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Nicholas Daniel Chinskey, Mark W Johnson; Acute Macular Neuroretinopathy Following Trauma. Invest. Ophthalmol. Vis. Sci. 2014;55(13):5940.
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To describe the imaging characteristics and clinical course of acute macular neuroretinopathy (AMNR) following non-ocular trauma.
We retrospectively reviewed medical records of five patients who developed symptoms and fundus findings suggestive of AMNR following trauma to the face or chest. Imaging studies including optical coherence tomography (OCT), infrared imaging, fluorescein angiography (FA) and indocyanine green angiography (ICGA) were evaluated. Multifocal electroretinography (mfERG) was available for a single patient.
All five patients were identified as having AMNR based on reddish-brown macular lesions with corresponding scotomas. In each case, the visual symptoms started immediately after non-ocular trauma. One patient had partial resolution of symptoms by six months while the other four had persistent scotomas at last follow-up (ranging from 10 months to 5 years after trauma). There was no leakage of fluid by either FA or ICGA. OCT imaging within days of the trauma demonstrated focal areas of hyperreflectivity in the outer plexiform and outer nuclear layers. OCT performed at later time points showed thinning of the outer nuclear layer and loss of the ellipsoid and outer segment layers. mfERG demonstrated focal reduction of signal limited to the area corresponding to the wedge shaped defects. The results of each imaging study were similar to those of published cases of AMNR linked to other causative agents.
The imaging characteristics and clinical courses of our five patients with AMNR following non-ocular trauma were comparable to published cases caused by other known risk factors. We believe that an acute ischemic injury involving the deep retinal capillary plexus is the pathogenic mechanism that most plausibly explains both the time course and clinical features of traumatic AMNR.
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