Lamellar Macular Holes; Pathophysiology, Classification, Clinic, Diagnosis, and Treatment

Lamellar macular hole (LMH), first described as a macular lesion developing after the opening of the central cyst in an eye with cystoid macular edema, has been used to define an aborted stage in full-thickness macular hole (MH) development. Abnormal posterior vitreous detachment associated with contraction of vitreous cortex plays a role in its pathophysiology. As a result of foveal traction of the attached and contracted macular vitreous cortex, splitting of the inner and outer retinal layers is observed. Contraction of the frequently accompanying epiretinal membrane also has an effect on the development of LMHs. Classified as tractional, degenerative, and mixed types, LMHs are seen as reddish, round, oval or lobulated lamellar defects at the fovea with the fundoscopic examination. In the differential diagnosis, it can be mistaken with MHs, and pseudoholes. Its diagnosis is best made with optic coherence tomography (OCT) examination. The diagnostic criteria with OCT are, defects in inner retinal layers with irregular foveal contour, thinning of the base of the fovea, partial-thickness MH with preservation of photoreceptors, and intraretinal splitting. Epiretinal proliferation is seen in most of the eyes. A thick, homogenous layer consisting of unusual material on the epiretinal surface has been defined as LMH-associated epiretinal proliferation by OCT. Persistent vitreopapillary adhesion is demonstrated in one-third of eyes. Patients with LMHs stay stable with minimal complaints about a long time, and surgery is not needed in most of them. When the patients have serious visual complaints, or a decrease in visual acuity (VA) is noted, surgery is indicated. The anatomical and functional success rate is high with pars plana vitrectomy, peeling of ERM, and ILM, air/gas endotamponade. Patient selection is important. Low preoperative VA, disruption at the junction of inner-outer photoreceptor layers, and foveal thinning are poor prognostic indicators. Further studies are warranted to determine which patients will benefit from surgery.

Retinal Changes Induced by Epiretinal Tangential Forces

Two kinds of forces are active in vitreoretinal traction diseases: tangential and anterior-posterior forces. However, tangential forces are less characterized and classified in literature compared to the anterior-posterior ones. Tangential epiretinal forces are mainly due to anomalous posterior vitreous detachment (PVD), vitreoschisis, vitreopapillary adhesion (VPA), and epiretinal membranes (ERMs). Anomalous PVD plays a key role in the formation of the tangential vectorial forces on the retinal surface as consequence of gel liquefaction (synchysis) without sufficient and fast vitreous dehiscence at the vitreoretinal interface. The anomalous and persistent adherence of the posterior hyaloid to the retina can lead to vitreomacular/vitreopapillary adhesion or to a formation of avascular fibrocellular tissue (ERM) resulting from the proliferation and transdifferentiation of hyalocytes resident in the cortical vitreous remnants after vitreoschisis. The right interpretation of the forces involved in the epiretinal tangential tractions helps in a better definition of diagnosis, progression, prognosis, and surgical outcomes of vitreomacular interfaces.