We report our findings for a patient with orbital apex syndrome associated with herpes zoster ophthalmicus. Our patient was initially admitted to a neighborhood hospital because of nausea and loss of appetite of 10 days’ duration. The day after hospitalization, she developed skin vesicles along the first division of the trigeminal nerve, with severe lid swelling and conjunctival injection. On suspicion of meningoencephalitis caused by varicella zoster virus, antiviral therapy with vidarabine and betamethasone was started. Seventeen days later, complete ptosis and ophthalmoplegia developed in the right eye. The light reflex in the right eye was absent and anisocoria was present, with the right pupil larger than the left. Fat-suppressed enhanced T1-weighted magnetic resonance images showed high intensity areas in the muscle cone, cavernous sinus, and orbital optic nerve sheath. Our patient was diagnosed with orbital apex syndrome, and because of skin vesicles in the first division of the trigeminal nerve, the orbital apex syndrome was considered to be caused by herpes zoster ophthalmicus. After the patient was transferred to our hospital, prednisolone 60 mg and vidarabine antiviral therapy was started, and fever and headaches disappeared five days later. The ophthalmoplegia and optic neuritis, but not the anisocoria, gradually resolved during tapering of oral therapy. From the clinical findings and course, the cause of the orbital apex syndrome was most likely invasion of the orbital apex and cavernous sinus by the herpes virus through the trigeminal nerve ganglia.

We report a case of eosinophilic chronic rhinosinusitis (ECRS) associated with optic neuropathy. The visual acuity in the right eye was suddenly reduced to no light perception on awakening in the morning. Fundus examination of both eyes on the same day showed no remarkable changes. Emergency computed tomography showed pan-sinusitis bilaterally and a partial defect of the sphenoid bone on the right side. From the clinical findings, the case was diagnosed as optic neuropathy associated with chronic sinusitis. Endoscopic sinus surgery (ESS) was performed on the same day, and all of the major sinuses were found to be filled with highly viscous fluid. Part of the optic canal had a defect probably due to inflammatory invasion from the adjacent sphenoid bone. Steroid therapy was started immediately postoperatively. Histopathological examination of excised polyps showed that numerous eosinophils had invaded the polyps but no hyphae were present. The patient reported that he had bronchial asthma and had had nasal polypectomy. Six months after the ESS and steroid therapy, the patient had a recurrence of the sinusitis. At that time, laboratory examination showed an elevation of total IgE and eosinophil numbers. From the clinical findings and course, this case was diagnosed as ECRS accompanied by optic neuropathy. Although ECRS rarely has ocular complications, the inflammation can spread and the optic nerve can be affected.

BackgroundTo describe a retrospective study of macular retinoschisis that developed long after the onset of retinal artery occlusion (RAO) using optical coherence tomography (OCT).MethodsWe describe changes in macular findings and visual acuity (VA) of 29 patients (21 males and 8 females, mean age: 66.1 ± 16.9 years) with RAO (18 branch RAOs [BRAOs] and 11 central RAOs [CRAOs] who visited Osaka Medical College Hospital over an 8-year period based on a medical chart review.ResultsThe mean VA (logMAR) increased from 1.06 ± 1.08 (CRAO: 2.04 ± 0.99; BRAO: 0.37 ± 0.40) at the first visit to 0.71 ± 0.87 (CRAO: 1.46 ± 0.86; BRAO: 0.18 ± 0.30) at the final visit. Macular OCT revealed swelling or hyper-reflectivity of the inner retina in the early phase of RAO and retinal thinning in the late phase. Among the 29 patients, two patients (a patient with BRAO and a patient with CRAO) developed macular retinoschisis about 1 year after RAO onset. The VA of the patient with BRAO was 20/300 at the first visit, and it improved to 20/25 two days after onset following eye massage and anterior chamber paracentesis. However, his VA worsened, declining from 20/25 to 20/50, and retinoschisis occurred 13 months after RAO onset. The patient with CRAO showed macular changes including small cystoids at the first follow-up visit more than 3 weeks after onset and developed retinoschisis 11 months after the first visit. In addition, two patients with BRAO and one patient with CRAO developed macular changes including small cystoids 3 weeks after onset, with the BRAO complicated by retinal vein occlusion. In the CRAO patient, the cystoid macular edema was resolved 1 month after the first visit.ConclusionsMacular retinoschisis is unusual, but a possible complication of RAO that can develop long after the onset of the occlusion, potentially resulting in renewed VA deterioration.

BackgroundTo report the case of a patient with pseudoxanthoma elasticum (PXE) and proliferative diabetic retinopathy (PDR), and discuss the relationship between PXE and diabetic retinopathy (DR).Case presentationA 47-year-old man with PXE presented with angioid streaks and DR in both eyes, and bilateral panretinal photocoagulation was performed for treatment. Vitrectomy had previously been performed in his right eye for vitreous hemorrhage due to PDR. Systemic findings included multiple, discrete, symmetrical, small yellow papules bilaterally in the axilla and inguinal region. Examination on presentation showed vitreous hemorrhage in his left eye, and vitrectomy was performed for treatment. Intraoperative findings showed fibrovascular membrane around the optic disc and vascular arcade. A mottled fundus (peau d’orange appearance) associated with angioid streaks was also present, yet there was no evident choroidal neovascularization (CNV). The postoperative course was satisfactory, and corrected visual acuity improved from 0.02 to 0.7 diopters.ConclusionDespite the peau d’orange appearance in both eyes of this case, no CNV was evident. The vitreous hemorrhage was thus attributed to PDR. Moreover, we reviewed the published literature and discuss the relationship between PXE and DR.