Multimodal retinal imaging of diabetic macular edema

toward new paradigms of pathophysiology

Edoardo Midena, Silvia Bini

Research output: Contribution to journalArticle

4 Citations (Scopus)

Abstract

The pathophysiology of diabetic macular edema (DME) is multifactorial and partly still unknown. An increasing body of evidence suggests that neurodegeneration and retinal glial cells activation occur even before the earliest clinical manifestation of diabetic retinal vasculopathy. Nowadays, new non-invasive techniques are available to assess and characterize DME, not only in a quantitative perspective, but also making it possible to understand and quantify the pathogenic processes sustaining fluid accumulation. Optical coherence tomography (OCT) allows documenting not only parameters such as macular volume, central and sectorial retinal thickness, fluid localization, and integrity of retinal layers, but also new still poorly investigated reflectivity aspects. Hyperreflective intraretinal spots (HRS) have been detected on OCT scans through the retinal layers, with a presumptive migration pattern towards the external layers during the occurrence of diabetic retinopathy and DME. These HRS have been hypothesised to represent an in-vivo marker of microglial activation. Autofluorescence of the fundus (FAF) also offers a non-invasive imaging technique of DME. The area of increased FAF correlates with the presence of intraretinal fluid and probably retinal glial activation. Microperimetry allows the measurement of retinal sensitivity by testing specific selected retinal areas. Some studies have shown that increased macular FAF in DME correlates better with visual function assessed with microperimetry than with visual acuity, showing that new imaging and functional techniques may help to elucidate DME pathogenesis and to target therapeutical strategies.

Original languageEnglish
Pages (from-to)1661-1668
Number of pages8
JournalGraefe's Archive for Clinical and Experimental Ophthalmology
Volume254
Issue number9
DOIs
Publication statusPublished - 2016

Fingerprint

Multimodal Imaging
Macular Edema
Optical Coherence Tomography
Neuroglia
Diabetic Retinopathy
Visual Acuity

Keywords

  • Autofluorescence
  • Diabetic macular edema
  • En-face optical coherence tomography
  • Microperimetry
  • Optical coherence tomography

ASJC Scopus subject areas

  • Ophthalmology
  • Sensory Systems
  • Cellular and Molecular Neuroscience

Cite this

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abstract = "The pathophysiology of diabetic macular edema (DME) is multifactorial and partly still unknown. An increasing body of evidence suggests that neurodegeneration and retinal glial cells activation occur even before the earliest clinical manifestation of diabetic retinal vasculopathy. Nowadays, new non-invasive techniques are available to assess and characterize DME, not only in a quantitative perspective, but also making it possible to understand and quantify the pathogenic processes sustaining fluid accumulation. Optical coherence tomography (OCT) allows documenting not only parameters such as macular volume, central and sectorial retinal thickness, fluid localization, and integrity of retinal layers, but also new still poorly investigated reflectivity aspects. Hyperreflective intraretinal spots (HRS) have been detected on OCT scans through the retinal layers, with a presumptive migration pattern towards the external layers during the occurrence of diabetic retinopathy and DME. These HRS have been hypothesised to represent an in-vivo marker of microglial activation. Autofluorescence of the fundus (FAF) also offers a non-invasive imaging technique of DME. The area of increased FAF correlates with the presence of intraretinal fluid and probably retinal glial activation. Microperimetry allows the measurement of retinal sensitivity by testing specific selected retinal areas. Some studies have shown that increased macular FAF in DME correlates better with visual function assessed with microperimetry than with visual acuity, showing that new imaging and functional techniques may help to elucidate DME pathogenesis and to target therapeutical strategies.",
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