Vitreopapillary traction syndrome (VPT syndrome) is a condition characterized by persistent attachment of the vitreous cortex around the optic disc (peripapillary area) with incomplete posterior vitreous detachment (PVD). Traction from the vitreous cortex can cause morphological damage to the attachment site and lead to visual impairment.
In vitreomacular traction syndrome (VMT), eyes with vitreomacular traction may also show vitreous attached around the optic disc, observed as vitreopapillary traction. 1) This condition can be confused with optic nerve diseases such as optic disc edema. 1)
Patients are often over 50 years old, but all age groups can be affected, with reports of onset as young as 11 years. There is no gender difference.
Vitreomacular traction syndrome (VMT) is a condition where the vitreous attaches to the macula and causes traction, while vitreopapillary traction syndrome primarily involves attachment and traction around the optic disc. Both can coexist. 1)
Symptoms vary widely, and some patients are asymptomatic.
The following findings are confirmed by fundus examination, OCT, and ultrasound.
Fundus Findings
Incomplete PVD: Vitreous remains attached around the optic disc.
Optic disc elevation: Elevation of the optic disc is observed. Differentiation from papilledema is necessary.
Intrapapillary and peripapillary hemorrhage: Small amounts of bleeding may be seen. Most resolve within a few months.
Focal opacification of the nerve fiber layer: Appears as edematous changes in the retinal nerve fiber layer.
OCT Findings
Optic disc elevation: OCT clearly depicts the elevation of the optic disc.
RNFL thickening: Thickening of the retinal nerve fiber layer is confirmed.
Thickened hyperreflective posterior hyaloid membrane: A hyperreflective posterior vitreous cortex attached to the optic disc or its margin is visualized.
Peripheral PVD: Posterior vitreous detachment is observed to be progressing around the attachment site.
Visual acuity is often maintained at 20/25 (0.8) or better, relative afferent pupillary defect (RAPD) is mild or absent, and color vision abnormalities are usually not seen, although decreased red saturation may be noted.
Ultrasound may show optic disc elevation, thickening of the vitreopapillary interface, and partial attachment of the posterior vitreous to the disc or disc margin.
Ocular movement-induced transient monocular vision loss has been reported as a characteristic symptom of VPT syndrome, thought to be due to dynamic optic nerve ischemia from vitreous traction. In reported cases, improvement occurred over weeks to months. However, if there are progressive changes, consultation with a specialist is important.
Since the onset of VPT syndrome is related to incomplete PVD, risk factors are similar to those for PVD.
In addition to PVD, associations with the following diseases have been reported:
In diabetic patients, early vitreous liquefaction (synchysis) is more likely to occur, suggesting a potentially higher risk of VPT-related optic neuropathy. 2) Additionally, in “disk-at-risk” (crowded disc/small disc), the adhesion between the vitreous and axons is stronger, which is thought to increase the risk of VPT development. 2)
This is the most useful examination for confirming the diagnosis of VPT syndrome. OCT allows non-invasive and detailed assessment of the morphological features of the posterior vitreous membrane, retina, and vitreopapillary interface. 1)
In eyes with epiretinal membrane (ERM) or vitreomacular traction, OCT is a commonly used sensitive test for diagnosis and characterization. 1) OCT scans through the optic disc can help differentiate papilledema from (in bilateral cases) optic disc edema. 1)
These are conventional diagnostic methods that can identify incomplete PVD, optic disc elevation, intraoptic disc hemorrhage, peripapillary hemorrhage, and changes in the nerve fiber layer. Slit-lamp microscopy under mydriasis is recommended.
Useful when fundus observation is difficult. It can depict optic disc elevation, thickening of the vitreopapillary interface, and partial attachment of the posterior vitreous.
Visual field test results vary among patients. They can range from normal to various abnormalities such as generalized sensitivity reduction, arcuate scotoma, and enlargement of the Mariotte blind spot. The contralateral unaffected eye is usually normal, which is an important finding for differential diagnosis.
The main diseases to be differentiated from isolated VPT syndrome are as follows:
| Disease | Main differentiating points |
|---|---|
| Papilledema | Bilateral, evidence of increased intracranial pressure |
| Optic disc drusen | Autofluorescence, calcification on ultrasound |
Most cases of isolated VPT syndrome due to incomplete PVD are managed conservatively with observation.
In the initial case series by Katz and Hoyt, intra- and peripapillary hemorrhages resolved without sequelae or visual impairment at 6-month follow-up. In a second series by the same group on eye movement-induced transient monocular vision loss, visual disturbances and visual field defects resolved within weeks to months.
In VPT syndrome due to isolated or incomplete PVD, the visual prognosis with observation or conservative treatment is usually good, with best-corrected visual acuity (BCVA) of 20/25 (0.8) or better.
The most common surgical intervention to relieve vitreopapillary traction is pars plana vitrectomy (PPV).
PPV in patients with vitreopapillary traction due to proliferative diabetic retinopathy has shown improvement in best-corrected visual acuity (BCVA) and visual evoked potentials (VEP).
In a case report of isolated VPT syndrome, BCVA improved from 20/80 (0.25) to 20/25 (0.8) after PPV. In contrast, a 16-year-old patient with progressive vision loss over 6 years had only minimal recovery after PPV, with BCVA remaining at 20/300 (approximately 0.06).
PPV for VPT-related optic neuropathy with partial PVD, termed “papillary vitreous detachment neuropathy,” has also been reported to improve vision. 2) However, at present, clinical and instrumental data are insufficient to determine whether VPT plays a causal role in the development of NA-AION. 2)
The vitreous humor is composed of a network of collagen fibers containing hyaluronic acid, filling the central part of the eye as a gel. With aging, degradation of collagen fibers and loss of proteoglycans occur, leading to liquefaction of the gel and formation of lacunae.
According to Johnson’s study using OCT (2010), PVD typically begins at the perifoveal macula, progresses to the periphery, and the optic disc is the last site of attachment. Persistent adhesion of the posterior cortical vitreous around the optic disc leads to VPT syndrome.
Depending on the stage of PVD, both static and dynamic traction forces can cause visual symptoms and anatomical findings. Dynamic forces are thought to play a greater role. Large movements of the vitreous gel during eye movement generate additional traction.
Observational studies in patients with proliferative diabetic retinopathy and optic disc traction suggest that VPT may damage the optic disc through the following mechanisms.
It is hypothesized that dynamic stretch injury of axons due to VPT causes disruption of the axonal cytoskeleton and membrane, as well as blockage of axoplasmic flow. 2) The onset of optic nerve symptoms is thought to depend on the severity of axonal damage, with higher risk in elderly individuals (decreased axonal elasticity), disk-at-risk (firm vitreopapillary adhesion), and diabetic patients (early vitreous syneresis). 2)
The effects of each mechanism may be reversible in some cases, but can lead to irreversible damage in the long term.
In eyes with epiretinal membrane or vitreomacular traction, vitreous attached to the peripapillary area may be observed as vitreopapillary traction. This condition can be confused with optic nerve diseases such as papilledema, and OCT is useful for differentiation. Additionally, VPT has been suggested to be associated with visual loss and ischemic optic neuropathy in some cases. 1)
In a review by Salvetat et al. (2023), it is suggested that VPT and PVD (total or partial) may be associated with the development of NA-AION, and the term “papillary vitreous detachment neuropathy” has been proposed. 2)
The proposed mechanism is that acute VPT associated with partial or complete PVD causes dynamic stretch injury of axons, leading to disruption of the axonal cytoskeleton and membrane, and blockage of axoplasmic flow. 2)
On the other hand, the same review concluded that current clinical and OCT evidence is insufficient to demonstrate a causal role of VPT in the development of NA-AION. 2) No cases have been reported in which VPT was documented on OCT before the onset of NA-AION, and it has been noted that PVD (including pre-onset PVD) is frequently observed in NA-AION. 2)
This issue continues to be debated among experts, including in point-counterpoint articles by Dr. Parsa and colleagues.
Ocriplasmin is a recombinant protease with activity against fibronectin and laminin, and has been studied for the treatment of vitreomacular traction. Its application to VPT syndrome is theoretically possible, but no approved pharmacologic therapy currently exists.
