Naohiro Ikeda

Purpose: To describe the ophthalmoscopic changes of the choroidal vessels in the posterior pole of Vogt–Koyanagi–Harada disease patients whose choroid is thickened due to asymptomatic choroiditis. Methods: Three patients whose choroidal vessels are indistinct or not visible in the posterior pole by ophthalmoscopy were examined by fundus photography and enhanced-depth imaging optical coherence tomography (EDI-OCT). Results: They did not complain of vision problems, and visual acuity was good. Serous retinal detachment was not observed by ophthalmoscopy or by OCT. However, choroidal thickening was observed in the EDI-OCT, while choroidal vessels became blurred or invisible on ophthalmoscopy. After steroid therapy, choroidal thickness decreased to normal levels and the small and large choroidal vessels previously indiscernible became visible by ophthalmoscopy and fundus photography. Conclusions: Asymptomatic choroiditis not accompanied by serous retinal detachment can be detected and assessed by observing the changes in the choroidal vessels by ophthalmoscopy and fundus photography.

To reconsider the pathogenesis of traumatic myopia by describing two cases and literature review.

Refractive change can be caused by systemic illnesses such as Lupus erythematosus, thyroid deficiency, and diabetes mellitus. However, refractive change after pituitary tumor removal has so far not been reported. A 62-year-old woman presented with blurred near vision 10 days after trans-sphenoidal surgery (TSS) for a pituitary tumor. Around the same time, she experienced intercurrent hyponatremia. The corrected visual acuity of both eyes was 20/20, the spherical equivalent of the right eye was −2.125 diopters, and of the left eye was −2.0 diopters before TSS. However, 11 days after TSS, the spherical equivalent of the right eye changed to −0.75 diopters, and that of left eye changed to −1.125 diopters without hyperglycemia. There were no changes in the corrected visual acuity during the follow-up. We demonstrated a case with transient refractive change after TSS. The following mechanism is proposed: Hyponatremia induced by the pituitary tumor removal causes an osmotic change in the aqueous humor with lens swelling. This case report is a reminder to both ophthalmologists and neurosurgeons that ophthalmological factors such as lens thickness and axial length should be taken into account when conducting preoperative examinations especially for patients undergoing TSS.

To determine the cause of angle-closure glaucoma in a case of posterior scleritis. The patient was a 65-year-old woman with unilateral acute angle-closure glaucoma who did not respond to laser iridotomy. Slit-lamp examination demonstrated a shallow anterior chamber in the left eye. Intraocular pressure was 22 mmHg even after application of two antiglaucoma eye-drop preparations. B-scan ultrasonography demonstrated scleral thickening and choroidal detachment in the left eye. Ultrasound biomicroscopy showed a shallow anterior chamber with angle closure, annular ciliochoroidal effusion with ciliary body edema, and an anterior rotation of the ciliary body. After instillation of cycloplegics, the ciliary body and ciliary processes rotated posteriorly, resulting in the release of the pressure on the iris. These changes led to the opening of the angle and subsequent normalization of intraocular pressure. A diagnosis was made of ciliochoroidal effusion syndrome associated with posterior scleritis. Patients with posterior scleritis can develop ciliochoroidal effusion syndrome, which can lead to angle-closure glaucoma. The therapeutic strategy for acute angle-closure glaucoma induced by ciliochoroidal effusion syndrome differs completely from that for acute angle-closure glaucoma with pupillary block. In the case of ciliochoroidal effusion syndrome, it is important to relieve the compression of the angle by the iris by displacing the lens–iris diaphragm posteriorly by cycloplegics. Jpn J Ophthalmol 2007;51:49–52 © Japanese Ophthalmological Society 2007

Purpose: To determine the location of the lesions in the retina of a patient with multiple evanescent white dot syndrome (MEWDS) and to resolve the conflict in the cause of the hypofluorescent spots observed in the late phase of indocyanine green angiography (ICGA). Case report: A 27-year-old woman presented with a unilateral enlarged blind spot and a central scotoma. Fundus examination of the left eye showed many round, indistinctly circumscribed white dots extending from the posterior pole toward the periphery. Fluorescein angiography demonstrated hyperfluorescence due to staining at the location of the white dots. Staining was also observed on the venous wall which was consistent with periphlebitis. The location of the scotomas corresponded with the hypofluorescent spots observed around the optic disc and in the macula in the late phase of ICGA. The scotomas disappeared with the resolution of the hypofluorescent spots, and the sites of other hypofluorescent spots were in accord with the sites of periphlebitis. Visual evoked cortical potentials disclosed no laterality, and the critical fusion frequency was reduced but normalized with the disappearance of the scotoma. Conclusion: The initial lesions of MEWDS occur in the retinal pigment epithelium and photoreceptor cells, but when MEWDS is complicated by periphlebitis, the inflammatory lesions extend to the inner layers of the retina. The inflammatory changes involve the choroid and all layers of the retina, which then block the weak background fluorescence in the later phase of ICGA and cause the hypofluorescent spots. The visual field defects are probably caused by retinal dysfunction due to the inflammatory changes.