Neuroinflammatory responses in diabetic retinopathy

Table 1 Clinicopathologic and bioelectrical characteristics of retina in diabetes

Morphological features	Clinicopathologic features	Bioelectrical features	Model	References
No apparent retinopathy	–	mfERG: implicit times prolong	Human	[36, 37]
No apparent retinopathy	–	VEP: P100 implicit time delay	Human	[36, 37]
Microaneurysma	Loss of pericytes		Rat	[5]
Hard exudative	Degeneration of photoreceptor and neuronal elements in the outer plexiform layer		Human	[31]
Cotton-wool spot	Microinfarct of the nerve fiber layer	PERG: amplitude reduce	Human	[25, 32]
IRMA	Shunt vessels and re-vascularize the hypoxic neuropile		Human	[32]
Neovascularization	Disrupt local basement membrane	OPs amplitude is correlated with the grade of DR	Human	[28, 39]
Hemorrhage			Human	[38]
Dot-and-blot	Hemorrhage in the inner nuclear layer
Flame-shaped	Hemorrhage in the nerve fiber layer
Globular	Hemorrhage in the middle neural retinal layer
Confluent	Hemorrhage in all neural retinal layers
Massive	Hemorrhage break through internal limiting membrane
Retina detachment	Shrinkage of the fibroglial component
Fibrovascular membrane	Composed of blood vessels, fibrous, glial matrix tissue, fibroblasts, and glial cells
DME	Intracellular fluid collections in Müller cells, extracellular fluid in the outer plexiform and the inner nuclear layers	mfERG: P1 latency decrease	Human	[41, 44, 45]
DME		Macular OPs: reduced	Human	[41, 44, 45]
Diabetic optic nerve	Vascular leakage and axonal edema in and around the optic nerve head	Increased VEP latency	Rat	[26, 47]

ISSN: 1742-2094