From the Department of Ophthalmology, Gunma University, School of Medicine, Maebashi, Japan.
The authors have no financial or proprietary interest in the materials presented herein.
Address correspondence to Hirotaka Itakura, MD, Department of Ophthalmology, Gunma University School of Medicine, 3-39-15 Showa-machi, Maebashi, Gunma, 371-8511, Japan. E-mail: firstname.lastname@example.org
A posterior precortical vitreous pocket (PPVP) is a physiologic liquefied lacuna anterior to the macular area, the posterior wall of which is a thin layer of vitreous pocket.1 PPVP was first reported in autopsy eyes in which the vitreous gel was stained with fluorescein. The PPVP was confirmed recently during triamcinolone-assisted vitrectomy2 and by spectral-domain optical coherence tomography OCT (SD-OCT).3–5 The premacular vitreous cortex, or the posterior wall of the PPVP, gradually thickens with age and the incidence of perifoveal posterior vitreous detachment (PVD) increases in elderly individuals.5 The perifoveal PVD may cause various vitreoretinal interface diseases such as macular holes and vitreomacular traction syndrome.3 We also observed that the thickened vitreous cortex occasionally has a lamellar structure in elderly individuals, suggesting possible splitting of the vitreous cortex.
We encountered four eyes with vitreomacular traction syndrome in the outpatient clinic in which SD-OCT showed splitting of the posterior vitreous cortex.
Design and Methods
We retrospectively reviewed the medical records of 35 cases of vitreomacular traction syndrome diagnosed using SD-OCT between June 2007 and February 2011. The current report includes 4 eyes of 4 patients with vitreomacular traction syndrome who presented with possible splitting of the vitreous cortex on SD-OCT (Cirrus OCT; Carl Zeiss Meditec, Inc., Dublin, CA). The four eyes were examined by SD-OCT, with 6-mm horizontal or 6-mm vertical scans obtained through the fovea. Biomicroscopy using a Superfield Lens (Volk Optical Inc., Mentor, OH) showed no PVD.
The study was conducted according to the tenets of the Declaration of Helsinki. All individuals provided informed consent to the examination following a detailed explanation of the study.
A 72-year-old man (case 1) presented with floaters and metamorphopsia in the right eye and a 68-year-old man (case 2) presented with metamorphopsia in the right eye. The best-corrected visual acuity was 20/20 in both cases. SD-OCT showed a perifoveal PVD, the vitreous cortex separated at the perifovea, and the posterior lamella adhered to the retina, which induced retinal elevation at the perifovea and surface wrinkling nasal to the fovea (Fig. 1) in both cases.
Figure 1. Spectral-domain optical coherence tomography of a 72-year-old man (case 1) shows a perifoveal posterior vitreous detachment. The vitreous cortex is separated in the perifoveal area and its posterior lamella adheres to the retina, which induces retinal elevation at the perifovea and surface wrinkling nasal to the fovea (white arrow). The fovea is not elevated and the junction between the photoreceptor inner and outer segments is intact. The fundus is scanned in a 6.0-mm line along the horizontal axis through the fovea (yellow arrow).
A 61-year-old man (case 3) presented with metamorphopsia and decreased vision in the right eye. The best-corrected visual acuity was 20/100. SD-OCT showed a perifoveal PVD with foveal detachment (Fig. 2). The vitreous cortex was split at the perifoveal area. The detached fovea showed cystoid macular edema.
Figure 2. Spectral-domain optical coherence tomography of a 61-year-old man (case 2) shows a perifoveal posterior vitreous detachment with a foveal detachment. The vitreous cortex is split at the perifoveal area (white arrow). The detached fovea has cystoid macular edema. The blurred reflex in the vitreous cavity is an artifact (*). The fundus is scanned in a 6.0-mm line along the vertical or horizontal axis through the fovea (arrow).
An 82-year-old woman (case 4) presented with decreased vision in the left eye. The best-corrected visual acuity was 20/32. SD-OCT showed a perifoveal PVD with a foveal detachment. The vitreous cortex was split at the foveal area and the detached fovea had cystoid macular edema.
SD-OCT showed splitting of the vitreous cortex in 4 eyes of 4 cases with vitreomacular traction syndrome. The vitreous cortex split into two lamellae in the perifoveal area in two eyes and at the fovea in one eye.
We reported that the lamellar structure of the vitreous cortex and splitting of the vitreous cortex are seen in elderly patients.5 We found 4 eyes with splitting of the vitreous cortex among the 35 eyes with vitreomacular traction syndrome.
Yamashita et al. has supported similar findings during surgery when posterior vitreous cortex can split into lamellae, leaving the outermost layer of the posterior vitreous cortex attached to the macula in idiopathic epiretinal membranes.6 Those authors reported three patterns of intraoperative characteristics of the posterior vitreous cortex during triamcinolone-assisted vitrectomy in 15 eyes with an epiretinal membrane without a PVD. The first pattern was a round defect in the vitreous cortex after surgical PVD, leaving an epiretinal membrane on the macula, in 7 (47%) of the 15 eyes. This suggested that the posterior wall of the PPVP or premacular vitreous cortex is a component of the epiretinal membrane. The oval defect of the premacular vitreous cortex is seen frequently in eyes with an epiretinal membrane with a PVD. The second pattern was a complete detachment of the vitreous cortex along with the epiretinal membrane seen in 3 eyes (20%). This also suggested that the posterior wall of the PPVP was the origin of the epiretinal membrane. It has been reported that epiretinal membranes occasionally resolve along with PVDs. The third pattern was an epiretinal membrane on the macula after separation of an intact posterior vitreous cortex that was seen in 5 eyes (33%). There are two possible explanations for the third pattern, one being separation of vitreous cortex in the posterior wall of the PPVP and the other that the epiretinal membrane is a cellular membrane arising through the internal limiting membrane with no hyaloid component.
An immunohistochemical study showed the lamellar structure of the vitreous cortex.7 We reported that the precursor of the vitreous collagen is secreted persistently into the vitreous cavity even after vitreous surgery in adult human eyes.8 The lamellar structure of the vitreous cortex may develop as a result of persistent production of vitreous collagen from the retina.
Gupta et al.7 reported that vitreoschisis was detected in half of their eyes with macular hole and macular pucker. It suggested that anomalous PVD with strong vitreomacular adhesion may be pathogenic in vitreomacular diseases.
SD-OCT confirmed the splitting of the vitreous cortex in vitreomacular traction syndrome. The lamellar structure of the vitreous cortex in elderly patients may underlie this phenomenon.
- Kishi S, Shimizu K. Posterior precortical vitreous pocket. Arch Ophthalmol. 1990;108:979–982.
- Fine HF, Spaide RF. Visualization of the posterior precortical vitreous pocket in vivo with triamcinolone. Arch Ophthalmol. 2006;124:1663.
- Johnson MW. Perifoveal vitreous detachment and its macular complications. Trans Am Ophthalmol Soc. 2005;103:537–567.
- Mojana F, Kozak I, Oster SF, et al. Observations by spectral-domain optical coherence tomography combined with simultaneous scanning laser ophthalmoscopy: imaging of the vitreous. Am J Ophthalmol. 2010;149:641–650.
- Itakura H, Kishi S. Aging changes of vitreomacular interface. Retina. 2011;31:1400–1404.
- Yamashita T, Uemura A, Sakamoto T. Intraoperative characteristics of the posterior vitreous cortex in patients with epiretinal membrane. Graefes Arch Clin Exp Ophthalmol. 2008;246:333–337.
- Gupta P, Yee KM, Garcia P, et al. Vitreoschisis in macular diseases. Br J Ophthalmol. 2011;95:376–380.
- Itakura H, Kishi S, Kotajima N, Murakami M. Vitreous collagen metabolism before and after vitrectomy. Graefes Arch Clin Exp Ophthalmol. 2005;243:994–998.