Herpes zoster ophthalmicus complicated by orbital apex syndrome and varicella-zoster virus-associated meningitis: a case report

Abstract Background Herpes zoster ophthalmicus (HZO) rarely causes orbital apex syndrome and may be accompanied by central nervous system infection. Integration of ocular and neurologic manifestations with imaging and etiologic investigations facilitates recognition of these complex complications. Case presentation A 65-year-old woman developed left-sided ptosis, proptosis, esotropia, restricted ocular motility, and decreased vision after pain and a vesicular eruption in the distribution of the left ophthalmic division of the trigeminal nerve. On admission, visual acuity in the left eye was 0.16 and did not improve with refraction; exophthalmometry measured 20 mm in the left eye and 17 mm in the right eye. The left pupil was dilated and unreactive to light. Orbital magnetic resonance imaging on May 16, 2025 showed thickening and abnormal signal intensity of the left optic nerve and multiple extraocular muscles. During hospitalization, the patient developed headache and recurrent nausea and vomiting. The cerebrospinal fluid nucleated cell count was 56 × 10⁶/L, consisting entirely of mononuclear cells. Probe-capture high-throughput sequencing of cerebrospinal fluid detected both varicella-zoster virus (VZV) and Epstein-Barr virus. Based on the clinical manifestations, imaging findings, and cerebrospinal fluid results, HZO complicated by left orbital apex syndrome and VZV-associated meningitis was diagnosed. Following systemic antiviral therapy, methylprednisolone, and symptomatic treatment, the headache, vomiting, and ocular pain subsided, and the ptosis and ocular motility disturbance improved. Repeat orbital magnetic resonance imaging on May 30 showed marked improvement in the optic nerve and extraocular muscle abnormalities. Visual acuity in the left eye improved to 0.4 at discharge. Six days after discharge, best-corrected visual acuity was 0.5, and uncorrected visual acuity remained 0.4 at follow-up on September 2, 2025. Conclusion Orbital apex involvement should be suspected when HZO is accompanied by decreased vision, ptosis, and ocular motility disturbance. Neurologic infection should be further evaluated when headache and vomiting occur. Orbital imaging, cerebrospinal fluid analysis, and etiologic testing help define the extent of involvement, while detection of multiple pathogens should be interpreted in the context of the clinical phenotype.

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Publication Details

Journal
BMC Ophthalmology
Published
2026-11-09
DOI
https://doi.org/10.1186/s12886-026-05520-2
Primary Topic
Herpesvirus Infections and Treatments
Type
article
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article

Herpes zoster ophthalmicus complicated by orbital apex syndrome and varicella-zoster virus-associated meningitis: a case report

Chaoyang Zhao, Rui Wu, Ziyou Yuan, Ying Zhang et al.
BMC Ophthalmology
Herpesvirus Infections and Treatments
article

Herpes zoster ophthalmicus complicated by orbital apex syndrome and varicella-zoster virus-associated meningitis: a case report

Chaoyang Zhao, Rui Wu, Ziyou Yuan, Ying Zhang, Bo Zhang, Huilin Li, Yan Wang
article en

Abstract

Abstract Background Herpes zoster ophthalmicus (HZO) rarely causes orbital apex syndrome and may be accompanied by central nervous system infection. Integration of ocular and neurologic manifestations with imaging and etiologic investigations facilitates recognition of these complex complications. Case presentation A 65-year-old woman developed left-sided ptosis, proptosis, esotropia, restricted ocular motility, and decreased vision after pain and a vesicular eruption in the distribution of the left ophthalmic division of the trigeminal nerve. On admission, visual acuity in the left eye was 0.16 and did not improve with refraction; exophthalmometry measured 20 mm in the left eye and 17 mm in the right eye. The left pupil was dilated and unreactive to light. Orbital magnetic resonance imaging on May 16, 2025 showed thickening and abnormal signal intensity of the left optic nerve and multiple extraocular muscles. During hospitalization, the patient developed headache and recurrent nausea and vomiting. The cerebrospinal fluid nucleated cell count was 56 × 10⁶/L, consisting entirely of mononuclear cells. Probe-capture high-throughput sequencing of cerebrospinal fluid detected both varicella-zoster virus (VZV) and Epstein-Barr virus. Based on the clinical manifestations, imaging findings, and cerebrospinal fluid results, HZO complicated by left orbital apex syndrome and VZV-associated meningitis was diagnosed. Following systemic antiviral therapy, methylprednisolone, and symptomatic treatment, the headache, vomiting, and ocular pain subsided, and the ptosis and ocular motility disturbance improved. Repeat orbital magnetic resonance imaging on May 30 showed marked improvement in the optic nerve and extraocular muscle abnormalities. Visual acuity in the left eye improved to 0.4 at discharge. Six days after discharge, best-corrected visual acuity was 0.5, and uncorrected visual acuity remained 0.4 at follow-up on September 2, 2025. Conclusion Orbital apex involvement should be suspected when HZO is accompanied by decreased vision, ptosis, and ocular motility disturbance. Neurologic infection should be further evaluated when headache and vomiting occur. Orbital imaging, cerebrospinal fluid analysis, and etiologic testing help define the extent of involvement, while detection of multiple pathogens should be interpreted in the context of the clinical phenotype.

BMC Ophthalmology
Herpesvirus Infections and Treatments
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