Advancements in Myopic Macular Foveoschisis Research

Macular foveoschisis (MF) refers to the separation of the neuroepithelial layer of the retina in patients with an abnormal vitreoretinal interface or in those with high myopia accompanied by posterior staphyloma. This separation creates one or multiple gaps within the retina, interconnected by columnar structures, potentially consisting of Müller cells [1]. Kamal-Salah [2] identified high myopia as an independent risk factor for MF. High myopia is characterized by a refractive error of ≥−6 diopters (D) or an axial length exceeding 26 mm [3]. Pathological myopia is obviously different from high myopia. Pathological myopia refers to the presence of typical complications in the fundus (such as posterior scleral staphyloma, myopic maculopathy or diffuse choroidal atrophy). Pathological myopia usually occurs in individuals with high myopia [4]. Presently, the global prevalence of myopia and high myopia reaches approximately 1.95 billion and 277 million individuals, respectively [5]. Projections suggest that by 2050, the number of people with myopia may rise to 4.758 billion and those with high myopia to 938 million [6]. In highly myopic eyes, the occurrence of MF is reported to be as high as 8–33% [7]. Given the escalating prevalence of MF and its impact on vision, significant attention should be directed toward understanding and managing MF.

Currently, there is no recognized classification system for MF. However, an associated classification system exists. Firstly, Shimada et al. [8] classified myopic traction maculopathy into five grades according to the size of the macular retinoschisis: no macular retinoschisis (S0), outside the macular fovea (S1), only in the macular fovea (S2), involving the fovea but not the entire macula (S3), the entire macula (S4). Secondly, according to histologic classification, retinoschisis can be classified into outer layer splits, inner layer splits, and splits with detachment of the inner limiting membrane. In patients with high myopia, outer layer splits are the most common, occurring predominantly in the outer plexiform layer. The precise mechanism is still uncertain but a possible hypothesis is that the thinning and atrophy of the choroid in patients with high myopia, leading to insufficient blood supply to the outer retinal layer cells (mainly photoreceptors) and the retinal pigment epithelium (RPE) layer. Consequently, this results in a decrease in the strength of retinal adhesion, leading to the occurrence of myopic foveoschisis [9]. In addition, a staging system for myopic tractional maculopathy based on optical coherence tomography (OCT) features [10] describes four stages (1–4) in the retinal pattern and three stages (a–c) describing the central concave pattern, as shown in Table 1.

The pathogenesis of MF is currently believed to be a combination of outward traction caused by posterior scleral staphyloma and inward traction due to vitreoretinal adhesions and rigidity of the inner limiting membrane. This leads to retinal structural and functional disorders in the macula retina. Studies suggest that outer retinoschisis is mainly caused by outward traction from posterior scleral staphyloma or ocular axis elongation, while inner retinoschisis is primarily due to vitreous traction or posterior vitreous detachment (PVD) [11]. Based on findings from OCT display, several pathogenic mechanisms have been proposed, as illustrated in Figure 1.

(1) Residual vitreous cortex and epiretinal membrane (ERM) after PVD: in high myopia patients, the vitreous body adheres more strongly to the central fovea compared to the surrounding retina [12]. During PVD, this can result in macular traction. Incomplete PVD often leads to Müller cells activating the residual cortex, which then contributes to anterior macular membrane development. This process exerts tangential traction on the macula, furthering MF formation [13]. (2) Internal limiting membrane (ILM) elasticity reduction: increased ILM hardness is a notable feature in patients with MF. This change is attributed to Müller cells and astrocytes reacting to mechanical stresses associated with ocular axis elongation, which stimulates glial cell proliferation and consequently enhances ILM rigidity [14].In addition, the presence of both ERM and residual vitreous cortex lead to reduced ILM elasticity. This decrease intensifies tangential traction at the vitreoretinal interface, which is a pivotal factor in MF development. (3) Retinal vasculature factors: vitreous adhesion to the retinal vasculature may play a more important role in MF pathogenesis than its adhesion to the central fovea [15]. Additionally, retinal vasculature stiffening induces inward traction on the retina, potentially leading to perivascular retinal abnormalities such as perivascular micro folds, cysts, and lamellar macular holes (LMHs) [12].

Posterior scleral staphyloma formation: in highly myopic eyes, ocular axis elongation causes the thinning at the posterior pole of the sclera, predisposing it to posterior scleral staphyloma formation, coupled with weaker retinal adhesion at the staphyloma site, generates an outward traction on the macula. This scleral dilatation-induced traction is a key factor in MF development [16].

Additionally, the dome-shaped macula (DSM) is a specific fundus phenotype in high myopia patients, potentially playing a protective role against MF [17]. Characterized by an inward bulge of the retinal choroid (>50 μm) in posterior scleral staphyloma (as observed on OCT), DSM alters the stress distribution on the fundus. In patients without DSM, the posterior fundus wall deforms outward, concentrating maximum stress at the macular central fovea, hence elevating MF risk at this location. Conversely, in patients with DSM, simultaneous inward and outward forces on the eye’s posterior wall shift the maximum stress from the central to the peripheral area, reducing central foveal traction and thereby lowering central foveal MF incidence while increasing peripheral retinoschisis [18]. Figure 2 illustrates the fundus stress state in DSM.

For adolescents’ high myopia patients with MF, Sun [19] found that the affected eyes typically lacked anterior abnormal retinal traction, severe macular degeneration, or even significant posterior scleral staphyloma. They concluded that the posterior sclera’s retained elasticity in these adolescents counteracts the external protrusion of the eyeball’s posterior segment, leading to diffuse posterior scleral dilatation. This dilation, in turn, progressively extends the choroid, retinal pigment epithelial layer, and retinal nerve fiber layer. However, the inner limiting membrane and retinal vasculature have limited extensibility, resulting in inward retinal traction beyond their dilation limit. Consequently, an imbalance between outward and inward traction culminates in retinal MF. Their findings indicated a tendency in adolescent high myopia patients toward shorter axial lengths, better best-corrected visual acuity (BCVA), and lesser refractive errors in MF eyes without posterior scleral staphyloma compared to those with it.

The prevalence of MF in highly myopia eyes with posterior scleral staphyloma has been reported to range from 9 to 34% [20]. MF typically follows a chronically progressive course. Studies indicate a significant disparity in progression rates: as high as 42.9% in stage S4 (entire macular area splitting) compared to a mere 7.8% in stages S1 (splitting outside the central fovea), S2 (central fovea splitting), and S3 (central fovea involvement without entire macula splitting) [8]. It has also been suggested that the progression likelihood is relatively high if the split involves the central fovea, irrespective of its extent across the macula [21].

MF can remain stable for many years without visual impairment, often eluding detection through fundus examination. Consequently, therefore, its diagnosis relies mainly on OCT [22]. Sayanagi et al. [23] conducted OCT in 21 eyes with MF and observed frequent co-occurrence with other abnormalities, including retinal microfolds (71%), internal limiting membrane detachment (38%), macular holes (MHs) (14%), paravascular hiatuses (24%), ERMs, and IS/OS defects. These microstructural retinal abnormalities are closely linked to patient prognosis.

Further, MF combined with anterior retinal traction and central foveal detachment presents a heightened risk for disease progression, potentially leading to MH and even retinal detachment (RD) [24]. Gaucher et al. [24] monitored 29 eyes with MF over an average of 31.2 months. OCT scans revealed that 13 eyes (44.8%) had anterior macular abnormalities, of which 8 eyes (27.6%) had ERMs and 5 eyes (17.2%) had vitreomacular traction; 10 eyes (34.5%) had RD of the macula; 7 eyes (24.1%) had MH; and 4 eyes (13.8%) were simple MF. Visual symptoms’ onset in patients often signals central macular fovea complications like MHs or RD. Interestingly, some cases exhibited spontaneous improvement or healing, possibly due to ILM rupture or PVD releasing tangential traction forces [25].

Shimada et al. [26] found that traction on the inner retina can transmit to the outer retina through the columnar structures between retinal split layers, potentially progressing MF to LMH, full-thickness macular holes (FTMHs), and even RD.

Sun et al. [27] identified two patterns in the OCT-based natural progression from MF to FTMH. Pattern 1 involves an initial focal elevation of the retinal pigment epithelial layer, leading to a small outer lamellar macular hole (OLMH) and RD. The OLMH gradually expands horizontally, while the RD extends vertically, culminating in FTMH formation following the rupture of the overlying inner retina. Pattern 2 is marked by a central foveal pseudocyst leading to an inner LMH. While retinoschisis may subside, leaving residual MF beneath the inner LMH, the remaining outer retinal tissue continues to split until it reaches the RPE, eventually progressing to FTMH and possibly leading to localized or rhegmatogenous RD [28]. At this point, the patient typically perceives a relative dark spot at the RD site, intensifying into an absolute dark spot with MH formation. Extensive RD may also result in noticeable visual field loss [4].

The International Vitreomacular Traction Study (IVTS) research group categorized MH based on its narrowest horizontal width: small (≤250 μm), medium (250–400 μm), and large (>400 μm) [29]. MHs can also be categorized by shape: MHs can also be categorized by shape: V-shaped (narrower medial diameter) and A-shaped (wider medial diameter). V-shaped MHs, with their narrower openings, are more prone to progress to FTMH, whereas A-shaped configurations may exert a protective effect against disease progression [30]. Tao et al. [31] observed similar cord-like structures at the edge of MHs in some cases using intraoperative OCT (iOCT). This “hole-door” phenomenon, possibly comprising residual ILM or other retinal tissue, is often associated with better MH prognosis, particularly in larger holes, where it correlates with higher closure rates [32].

It has been concluded that longer ocular axes in highly myopic patients have been linked to lower postoperative MH anatomical success rates. Alkabes et al. [33] examined 52 eyes after pars plana vitrectomy (PPV) combined with internal limiting membranes peeling. They found that the final MH closure rate was 73.3% in highly myopic eyes with an axial length greater than 26.0 mm, in eyes with an axial length of less than 26.0 mm, the anatomical closure success rate was 100%, and in eyes with an axial length of greater than 30 mm, the anatomical closure failure rate was 100%. Recent advances include the inverted ILM flap covering technique. Michalewska et al. [34] noted that this technique achieved MH closure rates of 100%, outperforming standard ILM peeling, which showed closure rates of 88%. The inverted ILM technique’s efficacy is attributed to the proliferation of glial cells, facilitated by Müller cell fragments in the inverted ILM, which aid in filling and closing the MH.

In some cases of MF, RD is an intermediate-stage change in the progression toward FTMH [27]. Patients with high myopia experiencing macular hole retinal detachment (MHRD) in one eye are at an increased risk of MHRD in the contralateral eye [35]. The progression from myopic retinoschisis (MRS) to early RD typically undergoes four stages. (1) Outer retinoschisis: Initial splitting in the outer retinal layers. (2) OLMH and small RD formation: development of an OLMH within the split area, accompanied by a localized RD. (3) Horizontal separation and enlargement: the MRS extends horizontally, while the OLMH and RD simultaneously expand vertically. (4) Adhesion and RD progression: the upper edge of the OLMH adheres to the upper edge of the original splitting structure. This phase is characterized by a reduction in the cleavage around the MH and further RD enlargement [26]. It is posited that MRS evolves from a splitting process beginning in the inner layers, extending outwardly, and culminating in central fovea detachment [10]. However, some studies have reported an alternative onset, where MRS begins in the outer plexiform layer of the central fovea and progresses outward from the foveal center [36].

Among patients with myopic MF, several factors correlate with improved postoperative visual outcomes: better preoperative visual acuity, shorter axial length, and successful reattachment of central fovea photoreceptors in eyes with central fovea detachment [37]. To mitigate the progression of MF to MH or even RD, surgical intervention is recommended upon the onset of symptoms such as decreased visual acuity or significant visual distortion. Eyes undergoing surgical intervention often present with poorer visual acuity compared to those receiving conservative treatment. Consequently, the decision to proceed with surgical intervention primarily depends on the patient’s visual symptoms and OCT features, including the stage of splitting, chamber height, and macular central fovea thickness [38]. Currently, no standardized clinical protocol exists for MF treatment. The mainstream surgical options include PPV, macular buckle, and posterior scleral reinforcement (PSR). However, there is ongoing debate regarding the necessity and efficacy of inner limiting membrane peeling and the use of gas tamponade in these procedures.

Research indicates that internal limiting membrane peeling (ILMP) effectively removes anterior vitreous traction and mitigates retinal stiffness, thereby facilitating retinal adaptation to posterior scleral staphyloma and preventing macular retinoschisis [39]. It also facilitates retinal elongation to conform to the posterior scleral staphyloma [40]. ILMP can stimulate the regeneration of Müller cells and the proliferation response of retinal glial cells, thereby aiding in the recovery of macular tissue [19]. However, this procedure can also damage Müller cells in the stripped area, crucial for the integrity of photoreceptor cells in the central macular fovea. Such damage may lead to complications like MHs, Müller cell dysfunction, and visual field defects [41, 42]. In cases of ultra-high myopia or MF due to posterior staphyloma along an extra-long axis, ILMP can exacerbate retinal thinning at the macular fovea, increasing the risk of MHs and RD [7]. The use of indocyanine green staining for ILMP also poses risks of toxicity and RPE atrophy [41]. Postoperative complications can include macular shift and nerve fiber layer depression [43].

Therefore, subsequent studies introduced fovea-sparing internal limiting membrane peeling (FSILMP) as an alternative, FSILMP was introduced as an alternative, showing improved anatomical repositioning rates of the macular central fovea and superior postoperative BCVA compared to ILMP. It also significantly reduces the risk of postoperative MHs. However, Russo et al. [44] found that up to 60% of FSILMP patients experienced thickening and crumpling of the remaining ILM 3 months post-surgery, potentially altering macular morphology and leading to decreased visual function. This complication may arise from inadequate proximity of the peeled area to the foveal center or incomplete tangential traction release due to residual posterior vitreous cortex on the retained ILM [44]. In 2016, Lee et al. [45] refined the FSILMP technique by limiting ILM retention to the central foveal area, using a 25-gauge high-speed cutter for precise ILM trimming. After 6 months of the surgery, no ILM proliferation, wrinkling, or MH formation was observed. However, accurately locating the true fovea during surgery is challenging, and inappropriate ILM retention may exacerbate MRS or MH development. Tao et al. [46] found that BCVA remained stable in patients with postoperative ILM crumpling over long-term follow-up, suggesting that the impact of ILM thickening and crumpling on long-term visual function requires further investigation.

Chen and Chen [47] also observed that patients who underwent ILM stripping in the preserved central fovea developed central fovea ERMs on the residual ILM after an average of 6 months. ERMs are nonvascularized fibroblastic membrane that proliferates on the inner surface of the retina. The remaining ILM is believed to act as a scaffold for fibroblast membrane proliferation, leading to secondary ERM formation. This process, characterized by inward contraction, results in central fovea aberration evident on OCT as well as significant visual impairment. Many patients subsequently require revision surgery to rectify the central fovea contour and improve visual acuity. A study involving 4 patients who underwent central fovea ERM and ILM removal surgery reported no statistically significant differences in foveal thickness and visual acuity postoperatively, yet both parameters exhibited notable improvement following an average follow-up of 5.8 months.

To enhance the precision of ILM peeling during vitreoretinal surgery, a new technique has been proposed that incorporates real-time examination in the supine position using iOCT [48]. iOCT enables the observation of microscopic damage during membrane stripping, which predominantly includes mechanical damage and vitreous hemorrhage resulting from the exposure and rupture of microvessels [49]. Furthermore, iOCT images assist surgeons in adjusting their peeling techniques and intensity in response to detected intraoperative microinjuries [31]. These images are also crucial for identifying and managing intraoperative microdamage or abnormalities, such as residual ERMs, ILM curls, nerve fiber layer irregularities, and cystic changes in the central fovea. This capability is particularly important for preventing complications like MHs or residual traction following successful ILM stripping [50]. In summary, iOCT holds significant clinical value in the treatment of patients with high myopia and myopic traction maculopathy, offering enhanced surgical precision and reduced risk of intraoperative complications.

Recent studies suggest that gas filling facilitates the reattachment of a split retina by exerting external forces to encourage the drainage of subretinal fluid. This process may also create a dry environment conducive to fluid reabsorption [51, 52]. However, contrasting evidence indicates no significant difference in postoperative BCVA, visual changes, or anatomical success between patients with and without gas filling. Notably, gas filling appears to expedite the resolution of macular splitting [53].

Meng et al. [52] observed that gas filling did not enhance resolution in patients with macular folds, and it potentially increased the risk of complications like MHs due to surface tension effects. There is a concern that intravitreal gas may direct subretinal fluid into the central fovea, a region with a relatively weaker retina, potentially leading to MH formation [54]. Given that the gas remains in the retina for only 1–2 months and retinoschisis repair demands a longer duration, some researchers argue against the necessity of gas filling in MF patients without MHs [53]. Conversely, gas filling has been shown to aid in the healing of minor macular splits, possibly incurred during ILM removal surgery. It may also reduce postoperative complications like low intraocular pressure and intraocular hemorrhage in highly myopic patients [55]. Clinicians currently adopt a personalized approach to gas filling, considering the patient’s specific condition. Jiang et al. [56] found that in mild to moderate MF cases, no significant difference was observed between C3F8 and air filling regarding BCVA improvement and retinal recovery. However, in severe MF cases, C3F8 demonstrated superior benefits in healing rates and reduction of splitting height. This advantage is attributed to the longer recovery time required for severe MF cases and the longer retention time of C3F8 compared to air. Consequently, the choice of gas fillers should be contingent on the severity of MF. Air is deemed adequate for patients with MF less than 400 μm, while C3F8 is recommended for those with MF greater than 400 μm. Currently, SF6 and C3F8 are the predominant inert gases used. SF6 offers benefits such as shorter filling time and lower incidence of cataract and glaucoma, whereas C3F8 is more effective in closing anatomical gaps [57].

Recent research posits that silicone oil (SO) should be considered a superior choice for intraocular tamponade in certain scenarios due to its potential to mitigate the reopening of MHs after the dissipation of gas. Additionally, SO has been documented to expedite the reabsorption of residual subretinal fluid [58]. The advantages of employing SO include a reduction in hyperopic shift, an extended duration of tamponade effect, enhanced promotion of MH closure, and diminished necessity for the patient to maintain a prone position postoperatively. Nonetheless, it is important to acknowledge that the utilization of SO as a tamponade agent necessitates an additional surgical intervention for removal. Moreover, SO is associated with an increased risk of postoperative complications, such as secondary glaucoma and potential retinal or optic disc atrophy. Consequently, evidence from some studies suggests that, particularly in cases of recurrent or initially untreated MHRD, intraocular gas remains an effective tamponade alternative [59].

While vitreoretinal surgery effectively addresses the internal tangential traction of the vitreous body on the retina, it does not counteract the external traction exerted by the sclera. Consequently, this can result in postoperative complications such as the persistence or recurrence of MHs, RD, or the formation of secondary MH [60]. Conversely, macular buckling (MB) can mitigate the outward traction of posterior scleral staphyloma by effectively shortening the axial length of the eye. Liu et al. [61] presented data suggesting that a sole MB procedure, without concurrent PPV, might suffice in managing eyes with MF absent of FTMH. Further research by Wu et al. [62] observed the formation of a DSM post-MB surgery in all subjects. Zhao et al. proposed that DSM might serve as a protective factor against the progression of myopic foveoschisis, attributing this to the inward bulging of the sclera at the central fovea in DSM, which reduces both the outward staphylomatic traction and the inward traction from preretinal pathologies [11, 17]. Comparative studies have indicated that highly myopic eyes with DSM exhibit greater myopia severity, longer axial lengths, increased subfoveal scleral thickness, and a reduced incidence of MF relative to eyes without DSM. Notably, these variations did not translate into significant differences in BCVA [18, 63].

In their evaluation of MB utilizing silicone sponge titanium explants, Zhao et al. [64] treated 28 eyes with MF and 21 eyes with FTMH accompanied by central fovea detachment. They achieved a retinal reattachment rate of 100%, with an MH closure rate of 79.16%, and noted significant improvement in BCVA across the cohort, alongside a mean AL reduction of 2.09 mm. Ripandelli’s investigation corroborated these findings, reporting retinal reattachment and MH closure rates of 93.3% post-MB surgery, contrasting with 73.3% and 36.3%, respectively, after PPV [65]. Alkabes and Mateo’s retrospective analysis further underscored the efficacy of MB over PPV in achieving higher success rates in retinal reattachment and MH closure, with no instances of retinal re-detachment in the MB group as opposed to a 21–50% re-detachment rate following PPV for persistent MH in MHRD cases [66].

Despite these promising outcomes, the application of macular band buckles is challenged by their lack of customization, as their universal designs may not accommodate the unique geometrical variations of all eyes, particularly in cases of posterior scleral staphyloma. In response, a novel approach has been proposed that leverages pattern recognition algorithms to generate precise three-dimensional (3D) models of ocular geometry from patient-specific computed tomography (CT) data. This model informs the fabrication of a tailored macular buckle using 3D printing with biocompatible polymers, such as polyether ether ketone (PEEK). The custom-fitted buckle is then positioned externally to the sclera, directly over the area of retinoschisis, and exerts targeted pressure to realign the retina anatomically (refer to the flowchart and simulation diagram in Fig. 3). While this technique is subject to ongoing refinement, it holds potential for highly accurate, individualized treatment, with significant implications for patient outcomes [67].

Postoperative complications associated with macular buckle surgery may manifest, including elevated intraocular pressure potentially attributable to the indentation from the buckle, as well as post-surgical swelling and inflammation of periorbital soft tissues [64]. Most patients report transient restrictions in ocular motility and diplopia during the initial postoperative phase, symptoms that typically subside within 6 months. This transient morbidity is likely related to edema of the extraocular muscles due to mechanical compression and inflammatory responses, along with an immunological reaction to the buckle implantation. Additionally, the volumetric prominence of the macular buckle may contribute to these symptoms. Considering the structural fragility in highly myopic eyes, where the choroid and retina are inherently thinner, the external pressure from the implant might exacerbate choroidal ischemia, culminating in a constrained atrophy of the RPE [68]. Future considerations might include the utilization of smaller buckle sizes to potentially mitigate the incidence and severity of complications such as postoperative ocular hypertension, choroidal hemorrhage, and restricted ocular movement [61].

PSR is designed to fortify the attenuated and ectatic scleral tissue, arrest progressive axial elongation, and remodel the posterior scleral contour. This procedure has demonstrated efficacy in mitigating outward retinal traction and facilitating the reapposition of the RPE to the neurosensory retina, especially in patients with myopic foveoschisis and posterior scleral staphyloma [69]. Moreover, PSR circumvents intraocular interventions, thereby reducing the risk of iatrogenic MHs often associated with PPV and membrane peeling [70]. Additionally, PSR has been reported to enhance macular blood flow and contribute to an increase in choroidal thickness [71]. A study documented a mean reduction in axial length of 2.46 ± 0.39 mm 1 week postoperatively, substantiating PSR’s efficacy in axial shortening. Incremental reattachment rates of MF were observed postoperatively at 1 week (8.3%), 3 months (16.7%), 6 months (50.0%), and 1 year (95.8%), delineating a progressive process of fluid resorption from the retinal schisis and MF reattachment. Concurrent with anatomical restoration, there was a significant improvement in BCVA, underscoring PSR’s role in anatomical and functional recovery by modulating ocular axial length, optimizing fundus circulation, and increasing choroidal thickness [72]. Despite the benefits, PSR surgery presents certain risks. The requisite exposure of the deep macular sclera poses a risk of intraoperative damage to the ophthalmic artery, potential compression of the optic nerve, and various postoperative complications. Conjunctival congestion is the most frequent complication, with other issues including diplopia from extraocular muscle restriction, transient ocular hypertension, and some patients experiencing short-term visual distortion related to retinal folding-induced axial shortening [73]. Notably, these early postoperative complications generally ameliorate within 6 months following the procedure [74]. While some enhanced and novel surgical techniques have demonstrated preliminary effectiveness, they are also associated with a range of complications. For instance, traditional PPV surgery has been implicated in postoperative complications in patients with high myopia. Research indicates that approximately 11% of these patients may develop fovea-centered macular atrophy following PPV, with the affected area progressively enlarging over time. This postoperative macular atrophy could potentially represent a novel complication linked to pathological myopia [75]. Consequently, the management of MF warrants further investigation to optimize treatment outcomes and mitigate associated risks.

MF is increasingly recognized as a prevalent complication among patients with high myopia and posterior scleral staphyloma. The condition arises from a confluence of factors that induce structural and functional disruptions within the macular retina, consequent to the bidirectional tractional forces. While patients may experience a prolonged period of stable visual acuity, progression to a MH or RD poses a substantial risk of severe visual impairment. Timely surgical intervention is thus critical. Currently, vitreoretinal surgery stands as the primary therapeutic approach for myopic foveoschisis, with MB and PSR being particularly beneficial in cases accompanied by posterior staphyloma. Emerging questions persist regarding the necessity and technique of inner limiting membrane removal during these surgeries, as well as the decision-making process related to the use of intraocular tamponades. Future studies are imperative to refine surgical strategies, optimize patient outcomes, and determine the most efficacious practices tailored to the individual pathophysiological characteristics of myopic foveoschisis.

The authors have no conflicts of interest to declare.

The work was supported by grants from the National Natural Science Foundation (81970836) and the Natural Foundation Project of Science and Technology Department of Jilin Province (20200201570JC).

He Chen (co-first author): writing – original draft preparation. Jinling Fu (corresponding author): writing – review and editing. Lufei Wang (corresponding author): supervision. Xuan Liu (co-second author): visualization. Xuebin Zhou (co-third author): software.