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Cryosurgery of the retina
Published in A Peyman MD Gholam, A Meffert MD Stephen, D Conway MD FACS Mandi, Chiasson Trisha, Vitreoretinal Surgical Techniques, 2019
Ingrid Kreissig, Harvey A Lincoff
It should be pointed out that the cryosurgical application causes a deeper and more profound necrosis of tissue in the center of the lesion than in the periphery.19 Remodeling with villous proliferation is limited to those areas in the adhesion in which RPE has regenerated and recovered Bruch’s membrane. In the centers of moderate cryopexy lesions, there are sometimes areas in which RPE fails to recover Bruch’s membrane before Müller cell processes come into contact with it. In these areas, Müller cell processes secrete a basement membrane and adhere to it with hemidesmosomes.24 At some points, the surface of Bruch’s membrane is penetrated by processes of Müller cells; these processes distribute in the collagen lamellae of the membrane. There is no evidence of late remodeling in these areas.
The uveal tract
Published in Mary E. Shaw, Agnes Lee, Ophthalmic Nursing, 2018
The choroid lies between the sclera and retina and extends from the optic nerve forward to the ora serrata where it joins the ciliary body. The choroid is composed of four layers: The suprachoroid, containing pigment cells, elastic tissue and collagen.The vascular layer, comprising large and small blood vessels, with pigment cells contained in the stroma surrounding the vessels; the large vessels are mainly veins.The choriocapillaries, comprising fenestrated capillary vessels.Bruch’s membrane, which is a barrier with fenestrations which allow nutrients through to the underlying retina; it is also a supportive membrane.
Ophthalmology
Published in Shibley Rahman, Avinash Sharma, A Complete MRCP(UK) Parts 1 and 2 Written Examination Revision Guide, 2018
Shibley Rahman, Avinash Sharma
Macular degeneration is the most common cause of blindness in the UK. Degeneration of the central retina (macula) is the key feature with changes usually bilateral. Two forms of macular degeneration are seen: Dry macular degeneration: characterised by drusen – yellow round spots in Bruch’s membrane.Wet (exudative, neovascular) macular degeneration: characterised by choroidal neovascularisation. Leakage of serous fluid and blood can subsequently result in a rapid loss of vision. Carries worst prognosis.
Retinal findings in glomerulonephritis
Published in Clinical and Experimental Optometry, 2022
Heather G Mack, Deborah J Colville, Phillip Harraka, Judith Anne Savige, Alessandro Invernizzi, Samantha Fraser-Bell
Whether complement dysfunction in retinal disease reflects local ocular complement abnormalities, abnormal complement formed in the liver and deposited in the eye, or a combination, is unclear. Large complement molecules are prevented from entering the retina by the blood-retina barriers. The inner blood-retina barrier consists of tight junctions between the non-fenestrated retinal capillary endothelial cells, surrounded by end-feet of Müller glial cells and astrocytes which secrete factors enhancing or disrupting the integrity of capillary endothelial cells. The outer blood-retina barrier is controlled by the RPE and is composed of tight junctions between the RPE cells. Bruch’s membrane, the semipermeable membrane between the RPE and the choriocapillaris, best thought of as a vessel wall between the RPE and choriocapillary basal laminae, provides a further barrier for the diffusion of molecules from the choroidal circulation into the retina.22
Heinrich Müller (1820-1864) and the entoptic discovery of the site in the retina where vision is initiated
Published in Journal of the History of the Neurosciences, 2022
John S. Werner, Iwona Gorczynska, Lothar Spillmann
Despite his short career, Müller made a number of landmark discoveries about the histology and anatomy of the visual system, thanks, in part, to enucleated eyeballs provided by Albrecht von Graefe. His 1851 paper described the red coloration of the visual pigment, now known to be rhodopsin (Müller 1851). This was before the celebrated work of Boll (1876) and Kühne (1877), who credited him (Hubbard 1977). Additionally, in his 1851 paper, Müller described neuroglia in the retina now known as Müller cells (Müller 1851). He also published descriptions of the retinal vasculature, and Figure 2.1 shows an example in which he flattened a human cadaver retina and preserved it so that many of the finest capillaries could be traced, a work completed after his death by Becker (1881). Müller described muscles in the orbit and lids, and a double fovea in some species of birds (e.g., hawks). His interests in the pathology of the eye led to investigations of subcapsular cataract, pigmentary changes in retinitis pigmentosa, and age-related changes in Bruch’s membrane now essential to our understanding of age-related macular degeneration. Müller’s collected papers are contained in an anthology assembled by Becker (1872).
Temporal retinal thinning and increased foveal avascular zone blood vessel density in alport syndrome: a case report
Published in Clinical and Experimental Optometry, 2021
Christopher J Borgman, Jason Duncan, Mario Martinez
Temporal retinal thinning (81% cases) is the most common ocular finding in X-linked Alport syndrome (Table 1).1,3,5–7,9 The temporal macula is reportedly 59 microns thinner on average than the nasal macula in Alport syndrome patients.3 It is currently unknown how or when this temporal retinal thinning specifically occurs in Alport syndrome, but is likely related to the underlying collagen IV abnormality associated with X-linked Alport syndrome.3,6 Previous authors have speculated that the retinal thinning may occur during postnatal development with abnormal vitreoretinal tractional forces, and/or abnormal Muller cell adhesion in these areas.3,6 The temporal retinal thinning predominantly affects the superficial layers of the retina, but does not appear to have a large impact on vision in general.5–7,9,10 Newer studies also suggest the involvement of Bruch’s membrane and retinal pigmented epithelium due to the presence of type IV collagen networks in these layers.5,10