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Byline: Daisuke. Nagasato, Naohiro. Ikeda, Akiko. Masuda, Ryosuke. Kashimoto, Tomohiro. Ikeda A patient with glaucoma developed sudden blurred vision immediately after the nasal mucosal injection of a betamethasone acetate solution [...]

Dependence on lithium-ion batteries for automobile applications is rapidly increasing. The emerging use of anionic redox can boost the energy density of batteries, but the fundamental origin of anionic redox is still under debate. Moreover, to realize anionic redox, many reported electrode materials rely on manganese ions through π-type interactions with oxygen. Here, through a systematic experimental and theoretical study on a binary system of Li3NbO4–NiO, we demonstrate for the first time the unexpectedly large contribution of oxygen to charge compensation for electrochemical oxidation in Ni-based materials. In general, for Ni-based materials, e.g., LiNiO2, charge compensation is achieved mainly by Ni oxidation, with a lower contribution from oxygen. In contrast, for Li3NbO4–NiO, oxygen-based charge compensation is triggered by structural disordering and σ-type interactions with nickel ions, which are associated with a unique environment for oxygen, i.e., a linear Ni–O–Ni configuration in the disordered system. Reversible anionic redox with a small hysteretic behavior was achieved for LiNi2/3Nb1/3O2with a cation-disordered Li/Ni arrangement. Further Li enrichment in the structure destabilizes anionic redox and leads to irreversible oxygen loss due to the disappearance of the linear Ni–O–Ni configuration and the formation of unstable Ni ions with high oxidation states. On the basis of these results, we discuss the possibility of using σ-type interactions for anionic redox to design advanced electrode materials for high-energy lithium-ion batteries.

To elucidate the factors that affect the visibility of polypoidal lesions on OCT angiography (OCTA) based on indocyanine green angiography (ICGA) findings in eyes with polypoidal choroidal vasculopathy (PCV).

Leber's hereditary optic neuropathy (LHON) predominantly affects young men between 10 and 30 years of age. However, two cases of LHON during ethambutol administration have been reported in older men and one case in an older woman. We now report a second case of an older woman in whom administration of ethambutol triggered the development of LHON.A 70-year-old woman received ethambutol, rifampicin, isoniazid, and pyrazinamide for the treatment of tuberculosis.Three months after the beginning of this treatment, a marked decrease in visual acuity occurred in both eyes and ethambutol was discontinued. Her corrected visual acuity was 0.03 in both eyes. There was no hyperemia, swelling of the optic disc, or capillary dilatation in either eye. Centrocecal scotomas were found bilaterally. After 1 month, her visual acuity had further decreased to 0.01, and the scotomas had enlarged. At this time, genetic analysis revealed a point mutation in mitochondrial DNA 11778.Ethambutol can be a risk factor for LHON because the number of reported ethambutol-related LHON cases has increased to four, including the present one. Ethambutol administration to patients with a family history of LHON should be avoided. Jpn J Ophthalmol2006;50:280–283 © Japanese Ophthalmological Society 2006

Purpose To report differences in the coloration of fundus lesions between Asian and Caucasian patients with bilateral diffuse uveal melanocytic proliferation (BDUMP). Cases This syndrome was detected in 2 Japanese patients, 69 and 73 years old, with lung cancer who visited our department complaining of visual disturbances. The coloration of the fundus lesions was investigated in these 2 patients. Results The fundus lesions in the first patient appeared gray or grayish-brown in color at the first visit. Six months later, the fundus appeared as a mixture of white to dark-brown lesions. The fundus in the second patient exhibited a mixture of white, gray, and dark-brown lesions from the first visit. Conclusions The fundus lesions in these BDUMP patients appeared gray or grayish-brown in color at the early stage of the disease, probably because of the abundance of melanin pigments in the uveal melanocytes. At the advanced stage, the fundus exhibited a mixture of dark-brown lesions due to melanin deposits and white, depigmented lesions caused by atrophy and/or necrosis of the melanocytes.

Abstract. 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.

The jitter phenomenon of extraocular muscles (EOMs) was investigated in 11 healthy controls and 42 patients with diplopia and/or blepharoptosis using single fiber electromyography (SFEMG). The authors compared the usefulness of SFEMG of EOMs with two other diagnostic techniques (Tensilon test and the titers of anti-acetylcholine receptor antibodies: Anti-AChR ABs) in the differential diagnosis of myasthenia gravis (MG). The Tensilon test was positive in 72.7% of MG patients. Anti-AChR ABs were detected in 100% of generalized MG patients and in 63.6% of ocular MG patients. SFEMG demonstrated an abnormal jitter phenomenon in all MG patients. The authors conclude that SFEMG of EOMs is the most decisive examination in the differential diagnosis of ocular MG, and recommend its use when the etiology of fluctuating diplopia and blepharoptosis cannot otherwise be established.

A recording of a single NMU discharge of the human extraocular muscle is suitable for obtaining information about several muscle fibers together with the activity of their original motoneuron in eye movement disorders.Neurogenic extraocular muscle paralysis in 46 cases was analysed by a single NMU discharge recorded by EMG examination. One of the most important electromyographical findings in anticipating recovery was the regularity of a single NMU discharge. Regularity was recognized about one week after the onset of incomplete paralysis and about three weeks after the onset of complete paralysis. Good recovery can be expected when the regularity of the single NMU discharge is recognized three to four weeks after onset and the discharge rate has increased in the intact eye even when the paralysed muscle did not show any clinical movement. The prognosis is poor when regularity is not recognized in the paralysed muscle about four weeks after onset.