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Visual Fields Rene Understanding of Diabetic Retinopathy


Progression

Diabetic retinopathy is a leading cause of irreversible blindness in developed countries.

Visual eld sensitivity is the ability to detect a dim white spot presented at various locations on a white
background and has important functional implications: It is important for mobility, driving, and other
important tasks of daily living. It has been shown that patients with good visual acuity (e.g., 20/20) but
poor visual elds have diminished quality of life

The study by Hellgren et al. suggests that diabetes has a direct and pronounced effect on the neural
retina, and this impact may be independent from the microvascular lesions that are typically used to
classify disease severity. It is notable that deterioration of the neural retina may occur for years
without a clinically detectable change in the microvasculature using traditional imaging tools. It also
may be the case that neural retinal changes precede microvascular changes or that we currently lack
the advanced imaging technology necessary to detect subclinical changes in the microvasculature.
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Diabetic Retinopathy An Update on Pathophysiology,
Classification, Investigation and Treatment

Neurodegeneration in the retina As well as the changes already described, structural and functional
alterations can injure certain non-vascular cells.[38] It is believed that neurodegeneration of retinal
neurons and glia may even precede microaneurysm development.[97]

Optical Coherence Tomography (OCT)

Optical Coherence Tomography is a non-invasive imaging technique which is non-contact and


facilitates high resolution cross-sectional imaging of the anterior segment, vitreous, retina and optic
nerve head. Rather than the sound waves of B-scan ultrasonography, OCT uses light interferometry
(near-infrared) to interpret the interference patterns of wave superposition. OCT is useful is very
sensitive in detecting change in macula thickness and therefore useful in the diagnosis of diabetic
macula oedema. It is also able to identify the loss of ganglion cells in the retina, which precedes
vascular changes. Because OCT gives a quantitative measure of retinal thickness it is critical in
monitoring retinal thickness in response to treatment e.g. Macula laser or Anti-VEGF agents. Different
tissue reflectivities are depicted by different colours; red denotes high reflectivity, green-yellow
intermediate reflectivity and blue-black low reflectivity. In addition to numerical measures of retinal
thickness a topographical map is created which is colour coded according to thickness.
Review neuroinflammatory responses in diabetic retinopathy
Diabetic retinopathy PPP
ICO Guidelines
Epidemiology of Diabetic Retinopathy In many countries, DR is the most frequent cause of preventable
blindness in working-aged adults. A Global metaanalysis study reported that 1 in 3 (34.6%) had any
form of DR in the US, Australia, Europe and Asia. It is also noted that 1 in 10 (10.2%) had vision
threatening DR (VTDR) i.e., PDR and/or DME. In the 2010 world diabetes population, more than 92
million adults had any form of DR, 17 million had PDR, 20 million had DME and 28 million had VTDR.

Pathophysiology and Pathogenesis of Diabetic Retinopathy


Xu, Heping, Curtis, Timothy, Stitt, Alan. Pathophysiology and Pathogenesis of Diabetic
Retinopathy [internet]. 2014 Aug 13; Diapedia 7104343513 rev. no. 14. Available
from:

Neurodegeneration & Glial dysfunction

As outlined above, dysfunction and degeneration of the retinal vasculature is a hallmark of diabetic
retinopathy. However, in recent years there has been strong clinical and pre-clinical evidence to
indicate that retinal neuronal degeneration also occurs as diabetes progresses[23].

Recent research has been conducted in rodents at various stages of diabetes and they indicate a range
of neural retina abnormalities ranging from neurotransmitter changes to overt loss of retinal ganglion
cells, amacrine cells or even photoreceptors[24]. Glial cells interface closely with the retinal neurons and
in particular the Mller glia over-produce glutamate which may contribute to excitotoxicity and
eventual depletion of retinal neurons.

In summary, the scientific literature strongly suggests that neural and glial abnormalities are an
important factor in diabetic retinopathy. There is a highly complex interplay between neurons, glia and
vascular components of the retina and diabetes is likely to profoundly alter the function of these cell
interactions. As this evidence accumulates, diabetic retinopathy may become viewed more accurately
as a disease of the neuro-vascular unit, resulting in degenerative pathology of many key cells in the
retina, each of which is vital for normal function of this delicate tissue.

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