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A case of a young woman who developed diplopia with midbrain infarction during treatment for herpes zoster virus uveitis Kohei Terada 1 , Taiga Inooka 2 , Yuri Tanaka 2 , Haruka Ando 2 , Sayuri Yasuda 2 1Department of Ophthalmology, Shizuoka Saiseikai General Hospital 2Department of Ophthalmology, Nagoya University Graduate School of Medicine pp.605-611
Published Date 2025/5/15
DOI https://doi.org/10.11477/mf.037055790790050605
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Abstract Purpose:Varicella-zoster virus(VZV)causes chickenpox upon initial infection and reactivates to cause herpes zoster. Ocular shingles may be accompanied by paralysis of the external ocular muscles, and VZV vasculopathy is postulated to be one of the mechanisms of this paralysis. We report a case of VZV vasculopathy as a cause of sudden onset of ocular motility disorder.

Case:A 29-year-old woman with systemic lupus erythematosus. She was taking medication for systemic lupus erythematosus and the symptoms were well controlled. She developed uveitis associated with VZV on the right side of the face and was treated with acyclovir ophthalmic ointment and steroid eye drops, and her findings improved. Three months after the onset of uveitis, she suddenly developed diplopia and presented to our emergency department.

Findings:There were no abnormalities in the internal ocular findings including visual acuity, intraocular pressure, or fundus findings in either eye. Pupillary dilatation, adduction and retraction deficits were observed in the right eye. A magnetic resonance imaging(MRI)scan of the head showed a high-intensity area medial to the right midbrain on diffusion-weighted images. Blood tests showed no abnormality in the blood coagulation system, and cerebrospinal fluid tests showed no increase in the number of protein cells. Based on these findings, she was treated with Bayaspirin and supplemental fluids as if it were a cerebral infarction without VZV vasculopathy. One month after onset, her diplopia showed signs of improvement, and six months after onset, the ocular motility disorder had lessened.

Conclusions:In young patients with ocular motility disorder with a history of VZV infection, cerebral infarction should be considered as a differential diagnosis, and in particular, cerebral infarction associated with VZV vasculopathy should be kept in mind as a differential diagnosis to exclude. If there is any doubt, it is important to perform not only a head MRI but also a cerebrospinal fluid examination.


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