A 76-year-old patient attended the emergency department for right frontal TBI with loss of consciousness, caused by a casual fall at home. The patient reported loss of vision in the right eye (OD) when she regained consciousness.
Her medical history included type 2 diabetes mellitus treated with oral antidiabetics and osteoarthritis. There was no other personal or family history of interest.
Examination revealed an infraciliary incised-contuse wound and a diffuse right fronto-orbital haematoma. Visual acuity (VA) was no light perception with a relative afferent pupillary defect (ARPD) in the OD and 0.6 in the left eye. The anterior pole was within normal, as were intraocular pressure and fundus.
Computed tomography (CT) of the skull with orbital slices was normal and magnetic resonance imaging (MRI) showed increased perineural fluid in the right NW sheath.
Given the persistence of symptoms, a sagittal reconstruction of the optic canal of the helical CT scan was performed, showing a linear fracture of the roof of the right orbit extending to the lesser wing of the right sphenoid, in the region of the OC, with minimal subsidence of the lateral fragment that reduced the internal diameter of the OC.
Visual evoked potentials were performed using monocular stimulus (Medelec® Synergy. Oxford. Instruments, England) with Googles at 2 cycles per second, showing a great asymmetry in the morphology of the responses to stimulation of both eyes, suggesting an absence of conduction of the visual stimulus in the right NW.
The patient was diagnosed with traumatic optic neuropathy (TON) with a mixed mechanism of production due to a closed frontal trauma that was transmitted indirectly to the OC and a direct lesion of the NO when the lesser wing of the sphenoid was displaced inside the OC.
Treatment with megadoses of corticosteroids (1 g of methylprednisolone followed by 250 mg every 6 hours for 48 hours) was started, without improvement.