Acute Macular Neuroretinopathy Following Non-Ocular Trauma: A Hypothesis Regarding Pathophysiologic Mechanism

To describe the imaging characteristics and clinical course of acute macular neuroretinopathy (AMN) following non-ocular trauma, and to hypothesize a pathophysiologic mechanism for this syndrome.

The records of five patients who developed symptoms and findings suggestive of AMN following trauma to the face or chest were retrospectively reviewed. Optical coherence tomography (OCT), infrared reflectance, fundus autofluorescence, fluorescein and indocyanine green angiography, and multifocal electroretinography were evaluated.

Visual symptoms started immediately or very soon after non-ocular trauma, and scotomas persisted at last follow-up (2 weeks to 10 years after trauma). OCT imaging performed within days of the trauma demonstrated focal areas of hyper-reflectivity in the outer plexiform and outer nuclear layers with eventual thinning of the outer nuclear layer, as well as variable loss of the ellipsoid and interdigitation zones.

Acute ischemic injury caused by trauma-induced hypotension and/or catecholamine release and involving the deep retinal capillary plexus is the pathogenic mechanism that most plausibly explains trauma-associated AMN.