OCT-Angiography in Neuro-Ophthalmology

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OCT has become one of the most important imaging modalities in ophthalmology, since its invention in 1990's. OCT is a noninvasive technique based on the principle of low-coherence interferometry, which generates high-resolution, cross-sectional images from backscattered light, and helps to assess the structural changes in different retinal diseases, low contrast between capillaries and retinal tissue, hinders OCT to be used to monitor vascular changes.

Fluorescein angiography (FA) and indocyanine green angiography (ICGA) are conventionally used for qualitative clinical assessment of retinal and choroidal circulations,but both the techniques require intravenous injection of contrast agents, which is time-consuming and can have potentially serious side effects. FA and ICGA provide two-dimensional (2D) images of ocular circulations, and do not give information regarding the depth of involvement. OCT- Angiography is a non invasive method which gives a three dimensional visualisation of blood vessels present at different levels.


OCTA identifies blood vessels by detecting blood flow-induced change in the OCT reflectance signal. Flowing red blood cells causes more variation in the OCT signal between repeated scans than static tissue. Multiple approaches have been described for quantifying this change through assessment of the intensity and phase of the OCT signal. Intensity-based technique was later introduced to visualize retinal and choroidal microvasculature called split-spectrum amplitude-decorrelation angiography (SSADA). The SSADA algorithm divides the OCT spectrum into narrower bands and then averages the intensity decorrelation detected in each band. This method significantly improved the signal-to-noise ratio. OCT-A employs two methods for motion detection: amplitude decorrelation or phase variance. The former detects differences in amplitude between two different OCT B-scans. Phase variance is related to the emitted light wave properties, and the variation of phase when it intercepts moving objects. In order to improve visualization and to reduce background noise from normal small eye movements, two averaging methods - split spectrum amplitude decorrelation technique and volume averaging - were developed. These OCT-A algorithms produce an image (3mm2 to 12mm2) that is segmented, into four zones: the superficial retinal plexus, the deep retinal plexus, the outer retina and the choriocapillaries.

Indications of OCT-A in neuro-ophthalmology

  • Multiple Sclerosis
  • Papillitis
  • Papilledema
  • Non arteritic anterior ischemic optic neuropathy (NAION)
  • Anterior arteritic ischemic optic neuropathy (AAION)
  • Hereditary optic neuropathy (Leber Hereditary Optic Neuropathy)
  • Glaucoma

Multiple Sclerosis

Nerve fiber layer( NFL) loss is a well-documented OCT parameter in patients of multiple sclerosis (MS) with or without optic neuritis [1] and is also predictive of the clinical visual outcome.OCTA measurements in MS patients can help to detect retinal vascular impairment. Wang et al. have reported a significant decrease in Optic Nerve Head flow index in MS patients with a history of optic neuritis as compared to healthy controls or MS patients without ON. But no significant changes were observed in the parafoveal region.[2] These findings have demonstrated the usefulness of OCTA in studying vascular abnormalities associated with MS.


Rougier et al, [3] found that in inflammatory optic disc edema, no vascular drop out was present. A significant peripapillary edema can hide, the underlying capillaries, but capillaries were visible above the edematous area. The radial distribution of peripapillary capillaries is usually preserved.


In patients with papilledema, radial peripapillary network remains unchanged, capillaries present at the surface of optic nerve head are dilated and tortuous and appear like a tangled ball of vessels, with no associated areas of vascular dropout. [3]


Nonarteritic anterior ischemic optic neuropathy (NAION) is the consequence of an acute ischemic event of the optic nerve head. The pathophysiology of NAION is believed to be the result of occlusion of the posterior ciliary artery, resulting in hypoperfusion of optic disc microcirculation. NAION is also known to be associated with structural crowding of the optic disc, hypertension, diabetes, and hyperlipidemia and hypercoagulable disorders, sleep apnea, and nocturnal hypotension are the known risk factors. [4] It is the most common acute optic neuropathy among patients older than 50 years.

OCT-A features

Wright Mayes et al, [5] in their retrospective study in NAION patients have demonstrated, flow impairment in OCTA in the retinal peripapillary capillaries which also correspond to the structural OCT deficits of retinal nerve fiber layer (RNFL) and ganglion cell layer complex (GCC) as well as with the automated visual field deficits.

A potential clinical application of OCT-A in NAION is monitoring recovery, early OCT-A study has revealed partial recovery of peripapillary vascular flow with improvement in visual function. [6] Rougier MB et al , have shown that in NAION patients peripapillary network is less visible and there are vascular dropout areas associated with tortousity. [3]


Superficial peripapillary capillary dilation has been reported in eyes with acute AAION and also in fellow eyes.

The cause of dilation can be explained by luxury perfusion in setting of short posterior ciliary arterial compromise. Alternatively, the dilation may represent centrally mediated autoregulatory mechanisms in the setting of reduced perfusion of the optic nerve These retinal capillary perfusion defects also correspond to visual field loss. [7]

Hereditary optic neuropathy

Microangiopathy is a well-known feature of eyes with LHON. The telangiectatic vessels with focal tortuosity can be clearly made visible by OCTA in patients with pseudoedema of the optic disk secondary to LHON. Moreover, temporal optic atrophy and NFL thinning in the papillomacular bundle is a general feature for LHON.

Different patterns of loss of choriocapilaries have been reported in different stages of LHON, by Balduci et al.[8]

In the early sub acute stage of LHON, vascular density is reduced chiefly in the temporal sector, in late sub-acute stages of LHON-l, vessel density is reduced in temporal, superotemporal and inferotemporal sectors and in chronic stages of LHON, vessel density is reduced in all sectors , further it was found that vessel density changes occur earlier than RNFL thickness changes, suggesting that OCT-A can be a useful biomarker to monitor the disease progression and treatment

Optic atrophy

In cases of optic atrophy, a decrease in peripapillary microvasculature has been noted. A possible explanation for decreased visibility of microvasculature in optic atrophy is a smaller number of nerve fibers in the peripapillary area which reduces the metabolic activity and in turn, lowers the blood flow via autoregulatory mechanisms. [9]


OCT-A has been reported to be a useful tool for evaluating optic disc perfusion in glaucomatous eyes, as attenuated peripapillary and macular vessel density has been detected in pre-perimetric glaucoma patients. Therefore, OCT-A can help in early detection of glaucomatous damage. Moreover, the quantitative data from these retinal vessels may prove useful in analysing metabolic activity from the inner layers of the retina and thus provide further advances in monitoring function and progression in this disease. [10]


1) Petzold A, de Boer JF, Schippling S, Vermersch P, Kardon R, Green A, et al. Optical coherence tomography in multiple sclerosis: A systematic review and meta-analysis. Lancet Neurol. 2010;9:921–32.

2) Wang X, Jia Y, Spain R, et al. Optical coherence tomography angiography of optic nerve head and parafovea in multiple sclerosis. Br J Ophthalmol 2014;98:1368–1373

3) Rougier MB et al Optical coherence tomography angiography at the acute phase of optic disc edema Eye Vis (Lond). 2018 Jun 23;5:15

4) Arnold AC. Pathogenesis of nonarteritic anterior ischemic optic neuropathy. J Neuroophthalmol. 2003;23:157–163.

5) Wright Mayes E, Cole ED, et al. Optical coherence tomography angiography in nonarteritic anterior ischemic optic neuropathy.J Neuroophthalmol 2017;37:358‑64

6) Sharma S, Ang M, Najjar RP et al. Optical coherence tomography angiography in acute non‑arteritic anterior ischaemic optic neuropathy. Br J Ophthalmol 2017;101:1045‑51.

7)Gaier ED,  Gilbert AL Optical coherence tomographic angiography identifies peripapillary microvascular dilation and focal non-perfusion in giant cell arteritis Br J Ophthalmol.2018 Aug;102(8):1141-1146.

8) Balducci N et al Peripapillary vessel density changes in Leber's hereditary optic neuropathy: a new biomarker. Clin Exp Ophthalmol. 2018 Dec;46(9):1055-1062.

9) Ghasemi Falavarjani K, Tian JJ, Akil H, Garcia GA, Sadda SR, Sadun AA. Swept source optical coherence tomography angiography of the optic disk in optic neuropathy. Retina. 2016;36(Suppl 1):S168–S177.

10) Yarmohammadi A, Zangwill LM, Diniz-Filho A, et al. Peripapillary and Macular Vessel Density in Patients with Glaucoma and Single-Hemifield Visual Field Defect. Ophthalmology. 2017;124(5):709-719.