uveitis, basic systemic inflammation markers and targeted infectious/autoimmune panels (guided by history) help determine secondary causes of adhesion.

11. Coagulation/vascular risk screening (as indicated)
    In selected patients with peripapillary hemorrhages or vascular signs, coagulation and vascular risk profiles may clarify contributors to tissue fragility and scarring.

D) Electrodiagnostic Tests

12. Standard automated perimetry (SAP)
    Computerized visual field testing detects arcuate defects, notches, or paracentral scotomas that correlate with nerve fiber layer stress from traction.

13. Optokinetic or saccadic function testing (clinical)
    Observing rapid eye movements and how symptoms fluctuate with gaze supports the idea of dynamic traction.

14. Visual Evoked Potential (VEP)
    Measures the electrical response of the visual pathway to light stimuli. Delays or amplitude changes suggest optic nerve dysfunction and help differentiate traction effects from true neuropathies.

15. Electroretinography (ERG) (selected cases)
    Assesses retinal function. A normal ERG with abnormal VEP suggests post-retinal (optic nerve) issues, whereas traction typically shows structural rather than global retinal dysfunction.

E) Imaging Tests

16. Spectral-domain Optical Coherence Tomography (SD-OCT) of the optic nerve head and peripapillary retina
    OCT is the key test. It provides cross-sectional images showing posterior vitreous adhesion, elevated disc contour, peripapillary folds, and vitreous cortex lines attached to the papilla. It can quantify retinal nerve fiber layer (RNFL) thickness and reveal traction shadows.

17. OCT of the macula and vitreomacular interface
    Because traction often extends toward the macula, macular OCT looks for vitreomacular traction, epiretinal membrane, or cystic changes, explaining distortion or blur.

18. B-scan ocular ultrasonography
    When media are hazy or the vitreous is hard to visualize, B-scan ultrasound shows vitreous strands, posterior hyaloid position, and dynamic movement with eye motion, supporting a traction diagnosis.

19. OCT Angiography (OCTA)
    Non-invasive imaging of capillary flow around the disc can show microvascular crowding or flow changes related to mechanical distortion, helping distinguish traction-related pseudo-swelling from inflammatory or ischemic disc edema.

20. Color fundus photography ± autofluorescence
    Photographs document disc elevation, folds, and tiny hemorrhages over time. Autofluorescence can highlight peripapillary RPE stress from chronic traction.

Non-pharmacological treatments

1. Watchful observation with scheduled OCT
   What it is: Regular eye exams and OCT scans without immediate intervention.
   Purpose: Monitor if traction stabilizes, worsens, or resolves; avoid unnecessary procedures.
   Mechanism: Many vitreoretinal interface problems evolve over time; OCT tracks the adhesion and optic nerve head contour. EyeWiki

2. Education about symptoms that need urgent review
   Purpose: Early detection of complications (sudden vision drop, new floaters/flashes, field loss).
   Mechanism: Rapid triage prevents delayed care if hemorrhage or acute traction develops.

3. Activity modification during acute symptoms
   What: Temporarily reduce heavy straining (very heavy lifting) if it repeatedly triggers transient dimming.
   Purpose/Mechanism: Decrease momentary vitreous tugging on the disc in rare, symptomatic cases; note evidence here is pragmatic rather than trial-based.

4. Optimize systemic health (especially diabetes, blood pressure)
   Purpose: In patients with diabetic eye disease, better systemic control supports overall retinal health and post-op outcomes.
   Mechanism: Reduces vascular stress and edema drivers that can coexist with traction. PubMed

5. Manage sleep apnea if present
   Purpose/Mechanism: Sleep apnea contributes to vascular stress in the optic nerve in other diseases; treating it supports overall optic nerve health (indirect support; not a VPTS cure).

6. Blue-light and glare management
   What: Use appropriate lighting and anti-glare strategies.
   Purpose: Comfort and contrast while traction is monitored.
   Mechanism: Improves visual function in borderline quality conditions.

7. Low-vision aids (if persistent field loss)
   Purpose: Improve function for reading/navigation if defects persist even after traction release.
   Mechanism: Magnification and contrast support.

8. Nutritional optimization (general eye-healthy diet)
   Purpose: Support retinal metabolism; not a direct traction fix.
   Mechanism: Antioxidants and omega-3s support retinal cells; evidence is stronger in AMD than VPTS.

9. Smoking cessation
   Purpose: Improve vascular and retinal health.
   Mechanism: Reduces oxidative stress and microvascular compromise.

10. Blood lipid control
    Purpose: Support retinal microcirculation.
    Mechanism: Lowers atherosclerotic burden that may affect perfusion.

11. Hydration and regular breaks for near work
    Purpose: Reduce visual strain and dryness that can mask symptoms.
    Mechanism: Comfort measures; do not change traction.

12. Treat coexisting ocular surface disease
    Purpose: Clearer vision and better imaging quality (OCT).
    Mechanism: Less surface blur, better monitoring.

13. Protective eyewear in risky environments
    Purpose: Prevent trauma that could acutely worsen vitreoretinal traction.
    Mechanism: Minimizes sudden vitreous traction events.

14. Glycemic targets before/after eye surgery (if diabetic)
    Purpose: Better wound healing and edema control.
    Mechanism: Metabolic stability around surgical stress. PubMed

15. Stepwise decision-making (shared decision tools)
    Purpose: Balance observation vs. surgery based on symptoms, fields, and OCT.

16. Visual field training/compensation
    Purpose: If residual field defects persist, teach scanning strategies.

17. Ergonomic screen settings & larger fonts
    Purpose: Reduce strain while monitoring.

18. Address medications that worsen perfusion (case-by-case)
    Purpose: Coordinate with primary care to optimize systemic perfusion if appropriate.

19. Treat coexisting macular traction separately when present
    Purpose: Macular traction (VMT) may coexist and need its own plan.
    Mechanism: Different adhesion site; options may include vitrectomy or pharmacologic vitreolysis in selected VMT (see below for surgery notes). EyeWikiPMC

20. Pre- and post-op counseling for vitrectomy
    Purpose: Set expectations, improve adherence to drops and follow-ups.
    Mechanism: Better post-op outcomes when surgery is chosen.

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Drug treatments

1. Topical corticosteroid (e.g., prednisolone acetate 1% q.i.d., taper)
   Purpose: Calm secondary inflammation around the disc if present.
   Mechanism: Inhibits inflammatory cascades that may worsen swelling.
   Side effects: Eye pressure rise, cataract with prolonged use.

2. Topical NSAID (e.g., nepafenac 0.1–0.3% q.d.–t.i.d.)
   Purpose: Reduce inflammatory mediators contributing to peripapillary discomfort/edema.
   Mechanism: COX inhibition reduces prostaglandins.
   Side effects: Surface irritation; rare corneal effects with prolonged use.

3. IOP-lowering beta-blocker (e.g., timolol 0.5% b.i.d.)
   Purpose: If intraocular pressure is elevated or there is coexisting glaucoma risk.
   Mechanism: Decreases aqueous production.
   Side effects: Bradycardia/bronchospasm in susceptible patients (systemic absorption).

4. Prostaglandin analog (e.g., latanoprost nightly)
   Purpose: Adjunct if IOP control is needed.
   Mechanism: Increases uveoscleral outflow.
   Side effects: Redness, lash growth, iris darkening.

5. Carbonic anhydrase inhibitor drops (e.g., dorzolamide t.i.d.)
   Purpose: IOP control or adjunct for cystoid macular edema in other settings.
   Mechanism: Reduces aqueous or alters retinal fluid transport.
   Side effects: Bitter taste, allergy.

6. Alpha-agonist (e.g., brimonidine t.i.d.)
   Purpose: Additional IOP control.
   Mechanism: Lowers aqueous production, increases uveoscleral outflow.
   Side effects: Allergy, fatigue.

7. Oral acetazolamide (e.g., 250–500 mg b.i.d.–q.i.d., short course)
   Purpose: Short-term edema control in selected cases with coexisting macular fluid; off-label.
   Mechanism: Carbonic anhydrase inhibition changes fluid dynamics.
   Side effects: Paresthesias, kidney stone risk, metabolic acidosis.

8. Anti-VEGF intravitreal agents (e.g., ranibizumab/aflibercept)
   Purpose: Only when diabetic macular edema or neovascular complications coexist. They do not release papillary traction but can treat the edema part.
   Mechanism: VEGF inhibition reduces vascular leakage.
   Side effects: Endophthalmitis risk (rare), transient IOP rise. PubMed

9. Topical antibiotic (peri-op prophylaxis as directed)
   Purpose: Around surgery to lower infectious risk.
   Mechanism: Reduces surface bacteria.

10. Cycloplegic (e.g., atropine 1% daily, short course if painful spasm)
    Purpose: Comfort if ciliary spasm contributes to ache.
    Mechanism: Paralyzes ciliary muscle; reduces spasm-related pain.

Evidence note: No medicine has proven to directly detach the vitreous from the optic disc in VPTS. When symptoms or objective damage are meaningful, surgery is the definitive option. EyeWikiPMC

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Dietary molecular supplements

These may support general retinal health but do not release vitreous traction. Always discuss with your doctor, especially if pregnant, on blood thinners, or with kidney issues.

1. Omega-3 (EPA/DHA 1–2 g/day) – supports photoreceptor membranes; anti-inflammatory signaling.

2. Lutein (10 mg/day) + Zeaxanthin (2 mg/day) – macular pigment support; antioxidant filtering.

3. Vitamin C (500–1000 mg/day) – aqueous antioxidant; collagen support.

4. Vitamin E (≤400 IU/day) – lipid antioxidant (avoid high doses if on anticoagulants).

5. Zinc (10–20 mg elemental/day) – cofactor in retinal enzymes (watch copper balance).

6. Astaxanthin (4–12 mg/day) – carotenoid antioxidant; visual fatigue research exists outside VPTS.

7. Alpha-lipoic acid (300–600 mg/day) – antioxidant; glucose metabolism support in diabetics (coordinate with MD).

8. Curcumin (500–1000 mg/day with pepperine for absorption) – anti-inflammatory; may support microglia modulation.

9. CoQ10 (100–200 mg/day) – mitochondrial support; theoretical retinal energy benefits.

10. Bilberry extract (80–160 mg/day standardized) – flavonoids; microvascular support.

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Regenerative / stem cell drugs”

Important safety note: There are no approved “immunity booster,” regenerative, or stem-cell drugs for VPTS. Experimental cell-based or regenerative therapies are being studied for other retinal diseases; they are not standard of care for releasing vitreopapillary traction and should not be used outside regulated clinical trials. The only proven way to remove the traction is surgical release (vitrectomy) when clinically indicated. EyeWikiPMC

What you can safely consider instead: evidence-based surgery (below), plus risk-factor control and supportive care.

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Surgeries

1. Pars plana vitrectomy (PPV) with posterior hyaloid/epipapillary membrane release
   What: Micro-incision surgery removes the vitreous gel and peels or releases the adherent hyaloid from the optic disc (and macula if needed).
   Why: Definitively eliminates traction on the disc; can improve optic nerve head contour and sometimes improve visual fields and symptoms. PMCPubMed

2. Vitrectomy with epiretinal membrane (ERM) peel (if present)
   What: Removes any coexisting fibrocellular tissue.
   Why: Further reduces tangential traction, optimizes retinal shape. PMC

3. Vitrectomy with ILM (internal limiting membrane) peel (selected cases)
   What: Gentle peel of the ILM around peripapillary/macular region when traction extends.
   Why: Reduces recurrence risk of membranes and residual traction in complex interface disease. (Surgeon-dependent practice; not mandatory in every case.)

4. Adjunct endolaser or PRP (if proliferative diabetic retinopathy)
   What/Why: Treats neovascularization while the eye is already in surgery, reducing tractional recurrence and hemorrhage risk in diabetic eyes. PubMed

5. Gas or no-tamponade strategy (case-by-case)
   What: Some surgeons use a short-acting gas bubble if macular interface work was extensive; many VPTS releases need no tamponade.
   Why: Supports contour if macular traction was also addressed. (Technique varies.)

Case series and reviews show that releasing vitreopapillary traction with vitrectomy can normalize disc appearance and improve visual field sensitivity in selected patients. Earlier series suggest traction can harm axoplasmic flow and prelaminar blood flow—reasons some surgeons consider early vitrectomy when function is threatened. PMCWiley Online LibraryPubMed

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Preventions

We can’t always prevent anomalous vitreous separation. But these steps support overall eye health and help prevent missed diagnoses:

1. Regular comprehensive eye exams after age 50 or sooner if symptomatic.

2. Prompt OCT when the optic disc looks elevated or vision changes occur. JAMA Network

3. Control diabetes, blood pressure, lipids. PubMed

4. Stop smoking.

5. Wear eye protection during high-risk activities.

6. Manage sleep apnea and cardiovascular risks (general optic nerve health).

7. Keep follow-up schedules if VPTS is observed.

8. Seek urgent care for sudden floaters/flashes or curtain-like shadow.

9. Optimize post-op drop adherence if surgery is done.

10. Keep a personal symptom diary to track triggers and timing.

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When to see a doctor (red flags)

• Sudden or progressive blurred vision, new visual field defects, or metamorphopsia.

• New floaters or flashes of light; sudden “curtain” or shadow.

• Eye pain, headache with visual changes, or unequal pupils.

• Known VPTS with worsening OCT findings or new hemorrhages.

• Any uncertainty—especially if disc swelling is suspected; VPTS can mimic true edema but needs a different approach. BMJ Case Reports

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What to eat and what to avoid

1. Eat: Dark leafy greens (lutein/zeaxanthin), colorful veggies, citrus, berries.

2. Eat: Oily fish 2–3×/week (omega-3).

3. Eat: Nuts/legumes/whole grains for vitamin E and minerals.

4. Eat: Adequate protein for healing if surgery is planned.

5. Drink: Water regularly; avoid dehydration.

6. Limit: Added sugars—especially important if diabetic.

7. Limit: Ultra-processed foods and excess salt.

8. Limit: Smoking and second-hand smoke exposure.

9. Discuss: Any supplements with your doctor (interaction checks).

10. Maintain: Healthy weight and physical activity for vascular health.

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Frequently Asked Questions

1) Is VPTS the same as optic disc swelling?
No. It mimics swelling. In VPTS, the disc looks elevated because the vitreous is tugging on it. OCT helps tell them apart. JAMA NetworkBMJ Case Reports

2) Can VPTS make me go blind?
Severe, ongoing traction can harm function, but many cases are mild. If vision or fields are threatened, surgery can remove the traction. PMC

3) Will eye drops fix the traction?
No. Drops may treat inflammation or eye pressure, but they don’t detach the vitreous from the disc. EyeWiki

4) How do doctors confirm VPTS?
With exam and OCT, which shows the sticky attachment and the direction/shape of traction. EyeWiki

5) Can it improve on its own?
Sometimes traction stabilizes; rarely it may lessen. That’s why regular OCT is used when observation is chosen.

6) When is surgery recommended?
When there are bothersome symptoms, progressive OCT changes, visual field loss, or coexisting disease (like diabetic traction) making harm more likely. PubMed+1

7) What happens during vitrectomy?
Small instruments remove the vitreous; the surgeon releases the sticking points on the disc (and macula if needed). Most procedures are outpatient.

8) What are the risks of surgery?
Infection (very rare), bleeding, cataract progression, retinal tear/detachment, pressure changes. Your surgeon explains your individual risk.

9) If I also have macular traction, is treatment different?
Yes. Macular traction (VMT) can need additional steps (membrane or ILM peel). Planning is based on OCT patterns. PMC+1

10) Do anti-VEGF shots fix VPTS?
They do not release disc traction. They can treat diabetic macular edema or neovascularization if present. PubMed

11) Is VPTS an optic neuropathy?
It can behave like a more anterior optic neuropathy because the pull disrupts axoplasmic flow and perfusion right at the disc surface. Lippincott JournalsWiley Online Library

12) Why do some people get VPTS?
Because of an anomalous PVD where the vitreous liquefies but stays attached around the disc instead of letting go completely. EyeWikiPMC

13) Can glasses or contact lenses help?
They don’t change traction, but updated correction improves function while you’re monitored.

14) Will I need long-term follow-up after surgery?
Yes—post-op visits ensure traction is released and monitor for complications; many patients do very well when properly selected. PMC

15) Is there anything I can do daily to help?
Keep systemic conditions controlled, don’t miss follow-ups, and call promptly if symptoms change.

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 30, 2025.