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Understanding vitreomacular interface diseases is key to treatment.
With the development of optical coherence tomography (OCT), subtle changes in the posterior vitreous can be observed that are not clearly visible by slit lamp biomicroscopy. With the advent of swept-source OCT (SS-OCT) technology in particular, variations in normal changes can now be visualised, as well as those associated with ageing.
In most normal eyes, the premacular lacuna and connected Cloquet’s canal can be clearly detected by SS-OCT (Figure 1). However, these structures become less noticeable with advancing patient age. The contours of the premacular lacuna collapse, and the liquefaction of the vitreous gel progresses.
In cases in which the premacular lacuna and Cloquet’s canal are not visible (Figure 2) and in which advanced vitreous liquefaction is present, a presumed bursa premacularis/posterior pre-cortical vitreous pocket (PPVP) appears (Figure 3).
Occasionally, the premacular lacuna and bursa fuse into a large empty space (Figure 4, upper right; Figure 5, right).
Differentiation of the premacular lacuna and the bursa premacularis/PPVP is important. Early studies found that the bursa premacularis/PPVP is a liquefied space with a relatively large volume, and not a thin space like the premacular lacuna.1,2
In usual OCT examinations, the depth is emphasised (Figure 1, top) and the premacular lacuna looks relatively large. However, when viewing the premacular lacuna with vertical and horizontal scales on a 1:1 scale in young patients (Figure 1, bottom), the premacular lacuna is almost the same depth as the thickness of the retina.
The premacular lacuna seems to correspond to a sub-bursal space, referred to in one in vivo slit lamp microscopy study and later as an artefact.3 However, it is my opinion that the premacular lacuna corresponds to a sub-bursal space.
Posterior vitreous detachments
Details of the early phase of age-related posterior vitreous detachments (PVDs) were previously unknown because they were not visible by biomicroscopy, however, SS-OCT has furthered the understanding of these detachments.
Age-related PVD progression begins from the state of no PVD to the vicinity of the outer periphery of the macula, as seen in the OCT image on the upper left to lower left of Figure 4.4 The PVD progresses throughout the posterior pole, but it is relatively rare for the condition to progress without showing an oval defect in the detached posterior vitreous cortex (Figure 4, upper right).
In many cases, the oval defect in the posterior vitreous cortex forms as shown in the middle or lower right, and the thin posterior vitreous cortex remains on the macular retina. There are two types of shallow PVD with an oval defect in the posterior vitreous cortex: one with vitreous gel attachment to the macula through the premacular oval defect of the posterior vitreous cortex (Figure 4, middle right),5,6 and one with no vitreous gel attachment to the macula (Figure 4, bottom right).
The condition of vitreous attachment through the oval defect in the posterior vitreous cortex may be experienced during creation of a PVD during vitreous surgery. This type of PVD is thought to provide protection for the fovea, where the retina is thin and fragile. The failure to make such a circular defect in the posterior vitreous cortex may induce the development of macular holes in some cases (Figure 5).
The structure that was defined as a bursa has many variations in ageing. When the bursa fuses with the premacular lacuna/ sub-bursal premacular space, it appears as a large empty space. There are some variations in PVDs starting in the posterior pole, but some of them are related to macular holes and epiretinal membranes, so detailed observation is indispensable.
Although these descriptions are based on my personal experience and opinion, I hope they increase clinicians’ understanding of vitreomacular interface diseases.