Assessment of the optic nerve head is a key part of a dilated eye examination. The optic disc’s color, cup-to-disc ratio, neuroretinal rim, disc margins, and surrounding peripapillary region are routinely evaluated during the examination.
Normally, the margins of the optic disc are clear and well-defined. However, when the optic disc margins appear blurry or the optic disc appears elevated, it can be a sign of an underlying issue.
Overview of vitreopapillary traction syndrome
While papilledema and optic disc drusen are commonly considered when the optic disc margins look blurry or elevated, it is also important to think about structural changes caused by traction on the nerve.
One condition to keep in mind is vitreopapillary traction (VPT) syndrome. Though less common than other optic nerve conditions, vitreopapillary traction remains a clinical consideration in optic disc elevation and should be included in the differential.1
This article takes a closer look at vitreopapillary traction syndrome, using a case example to explore risk factors, diagnostic methods, and treatment options.
Epidemiology and pathophysiology of VPT syndrome
The vitreous is naturally connected to the retina, with stronger attachments at the vitreous base, optic disc, macula, and along the retinal vessels. As the eye ages, the vitreous begins to liquefy, and these connections weaken. This process often leads to a posterior vitreous detachment (PVD), where the vitreous pulls away from the retina.2-4
A PVD usually occurs in a consistent pattern, with the vitreous remaining attached to the optic nerve until the final stage. Typically, the detachment follows a predictable pattern, with the optic nerve being the last to separate.5
If the vitreous liquefies too quickly before the adhesions can weaken, an anomalous PVD occurs, causing traction at areas that are still attached to the retina.5 When this traction affects the optic disc, it results in vitreopapillary traction, where the vitreous continues to pull on the optic nerve after most of it has detached.2
Incidence of VPT
The exact prevalence of vitreopapillary traction syndrome is not well established, mainly because it is much less common than other vitreoretinal conditions like epiretinal membranes or vitreomacular traction.
However, it has been reported more frequently in eyes with full-thickness macular holes, lamellar holes, dry age-related macular degeneration, and epiretinal membranes.6
Risk factors of vitreopapillary traction
VPT syndrome frequently occurs alongside a PVD, so it is not surprising that the two conditions share several common risk factors, including:
- Age: The vitreous naturally undergoes liquefaction and structural changes as we age, increasing the likelihood of an anomalous PVD, which carries the risk of VPT.2
- Diabetic retinopathy: In proliferative diabetic retinopathy, neovascularization can lead to abnormal adhesions between the posterior vitreous cortex and the optic disc, setting the stage for vitreoretinal and vitreopapillary traction.7
- High myopia: In myopic eyes, vitreous liquefaction happens earlier, so PVD and potentially VPT can develop sooner than in non-myopic patients.8
- Previous ocular surgery: PVD tends to occur frequently following cataract surgery. Post-operative structural changes may contribute to earlier vitreous separation, which again raises the risk for traction-related issues.9
- Non-arteritic anterior ischemic optic neuropathy (NAION): Optic nerve head changes like decreased prelaminar blood flow or neuronal damage can also predispose the eye to abnormal vitreopapillary interactions.10
VPT presentation and symptoms
During a dilated fundus exam, VPT can present with a variety of optic nerve and peripapillary changes. The condition is typically unilateral, though bilateral involvement can occur in some cases. Its presentation tends to correlate with the amount of traction affecting the peripapillary area.
Patients with VPT syndrome may present with:2,11
- Elevation of the optic nerve head
- Blurred or indistinct disc margins
- Optic disc hemorrhages
- Peripapillary hemorrhages
- Subretinal hemorrhages
These signs can vary depending on the amount of traction that is present. VPT should be kept in the differential, especially in cases of optic disc elevation or hemorrhages without a clear underlying cause.
Symptoms of vitreopapillary traction syndrome
The symptoms of vitreopapillary traction syndrome can vary widely among patients.
Some patients remain asymptomatic, while others experience:
- Blurred vision
- Floaters
- Photopsia (flashes)
- Visual field defects, including enlarged blind spots or altitudinal defects
- Some studies suggest that visual field loss in VPT syndrome can correlate with the area of traction, particularly when the traction affects the optic nerve head or adjacent retinal nerve fiber layer (RNFL)2,12-14
- Gaze-evoked amaurosis (temporary vision loss), a less common but also relevant symptom15
Download the cheat sheet here!
Vitreopapillary Traction Syndrome Differential Diagnosis Cheat Sheet
Use this cheat sheet to review key signs, symptoms, diagnostics, and risk factors for VPT syndrome and conditions that present similarly, including optic disc drusen and papilledema.
Diagnosis of VPT syndrome
The following key tests can help to confirm a diagnosis of vitreopapillary traction syndrome:
Fundus photography
As noted above, funduscopic examination may reveal optic nerve head elevation with blurred optic disc margins, optic disc hemorrhages, or peripapillary or subretinal hemorrhages.
Figure 1: Fundus images of a patient with VPT syndrome demonstrating glial tissue nasal to the optic disc of the right eye (left) and blurred optic disc margins and peripapillary hemorrhage of the left eye (right).
Figure 1: VPT syndrome©Mohamed M Khodeiry et al. Image cropped and used under CC BY 4.0.
Optical coherence tomography (OCT)
Optical coherence tomography is one of the most useful tools for evaluating VPT syndrome. It can easily detect thickening of the peripapillary RNFL and highlight areas where the vitreous is exerting traction. Chronic traction can result in cellular proliferation, which often appears as a hyperreflective band along the posterior hyaloid.2,16
Figure 2: OCT of the optic nerve head showing vitreous traction on the optic discs of both eyes, with disc elevation of the left eye.17
Figure 2: VPT syndrome©Mohamed M Khodeiry et al. Image cropped and used under CC BY 4.0.
Figure 3: OCT scan of a patient diagnosed with VPT syndrome.18
Figure 3: VPT syndrome©Breyne Middleton et al. Image used under CC BY 4.0.
B-scan ultrasound
On B-scan, VPT usually shows up as a partial detachment of the posterior hyaloid around the optic nerve.19,20
Figure 4: B-scan ultrasound demonstrating an incomplete PVD adhered to the optic disc (red and yellow arrows).20
Figure 4: PVD© Xian Zhang et al. Image cropped and used under CC BY-NC 3.0.
Fluorescein angiography (FA)
Fluorescein angiography can help confirm the diagnosis by showing focal leakage from the optic disc.16
Figure 5: FA of the left optic disc in a patient with VPT syndrome showing focal leakage.
Figure 5: Vitreopapillary traction©Elizabeth Houle et al. Image cropped and used under CC BY 4.0.
Visual field testing
Visual fields may appear completely normal, but defects such as enlarged blind spots or altitudinal losses have also been seen in some cases.2
Figure 6: Humphrey 30-2 visual fields showing a full visual field of the right eye and supertemporal wedge-shaped scotoma in the left eye of a patient with VPT.17
Figure 6: VPT syndrome©Mohamed M Khodeiry et al. Image cropped and used under CC BY 4.0.
Management and treatment of VPT
Management of vitreopapillary traction is dependent upon the patient’s symptoms and any related eye conditions. Some cases only require monitoring, while others may require surgery.
Observation
If the patient is asymptomatic, observation is often enough.
Follow-up appointments should include the following tests:
- Dilated fundus exams
- Fundus photography
- OCT
- Visual field testing
Asymptomatic patients without any coexisting ocular disease can usually be seen every 6 to 12 months for routine exams, OCT, and visual field testing to monitor for any changes.
If VPT is present with other ocular conditions such as diabetic retinopathy, macular disease, vascular occlusions, or optic neuropathy, the risk for visual field loss increases. These patients should be monitored more closely and more often.2
Surgical treatment
When vision is affected or traction is worsening, pars plana vitrectomy (PPV) is the preferred treatment method. It relieves optic nerve traction by removing the posterior hyaloid, often improving vision and disc anatomy. Post-operatively, these patients need close follow-up appointments in the first few months, with intervals extended as recovery stabilizes.2
Although there is currently little data supporting early PPV for VPT, research indicates that it can enhance both anatomy and vision, particularly in patients with severe symptoms.
Since there are no precise rules about when to operate, the choice is typically made on an individual basis and is influenced by several factors, including visual acuity, the severity of the symptoms, and any associated complications, rather than just traction.2,21
Medical therapy
Ocriplasmin, an intravitreal injection, was studied as a non-surgical treatment option for VPT. It was developed to break down proteins anchoring the vitreous to the retina, helping to induce a posterior vitreous detachment.22,23,24
While early results were promising, its use declined because of side effects such as floaters, photopsia, temporary vision loss, and injection-related eye pain, as well as inconsistent outcomes. Approved in 2012, it was withdrawn from the US market in 2020.22,23,24
Prognosis of VPT
The outlook for patients with vitreopapillary traction varies depending on the severity of symptoms, severity of the condition, and associated ocular disease. Many patients with mild or asymptomatic VPT do well with regular monitoring and experience little to no progression.
However, when traction is more severe or linked to other retinal or optic nerve conditions, the risk of lasting visual field defects and optic nerve damage increases if it is left untreated.16
Don't forget to download the VPT Syndrome Differential Diagnosis Cheat Sheet!
VPT syndrome case report
A 77-year-old female with a history of hypertension, hyperlipidemia, depression, and bilateral hearing loss, presented for a 1-month post-operative eye examination with complaints of floaters OS > OD.
The patient described the floaters as looking like “droplets of rain on a windshield.” The patient denied eye pain, diplopia, or photopsia. Best-corrected visual acuity was 20/25 OD and 20/25-1 OS.
Pupillary reactions were normal, and no afferent pupillary defect was noted. Intraocular pressures were within normal limits. Dermatochalasis of the upper eyelids was noted.
Posterior chamber intraocular lenses were centered in both eyes with trace peripheral opacification OU. Funduscopic examination revealed moderate elevation and blurring of the right and left optic disc margins and peripapillary region. No hemorrhages or exudates were seen in the posterior segment.
Vitreous syneresis was also noted OU. Minimal dry drusen was noted in the macula OD and macula appeared normal OS.
OCT imaging OD revealed a partial PVD with persistent vitreopapillary adhesion and anterior-posterior traction on the optic disc. The average RNFL thickness was 139µm OD and 104 µmOS. There was localized elevation of the optic nerve head and moderate peripapillary thickening (Figure 7).
Figure 7: OCT of the right eye (OD) and left eye (OS) showing peripapillary elevation and RNFL thickening OD.
Figure 7: Courtesy of Stephanie Rowe, OD.
Visual field testing (Humphrey 24-2) showed a possible superior arcuate defect and nasal step OD, though the results were of low reliability (Figure 8). The visual field defect resembled glaucomatous damage but did not correspond with optic disc cupping or RNFL thinning (Figure 2). Visual field testing for OS showed mild scattered non-specific visual field changes OS (Figure 9).
Figure 8: Visual field OD highlighting a superior arcuate nasal step defect.
Figure 8: Courtesy of Stephanie Rowe, OD.
Figure 9: Visual field OS demonstrating mild scattered field defects.
Figure 9: Courtesy of Stephanie Rowe, OD.
A consultation was also made with the referring surgeon and a diagnosis of VPT syndrome was confirmed. Given the patient’s stable vision and lack of macular involvement, conservative management with close monitoring was selected.
At the 5-month follow-up appointment, the patient’s symptoms of floaters had improved. The average RNFL thickness on OCT images at the follow-up appointment was measured at 130µm OD and 95µm OS. The decision was made to monitor the condition at 6-month intervals.
Key takeaways
- Vitreopapillary traction happens when the vitreous stays abnormally attached to the optic disc, which can cause disc elevation and visual field changes. Its appearance can mimic optic nerve swelling, but the underlying cause is different.
- OCT is the main tool for diagnosing and following these patients. The OCT can reveal the traction and help track any changes over time.
- The biggest risk factors are older age, diabetes, high myopia, and a history of ocular surgery.
- Management can range from simple observation to vitrectomy, depending on how much traction is present and how the symptoms are progressing.
- This case example shows how OCT can help to confirm the diagnosis, avoid unnecessary systemic workups, and make it easier to choose the right treatment plan.
Conclusion
Recognizing vitreopapillary traction syndrome can be a challenge because it often resembles other optic nerve conditions. With advances in OCT, the ability to detect and monitor VPT has improved.
While many patients can be managed with observation alone, those with significant symptoms or other retinal and optic nerve disease often benefit from surgical treatment. Although medications like ocriplasmin initially showed potential, surgery remains the most effective and predictable option for managing advanced cases.
Early detection and timely intervention are critical for preserving visual function and reducing the risk of complications.
