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OPTOMETRY Letters to the editor Clin Exp Optom 2014; 97: 187–188
Re: Leber’s hereditary optic neuropathy masquerading as optic neuritis with spontaneous visual recovery Yu-Jiao Zhang MMed Yi Du MD Kaijun Li PhD Jian-Feng He MD Department of Ophthalmology, First Affiliated Hospital of Guangxi Medical University, Nanning, Guangxi, China E-mail: [email protected]
mitochondrial DNA mutation. He was diagnosed with LHON. Currently, it is challenging to differentiate Leber’s optic neuropathy from optic neuritis, especially in Chinese patients. One reason is that there is a relatively high proportion (29 per cent compared with 6.4 to 11 per cent in Caucasian populations4) of bilateral cases in Chinese patients with optic neuritis. Furthermore, up to 60 per cent of these patients have no ocular pain.4 We wish to remind practitioners that thorough clinical and laboratory examinations are necessary for an accurate diagnosis of LHON in Chinese patients.
EDITOR: We read with great interest the article by Hsu and colleagues1 describing a 28-year-old Chinese man with gradual bilateral visual loss treated with methylprednisolone pulse therapy. The patient recovered after 21 months of corticosteroid treatment and mitochondrial DNA analysis revealed a 14484 mutation. As reported by Hsu and colleagues,1 we also find that Leber’s hereditary optic neuropathy (LHON) often masquerades as other optic neuropathies. Du and colleagues2 reported upon a 16-year-old Chinese boy suffered from both LHON and fibrous dysplasia of the orbital bone. The boy had bilateral, painless loss of vision. He was suspected of suffering from compressive optic neuropathy and/or optic neuritis and was treated with methylprednisolone pulse therapy; however, he had no visual recovery. Eventually, an 11778 mitochondrial DNA mutation was detected, ultimately leading to a diagnosis of LHON. Hashemi and colleagues3 documented a 67-year-old Caucasian patient with thyroid eye disease, which had been misdiagnosed as dysthyroid optic neuropathy. His orbital computed tomography demonstrated an increase in fat volume and a stretched optic nerve. The patient was treated with bilateral orbital decompression surgery but his visual acuity worsened. Testing revealed a 14484
1. Hsu TK, Wang AG, Yen MY, Liu JH. Leber’s hereditary optic neuropathy masquerading as optic neuritis with spontaneous visual recovery. Clin Exp Optom 2013; DOI: 10.1111/cxo.12100. 2. Du Y, Jiang B, Li K, Chen Y, He J. Leber hereditary optic neuropathy in a boy with fibrous boney dysplasia. Eye Science 2013; 28: 48–50. 3. Hashemi N, Yalamanchili SS, Zhang J, Lee AG. Leber hereditary optic neuropathy mimicking thyroid-related optic neuropathy. J Neuroophthalmol 2012; 32: 95–96. 4. Du Y, Li K, Yang J, Xu X, Li JJ, Zhou RW, Zhang Y et al. Disc swelling and mild initial visual acuity loss predict a better short-term visual acuity outcome in bilateral acute optic neuritis. J Clin Neurosci 2012; 19: 1380–1382.
Limited blinking could also be involved in watchmakers’ glaucoma Julio González Martín-Moro*† MD PhD Yolanda Fernández de Miguel* MD * Department of Ophthalmology, University Hosopital of Henares, Madrid, Spain † University Francisco de Vitoria, Madrid, Spain E-mail: [email protected]
DOI:10.1111/cxo.12133 EDITOR: We have read with interest the article by Ascaso, Mateo and Grzybowski1 on watchmakers’ glaucoma. We think that it can provide some insight into the pathogenesis
© 2014 The Authors Clinical and Experimental Optometry © 2014 Optometrists Association Australia
of this disease; however, we believe that an alternative hypothesis can be proposed for the pathogenesis of glaucoma in this patient. The authors advanced the theory that a watchmaker’s loupe worn for long periods of time induced elevated intraocular pressure (IOP). They suggested that the stress generated by the orbicularis muscle to hold the loupe could have been directly transmitted to the sclera or could have increased venous pressure; however, we believe that the effect may have been the result of altered blink function. It is known that blinking induces IOP changes2–4 and that pressure oscillations are important for the perfusion of several tissues. Although the loupe is held in place by the orbicular muscle and the periocular muscles, it stretches the skin of the lid, limiting closure. Wearing the loupe could arrest blinking for long periods of time, lessening these beneficial IOP changes. A growing body of evidence relates sleep apnoea syndrome (SAS) and glaucoma. There is still some controversy about this topic because some population studies have failed to confirm this association. Nevertheless, most publications support this link and recent literature expands the spectrum of this association to other ocular diseases, such as non-arteritic ischaemic optic neuropathy, idiopathic intracranial hypertension and floppy eyelid syndrome (FES). Most clinicians accept that SAS produces glaucoma because it induces ischaemia and an altered cortisol cycle could also be involved; however, the mechanism that links SAS and glaucoma still remains unknown. The association between floppy eyelid and SAS is equally mysterious and to make things even more complex, recent studies have found an independent association between FES and glaucoma.5 The authors of that recent paper, could not explain this surprising association but considered that FES could have an effect independent and additional to that due to hypoxia. We think that FES could be part of the pathway that connects SAS and glaucoma. The eyelids are physically in a position to influence the external surface of the eye and each blink induces a transitory increase in Clinical and Experimental Optometry 97.2 March 2014