Purpose: To report novel spectral domain optical coherence tomography and electrophysiologic findings in diffuse unilateral subacute neuroretinitis.
Methods: Six patients with a diagnosis of diffuse unilateral subacute neuroretinitis were retrospectively ascertained. All patients had received oral treatment with albendazole; resolution of the inflammatory lesions without subsequent relapse was noted. Spectral domain optical coherence tomography was performed using a Spectralis HRA OCT (Heidelberg Engineering). The inner and outer retinal volumes were calculated for the macular area. The contralateral eyes acted as controls. All six patients underwent standardized full-field electroretinography and pattern electroretinography. Some had multifocal electroretinography.
Results: Inner retinal volume significantly differed between affected and control eyes (P < 0.02), but there was no significant difference in outer retinal volume. Electroretinography data showed a mixed pattern of inner and outer retinal dysfunction, with inner retinal dysfunction being greater; reduction in b:a ratio of the scotopic bright flash electroretinography was a consistent observation in those patients (5/6) with generalized retinal dysfunction. Two patients showed definite photoreceptor involvement, with probable involvement in a third. Of the four patients in whom serial data are available, there was definite evidence of progressive inner and outer retinal dysfunction in one patient, with inner retinal dysfunction being greater, and probably in a second patient.
Conclusion: The data provide anatomical and functional evidence of both inner and outer retinal dysfunction in diffuse unilateral subacute neuroretinitis, even though the worm is usually assumed to be located in the subretinal space. The mechanism is unclear.
In eyes affected by DUSN, spectral domain OCT and electroretinography show inner and outer retinal disruption and dysfunction of the previously affected areas after disease resolution.
*Medical Retina Department, Uevitis Unit, Moorfields Eye Hospital, London, United Kingdom; and
†Electrophysiology Department, Institute of Ophthalmology, University College London, London, United Kingdom.
Reprint requests: Diego Vezzola, MD, Moorfields Eye Hospital, City Road 162, London, United Kingdom; e-mail: firstname.lastname@example.org
This research has received a proportion of its funding from the Department of Health's NIHR Biomedical Research Centre for Ophthalmology at Moorfields Eye Hospital and UCL Institute of Ophthalmology.
None of the authors have any conflicting interests to disclose.