Sir,

We describe the fundus microscopy and the macular optical coherence tomography findings in a patient presenting with a unilateral paracentral scotoma following a whiplash injury.

Case report

A 24-year-old female suffered a car accident, inducing an extension–flexion movement of the neck. Within hours after the accident, she noted a paracentral scotoma in the left eye. Fundus examination of the affected eye demonstrated a macular swelling without posterior vitreous detachment. Six months later, the patient was referred to our clinic. She complained of a persistent scotoma close to her fixation area. Visual acuity was 20/20 in both eyes. However, using a laser beam, we revealed a left inferior paracentral scotoma, about 2 degrees in diameter (Figure 1a). Automated perimetry (Octopus 101, Interzeag) showed a loss in sensitivity at the nearest test location, left inferior to the fixation point (Figure 1b). Fundus examination revealed a whitish annular perifoveal lesion (Figure 1c). Macular optical coherence tomography (Stratus OCT III, Carl Zeiss) showed a hypereflective membranous lesion at the vitreoretinal interface (Figure 1d).

Figure 1
figure 1

(a) A left inferior paracentral scotoma is delineated using a laser beam and a Maddox cross. (b) Quantified Octopus automated perimetry (10-degree centromacular field) showing a deep sensitivity loss, left inferior to the fixation point. (c) Fundus photography of the left eye showing a perifoveal lesion 6 months after a whiplash injury. (d) Stratus OCT III imaging (Line program), showing a thin hypereflective parafoveal lesion at the vitreoretinal interface.

Full size image

Comment

Very few cases of whiplash maculopathy have been described since it was first reported some 30 years ago.1, 2 Although whiplash is a common injury in motor vehicle crashes, whiplash maculopathy is rarely reported, probably due to underdiagnosis.2 We describe here a perifoveal lesion associated with this condition. The annular aspect of the lesion in fundus microscopy and its localisation at the vitreoretinal interface, demonstrated by OCT, support the role of vitreoretinal traction as presumed pathophysiologic mechanism. However, the thin membranous lesion described does not entirely explain the deep sensitivity loss measured by quantified perimetry, suggesting an underlying retinal damage, probably resulting from vitreoretinal traction and/or shearing forces. Recent results of macular histological examination following a fatal whiplash injury support the pathogenic role of vitreoretinal traction in photoreceptors’ disruption.3

OCT can be useful in the detection of lesions at the vitreoretinal interface related with whiplash maculopathy, providing us with a supplementary tool in the diagnosis of this frequently under-recognized condition. Moreover, OCT findings emphasise the role of vitreoretinal traction in the pathogenesis of whiplash maculopathy.