Acute macular neuroretinopathy: pathogenetic insights from optical coherence tomography angiography.

Casalino, Giuseppe; Arrigo, Alessandro; Romano, Francesco; Munk, Marion; Bandello, Francesco; Parodi, Maurizio Battaglia (2019). Acute macular neuroretinopathy: pathogenetic insights from optical coherence tomography angiography. The British journal of ophthalmology, 103(3), pp. 410-414. BMJ Publishing Group 10.1136/bjophthalmol-2018-312197

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AIM

To describe the optical coherence tomography angiography (OCT-A) features of patients affected by acute macular neuroretinopathy (AMN).

METHODS

This is a prospective, observational, cross-sectional study. Multimodal imaging, including spectral domain OCT (Spectralis HRA+OCT; Heidelberg Engineering, Heidelberg, Germany) and 6×6 mm swept source OCT-A (ZEISS PLEX Elite 9000; ZEISS, Dublin, California), was performed on all patients. The primary outcome measure was assessment of the vascular alterations of the superficial (SCP) and deep (DCP) capillary plexuses and choriocapillaris (CC). A segmentation of the AMN lesions using enface OCT images of photoreceptors-retinal pigment epithelium complex was used to discriminate intralesional and extralesional regions on the OCT-A enface slabs of the DCP and CC reconstructions. Each OCT-A slab was imported into ImageJ V.1.50 and digitally binarised for quantitative analyses.

RESULTS

Overall, seven patients (mean age 19.4±3.2 years, six women) affected by AMN were included. The mean best-corrected visual acuity was 0.00±0.00 logarithm of the minimum angle of resolution. Twelve healthy age-matched subjects (mean age 22±3.4 years, 10 women) represented the control group. The quantitative analysis of global vessel densities showed that the CC vessel density was significantly lower in patients with AMN (0.495±0.03) compared with the age-matched controls (0.545±0.02) (corrected p=0.0003). The intralesional vessel density of the DCP was 0.349±0.04 in AMN and vs 0.497±0.02 in the controls (corrected p=0.0002).

CONCLUSIONS

Our study confirmed inner choroidal vascular flow void as a possible pathogenetic mechanism of AMN. We also found a focal impairment of the DCP within the AMN lesions. Future studies are needed to clarify which is the primary location of the vascular insult in this condition.

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