A 64-year-old woman presented with sudden painless visual loss in her left eye. She had no past history of systemic vascular diseases such as hypertension, diabetes mellitus, dyslipidemia, smoking, and trauma. Six weeks before her visual loss, she had developed ipsilateral HZO, characterized by painful rashes on the left forehead, eyelid, and side of the nose, and keratitis and received topical acyclovir, levofloxacin, and prednisolone from an ophthalmologist as well as topical fusidic acid, betamethasone, and neomycin sulfate from a dermatologist. Her condition partially improved after 3 weeks of the treatments. At onset, her visual loss was confined to upper half of her left visual field. Visual acuity was 0.03 in the left eye and normal in the right eye. She was diagnosed with herpetic uveitis and treated with topical ketorolac tromethamine, neomycin sulfate/triamcinolone acetonide, and acyclovir. Later, visual perimetry disclosed superior altitudinal and inferior peripheral defects in the left eye and an equivocal superior visual defect in the right eye (shown in Fig. 1). One week after visual loss, her left eye vision progressed to total visual loss. Ocular examination revealed visual acuity of 1.0 OD and light perception OS, with no signs of uveitis, cherry red spot, or anterior ischemic optic neuropathy (AION). Brain and orbit magnetic resonance imaging with contrast confirmed no evidence of acute stroke, infiltrative, or space-occupying lesions except old infarcts in the left basal ganglion. Herpes zoster-associated optic neuropathy was impressed, but she declined further survey and had received oral valaciclovir (500 mg three times per day) for 3 days after discharge. Two weeks after her visual loss, she was hospitalized with stationary vision.
On examination, the left eye had sluggish light reflex, relative afferent pupillary defect, and visual acuity of hand motion of 30 cm. The intraocular pressure was 19 mm Hg. Slit-lamp examination revealed a mild cataract, a clear anterior chamber, and no corneal lesions. Fundoscopy demonstrated a normal-appearing optic disc with normal retina, macula, and retinal vessels (shown in Fig. 2). The right eye had visual acuity of 1.0 and was otherwise unremarkable except for a mild cataract. A survey of optic neuropathy was performed. White blood cells' count was 6,700 with 68.1% neutrophils, 20.3% lymphocytes, 10.5% monocytes, and 0.6% eosinophils. Erythrocyte sedimentation rate was 46 mm/h, and C-reactive protein 4.3 mg/L. Laboratory examination including serum creatinine, alanine aminotransferase, lipid profile, thyroid-stimulating hormone, thyroxine, cobalamin, and autoimmune screening was within normal limits. Cerebrospinal fluid (CSF) studies revealed no pleocytosis or culture evidence of viral, tuberculosis, or syphilis infection. CSF polymerase chain reaction for herpes simplex virus type 1 and type 2 and varicella-zoster virus (VZV) DNA was negative. Sonography of the carotid and ophthalmic arteries was unremarkable. Cerebral digital subtraction angiography demonstrated no evidence of occlusion in ophthalmic arteries. Nonarteritic PION was diagnosed, and its association with previous herpes zoster was possible. She was treated with aspirin, topical brimonidine, and an additional 7-day course of oral valaciclovir (1 g 3 times a day).
After treatment, visual acuity of the involved eye slightly improved and reached counting finger of 20 cm and 0.02 at four and 6 weeks after visual loss, respectively. Six weeks after visual loss, visual perimetry revealed a total defect for the left eye, and despite the suboptimal quality, a superior defect for the right eye without impaired visual acuity or subjective visual problems (shown in Fig. 1). Optical coherence tomography disclosed left temporal pallor and a loss of the retinal nerve fiber layer in the left temporal eye (shown in Fig. 3). Seven weeks after the visual loss, visual evoke potential revealed prolonged P100 latency on both sides, with more severe latency on the left side (left, 146.7 ms; right, 119.1 ms; cutoff value, 110 ms). During the follow-up, she reported stationary vision. The CARE Checklist has been completed by the authors for this case report, attached as supplementary material (for all online suppl. material, see www.karger.com/doi/10.1159/000529837).