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Show Reply-Optic Disc Doubling or Pseudo-Optic Disc in Colobomatous Retinal Abnormality? We thank Gerth-Kahlert and Wildberger for their com-ments on our article dealing with optic disc doubling (1). In their case, the blood vessels that appear to arise from the coloboma inferior to the disc are actually a continuation of the blood vessels emerging from the optic disc. This is an example of a lesion simulating the optic disc or pseudo-disc doubling. In contrast, in our patient, there is no connection on the surface of retina between the 2 groups of vessels. The emerging retinal vasculature from the optic disc has a normal configuration except for an absent inferotemporal venous trunk. The superonasal part of the inferior disc is occupied by the cup, and the inferonasal portion shows the origin of another independent but incomplete retinal vascular sys-tem. It consists of superotemporal and inferotemporal venous and superotemporal and inferonasal arterial arcades, converging at one point. There is a single foveal avascular zone corresponding to the true optic disc at a level slightly lower than its normal position. The inferotemporal portion of the perifoveal capillary net is formed by the tributaries from the superotemporal vascular arcade from the second disc. Fundus fluorescein angiography shows simultaneous and similar filling patterns of both vascular systems. The arcuate visual field defect in our patient demon-strates that the inferior optic disc is nonfunctioning. The hypopigmented bridging track possibly indicates an embryological relationship between the 2 discs. The 2 separate vascular systems, the presence of 2 blind spots on visual field testing, and the crater-like depression over the inferior disc in optical coherence tomography (OCT) suggest that our patient has true doubling of the optic disc. With regard to our OCT findings, unfortunately we do not have a horizontal line scan passing across the inferior disc to show nasotemporal asymmetry of the nerve fiber layer. We agree with Gerth-Kahlert and Wildberger that discontinuation of the junction of the inner and outer photoreceptor segment is difficult to assess because of the quality and angulation in the scan. Ultrahigh resolution OCT passing across both optic discs would give better delineation of the adjacent retinal architecture. Tapas R. Padhi, MS Consultant, Department of Retina and Vitreous, LV Prasad Eye Institute, Bhubaneswar, India drtapasranjan@yahoo.co.in The authors report no conflicts of interest. REFERENCE 1. Padhi TR, Samal B, Kesarwani S, Basu S, Das T. Optic disc doubling. J Neurophthalmol. 2012;32:238-239. Idiopathic Intracranial Hypertension in a Child With Obstructive Sleep Apnea Cured by Tonsillectomy/Adenoidectomy We read with interest Dr Michael Wall's editorial on idiopathic intracranial hypertension (IIH) (1). We describe a surgically treatable case of IIH associated with obstructive sleep apnea (OSA). A 9-year-old girl presented to our emergency department with complaints of diplopia, headaches, nausea, and vomit-ing for 5 days associated with mild neck stiffness. She was taking no medications. Her height was 62 inches, weight 159 lbs for a body mass index of 29, (over the 95th percentile for girls her age and height). Visual acuity was 20/40, right eye and 20/25, left eye. Pupillary reactions, color vision, and confrontation visual fields were normal. Extra-ocular motility demonstrated limited abduction bilaterally. Funduscopic examination revealed mild bilateral optic disc swelling with dilated retinal vessels without hemorrhage or exudate. Neurological examination was normal. Automated visual fields performed 3 days later showed superior arcuate scotomas in each eye and a nasal step in the right eye. Magnetic resonance imaging of the brain was normal as was magnetic resonance venography. Opening pressure on lumbar puncture was greater than 50 cm H2O, and cerebro-spinal fluid analysis was normal. The patient was diagnosed with IIH and prescribed 500 mg of acetazolamide 4 times a day. This was eventually reduced to 500 mg twice a day. Her diplopia resolved, but 6 months later, she complained of Letters to the Editor: J Neuro-Ophthalmol 2013; 33: 412-423 413 Letters to the Editor Copyright © North American Neuro-Ophthalmology Society. Unauthorized reproduction of this article is prohibited. intractable headaches and had worsening papilledema. Open-ing pressure on repeat lumbar puncture was 44 cm H2O. At this point, the patient's mother reported that the child had OSA, which was diagnosed 2 years previously. Polysomnographic studies had demonstrated severe OSA with a respiratory disturbance index of 21 events per hour. The patient was irregularly using a continuous positive air-way pressure machine. On physical examination, the patient was found to have hypertrophic tonsils and adenoids with complete obstruc-tion of her nasopharynx. She underwent adenotonsillec-tomy and postoperatively reported immediate relief of her headaches. At her last visit, she had complete resolution of all symptoms referable to IIH and subjective improvement in her sleeping pattern. Recent studies have suggested a potential relationship between IIH and OSA (2-6). The nocturnal hypoxemia and hypercarbia present during apneic episodes cause ce-rebral vasodilation and secondary increased ICP (7). OSA may be a risk factor in the worsening of IIH, the impor-tance of which is compounded by the fact that the 2 con-ditions frequently coexist in patients with obesity. Screening for papilledema is recommended in all patients with OSA who have visual symptoms (8,9). In children who are found to have OSA and IIH, airway obstruction caused by adenotonsillar enlargement should be consid-ered. We are not aware of previously reported cases where the removal of adenotonsillar tissue led to significant im-provement in OSA and resolution of intracranial hypertension. Evelyne Kalyoussef, MD Nneka O. Brooks, MD Huma Quraishi, MD Roger Turbin, MD Larry Frohman, MD Departments of Otolaryngology-Head and Neck Surgery (EK, HQ), Ophthalmology and Visual Sciences (NO, RT, LF), and Neurology and Neurosciences (LF), Rutgers New Jersey Medical School, Newark, New Jersey The authors report no conflicts of interest. Presented at Triological Society Combined Sections Meeting, January 27-29, 2011, Scottsdale, AZ. REFERENCES 1. Wall M. Idiopathic intracranial hypertension and the idiopathic intracranial Hypertension Treatment Trial. J Neuroophthalmol. 2013;33:1-3. 2. Quinn AG, Gouws P, Headland S, Oades P, Pople I, Taylor D, Benton JS, Buncic JR, Henderson J, Fleming P. Obstructive sleep apnea syndrome with bilateral papilledema and vision loss in a 3-year-old child. J AAPOS. 2008;12:197-199. 3. Hanigan WC, Zallek SN. Headaches, shunts, and obstructive sleep apnea: report of two cases. Neurosurgery. 2004;54:764- 768; discussion 768-760. 4. Marcus DM, Lynn J, Miller JJ, Chaudhary O, Thomas D, Chaudhary B. Sleep disorders: a risk factor for pseydotumor cerebri. J Neuroophthalmol. 2001;21:121-123. 5. Lee A. Pseudotumor and sleep apnea. J Neuroophthalmol. 2001;21:235. 6. Wall M, Purvin V. Idiopathic intracranial hypertension in men and the relationship to sleep apnea. Neurology. 2009;72:300-301. 7. Purvin VA, Kawasaki A, Yee RD. Papilledema and obstructive sleep apnea syndrome. Arch Ophthalmol. 2000;118:1626-1630. 8. Waller EA, Bendel RE, Kaplan J. Sleep disorders and the eye. Mayo Clin Proc. 2008;83:1251-1261. 9. Jindal M, Hiam L, Raman A, Rejali D. Idiopathic intracranial hypertension in otolaryngology. Eur Arch Otorhinolaryngol. 2009;266:803-806. A Limited Form of Neuromyelitis Optica With a Lesion of the Fourth Nerve Nucleus We read with great interest the review article "Neuro-myelitis optica" by Morrow and Wingerchuk (1). The authors referred to several reports of abnormal eye move-ments in association with brainstem lesions in NMO (2-4). We evaluated a patient with a limited form of NMO with a fourth nerve palsy. A 62-year-old woman with a history of numbness in the legs, nausea, and repeated vomiting presented with vertical diplopia and numbness in the left arm and chest. Neuro-ophthalmic testing demonstrated visual acuity of 20/20 in both eyes, full visual fields, and normal ophthalmoscopy. The patient had a right hypertropia that increased in left gaze and head tilt to the right. Ocular motility was otherwise unremarkable. Magnetic resonance imaging (MRI) showed hyperin-tense areas in the midbrain, pons, and medulla (Fig. 1) and in the spinal cord from C5 to T1 (Fig. 2). NMO antibody was positive, whereas acetylcholine receptor, nuclear, SS-A, and SS-B antibodies were all negative. Cerebrospinal fluid analysis revealed no oligoclonal bands. The patient was diagnosed with a limited form of NMO due to the presence of NMO antibody and longitudinally extensive spinal cord lesions. She was treated with intravenous methylprednisolone pulse ther-apy (1,000 mg daily for 3 days) followed by oral prednisolone (10 mg/day with gradual taper). Two months after the third pulse, vertical diplopia had almost 414 Letters to the Editor: J Neuro-Ophthalmol 2013; 33: 412-423 Letters to the Editor Copyright © North American Neuro-Ophthalmology Society. Unauthorized reproduction of this article is prohibited. |
