Our patient had an acute monocular visual loss and a fundus that appeared normal except for the relatively delayed angiographic retinal filling time and enlarged disc cups. The RAPD, central scotoma and systemic complications made it difficult to determine the site of the alterations. The reduced FMERGs pointed to the retina as the site.
However, an abnormally long‐lasting visual decrease is not typical for amaurosis fugax,1
and ophthalmoscopy did not show retinal oedema typical of arteriolar occlusion. Conventional electrophysiological examinations such as full‐field ERGs and VEPs might be useful except when the ischaemic site is in the macular region.
The clinical course in our case was compatible with a transient retinal ischaemia with a possibility of a transient central retinal artery occlusion, although additional more generalised abnormalities cannot be completely excluded. The FMERG within the 5° area is similar to that of the ERG of a monkey treated with 2‐amino‐4‐phosphonobutyric acid (APB) and cis‐2,3‐piperidine dicarboxylic acid (PDA) to suppress both on and off synapses.4,5
This implies that the inner retinal layers have serious dysfunction. Because of the systemic complications, the risk of utilising prophylactic anticoagulant agents was discussed. However, the VA and central scotoma quickly recovered accompanied by an improvement in the FMERGs without any intervention.
These findings indicate that clinicians should consider focal macular dysfunction in cases of acute vision loss and normal retinal appearance; multifocal ERGs or FMERGs are useful in determining the site of the pathology.