Retrobulbar optic neuritis associated with trigeminal herpes zoster is very rare [1,2]. In most published cases, this condition was treated with steroids and acyclovir, but the efficacy of these treatments is controversial [3-7]. We report a woman with retrobulbar optic neuritis caused by varicella-zoster virus in whom loss of visual acuity was markedly improved by stellate ganglion block (SGB) and minimally improved by aggressive administration of steroids. Case Report A 50-yr-old woman developed herpes zoster in the first division of the left trigeminal nerve, including the nasociliary nerve. The skin lesions and pain gradually resolved with intravenous (IV) administration of acyclovir 750 mg/day for 5 days, followed by 250 mg/day for 3 days. Six weeks after the onset of herpes zoster, the patient noticed a gradual decrease in visual acuity in her left eye and severe itching of her left forehead. She developed complete loss of visual acuity in her left eye over a 24-h period and was admitted to the hospital. Her left eye had no light perception; the visual acuity of her right eye was normal. The mobility of her eyes was unaffected. The left pupil was slightly larger than the right one, with left eye reaction almost absent to direct light and normal to indirect light. Slit lamp examination and ophthalmoscopy disclosed no abnormal signs. Intraocular pressure was within the normal range in both eyes. General physical and neurologic examinations were normal. Brain computed tomography and magnetic resonance imaging revealed no abnormalities. The serum complement fixation titer of varicella-zoster virus was 1:128 (normal range less than 1:4). Retrobulbar optic neuritis due to varicella-zoster virus was suspected, and treatment was initiated with IV methylprednisolone 1000 mg/day for 3 days, followed by oral prednisolone 30 mg, which was tapered 10 mg/wk. She received a second course of IV methylprednisolone 1000 mg/day for 3 days from the 15th hospital day, when visual acuity gradually improved to finger counting at 30 cm. Visual field testing at that time revealed a central scotoma in her left eye. Left eye visual acuity remained 20/330 on the 29th hospital day. On the 30th hospital day, she was referred to the pain clinic for treatment of left visual disturbance and severe itching. We performed left SGB using 6 mL of 1% mepivacaine daily for 2 wk. Within 30 min after the first SGB, she noticed marked improvement of vision, and this improvement lasted until the following day, when her left eye visual acuity was 20/220. Visual acuity then improved to 20/70 after the third SGB and to 20/33 after the seventh SGB. Her severe itching eased slightly through the series of SGBs. Eight months after the onset of optic neuritis, left eye visual acuity remained at 20/33, and color perception was impaired. Ophthalmoscopic examination revealed temporal pallor of the disc, and brain computed tomography revealed left optic nerve atrophy. Discussion Optic neuritis after trigeminal herpes zoster appears weeks to months after the onset of skin lesions, and loss of visual acuity varies from severe bilateral impairment to moderate unilateral impairment. Because pathologic examination of the optic nerve cannot be performed, the definitive confirmation of the link between varicella-zoster virus and optic neuritis depends on clinical findings and the exclusion of other etiologies. In the present case, a diagnosis of retrobulbar optic neuritis associated with herpes zoster was made based on the history of herpes zoster infection, profound loss of vision, and absence of other abnormal findings. Optic neuritis after herpes zoster is usually treated with steroids but often has a fulminant course unresponsive to steroids [3-5]. In our patient, loss of visual acuity was markedly improved by SGB, and only minimally improved by aggressive administration of steroids. In some cases, steroids improved visual acuity disturbed by optic neuritis after herpes zoster [6,7], but these improvements were more gradual and slighter than the marked improvement in our patient with SGB. The process by which herpes zoster leads to subsequent optic neuritis is not well understood, but it may be related to multiple mechanisms, including viral spread, ischemic vasculitis, demyelination, and host-immune response to infection [8-10]. The mechanism by which SGB improves the visual acuity is equally unclear. SGB may relieve optic nerve ischemia, because sympathetic blockade by SGB increases central retinal blood flow [11]. Further clinical study is required to determine whether SGB should be used with steroid therapy for the treatment of optic neuritis after herpes zoster. In summary, we treated a patient with retrobulbar optic neuritis after herpes zoster. SGB performed 30 days after the onset of visual disturbance was more effective than steroid therapy. Early initiation of SGB may have the potential to improve visual acuity decreased by optic neuritis after herpes zoster.
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Feb 1, 2000
W Schlack + 1
Open Access