Progression of an Acquired Vitelliform Lesion to a Full-Thickness Macular Hole Documented by Eye-Tracked Spectral-Domain Optical Coherence Tomography

Natural course of adult-onset vitelliform lesions in eyes with and without comorbid subretinal drusenoid deposits

“…However, the numbers involved are small and caution should be made with reference to this incidence. In contrast to idiopathic FTMH, where vitreomacular traction (VMT) is the primary aetiology, SDOCT studies suggest, in the setting of AVL, progressive retinal thinning results in development of a macular hole [16]. In our study, both patients had attached posterior hyaloid with visible vitreomacular adhesion.…”

“…Full thickness macular holes (FTMH) have previously been reported as infrequent complications of juvenile [15] and adult-onset vitelliform macular disease [16]. Despite their rarity, they remain an important complication, requiring potential surgery, adding morbidity in subjects in whom they occur.…”

Macular Hole–related Retinal Detachment Complicating Autosomal Recessive Bestrophinopathy: Clinical Features, Multimodal Imaging, and Surgical Outcome

“…We believe that the MH found in our patient was a complication to the retinoschisis seen in the outer nuclear layer and inner nuclear layer which was more extensive in the same eye rather than progressive retinal atrophy. Progressive retinal atrophy was proposed as a probable cause for the development of macular hole in patients with best vitelliform macular dystrophy; 8 however, being a 3-year-old patient, progressive retinal atrophy could not be the cause of the hole formation in young age. Absence of subretinal vitelliform material in the right eye is thought to be due to its egress through the hole to the vitreous cavity which appeared as hyperreflective materials on the surface of the retina by OCT.…”

Spontaneous Closure of the Macular Hole in a Patient with Acquired Vitelliform Lesion

“…However, no studies have reported spontaneous closure of MH, as in the present case. Furthermore, it should be noted that the study by Goldberg and Freund [13] was the only previous study reporting a case of AVL associated with MH.…”

“…Arnold et al [12] examined the lesions with OCT, and reported that the disappearance of photoreceptor cells in the fovea prior to the onset of MH and subsequent thinning of the inner layer of the retina led to the formation of the MH. Goldberg and Freund [13] suggested a similar pathogenic mechanism; however, considering the presence of MH in patients without epiretinal membrane or retinal-vitreous body adhesions, they reported that retinal vitreous traction was less involved in the development of MH.…”