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Query: UMLS:C0851184 (thinning)
 11,252 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Previous studies have attributed changes in the retinal surface over or adjacent to large superficial retinal vessels to a variety of conditions, the most common being 'anomalous vitreoretinal attachments.' The fundamental nature of the lesions and their pathogenesis, however, has remained controversial. The present study was undertaken to categorize the ultrastructural alterations of the vitreoretinal juncture over retinal vessels in the posterior fundus of man, and to clarify the relationship of these fundamental changes to clinically significant lesions in this region. Results show no difference in vitreoretinal, or more specifically vitreolaminar attachments over vessels when compared with adjacent regions. The cause of the more significant anomalies, notably surface breaks and their sequelae, is apparently multifactorial and related to a sequence of events. Initially three events predispose to or cause small surface breaks: developmental thinning of the inner limiting lamina; subsurface retinal degeneration; and transmigrating macrophages. These small surface breaks, when complicated by vitreous incarceration or by simple epiretinal membrane formation, can during posterior vitreous detachment cause peeling of the retinal surface, and the resulting large surface breaks may in turn provoke more complex proliferative lesions of the vitreoretinal juncture.
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PMID:Vitreoretinal juncture over retinal vessels. 30 81

We identified a group of 93 patients (102 eyes) with involutional macular thinning which is a condition that predisposes the affected eyes to developing idiopathic macular holes. The fovea in these patients shows specific architectural changes that can be identified on ophthalmoscopy. On follow-up (mean, 50 months), 26 eyes (27%) developed a macular hole compared to 0% in normal fellow eyes (P less than 0.00001). Patients with pigment epithelial window defects on fluorescein angiography (12 of 15 eyes or 80%), or with no posterior vitreous detachment (15 of 34 eyes or 44%) had the highest risk of developing macular holes. There were seven eyes with involutional macular thinning, pigment epithelial window defects on fluorescein angiography and no posterior vitreous detachment; six (86%) developed a macular hole. Macular degeneration, estrogen supplements, cystoid changes (with normal fluorescein angiography), and poor visual acuity did not increase risk. We present a theory for the pathogenesis of idiopathic macular holes.
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PMID:Involutional macular thinning. A pre-macular hole condition. 395 21