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Show Letters to the Editor Ocular Motor Dysfunction Due to Brainstem Disorders I enjoyed the excellent review article by Lee et al (1) entitled "Ocular Motor Dysfunction Due to Brainstem Disorders." After reading the possible causes of internuclear ophthalmoplegia (INO), I did not see where giant cell arteritis (GCA) was referenced, and this reminded me of a patient whom I recently evaluated. A 72-year-old man reported a 7-day history of sudden-onset oscillopsia and horizontal diplopia accompanied bolization from inflamed segments of the vertebral or basilar arteries (4,8). This letter serves as a reminder of yet another neuro-ophthalmic disorder that GCA can produce. Michael S. Vaphiades, DO Departments of Ophthalmology, Neurology and Neurosurgery, University of Alabama, Birmingham, Alabama Supported in part by an unrestricted grant from the Research to Prevent Blindness, Inc, New York, NY. FIG. 1. Brain MRI. A. Axial fluid-attenuated inversion recovery image scan at the level of the pons is unremarkable but diffusion-weighted imaging (B) shows restricted diffusion in the area of the right medial longitudinal fasciculus, confirmed on the apparent diffusion coefficient map (C). by a headache. He denied jaw claudication, scalp tenderness, fever, or chills, but experienced a 20-pound weight loss thought to be related to a pancreatic cyst. He also had a history of thrombocytosis. On examination, his afferent visual system was normal. Ocular motility showed a right INO and rotary nystagmus with the fast phase toward the patient's left and gazeevoked vertical nystagmus. The remainder of the ophthalmic and neurologic examinations were unremarkable. He was hospitalized and sedimentation rate was 58 mm/ h, C-reactive protein was 127.5 mg/L (0-10.9 mg/L), and platelet count was 572,000/mm3 (normal: 150,000- 400,000/mm3). Brain MRI revealed a lacunar infarct on the right side of the pons involving the medial longitudinal fasciculus (Fig. 1). Intravenous methylprednisolone (IVMP) 1,000 mg was instituted and a temporal artery biopsy confirmed the diagnosis of GCA. After 3 days of daily IVMP and 1 week of 80 mg daily oral prednisone, the patient's eye movements and symptoms began to improve. On follow-up 10 weeks later, the INO had resolved completely. GCA is a rare cause of INO (2-7). It has been postulated that the cause of INO in GCA is likely due to thromboem566 The author reports no conflicts of interest. REFERENCES 1. Lee SH, Kim HJ, Kim JS. Ocular motor dysfunction due to brainstem disorders. J Neuroophthalmol. [published ahead of print November 2, 2017] doi: 10.1097/WNO.0000000000000583. 2. Thomson GT, Johnston JL, Sharpe JA, Inman RD. Internuclear ophthalmoplegia in giant cell arteritis. J Rheumatol. 1989;16:693-695. 3. Crompton JL, Burrow DJ, Iyer PV. Bilateral internuclear ophthalmoplegia-an unusual initial presenting sign of giant cell arteritis. Aust N Z J Ophthalmol. 1989;17:71-74. 4. Trend P, Graham E. Internuclear ophthalmoplegia in giant-cell arteritis. J Neurol Neurosurg Psychiatry. 1990;53:532-533. 5. Johnston JL, Thomson GT, Sharpe JA, Inman RD. Internuclear ophthalmoplegia in giant-cell arteritis. J Neurol Neurosurg Psychiatry. 1992:55:84-85. 6. Hughes TA, Wiles CM, Hourihan M. Cervical radiculopathy and bilateral internuclear ophthalmoplegia caused by temporal arteritis. J Neurol Neurosurg Psychiatry. 1994;57:764-765. 7. Ahmad I, Zaman M. Bilateral internuclear ophthalmoplegia: an initial presenting sign of giant cell arteritis. J Am Geriatr Soc. 1999;47:734-736. 8. Gibb WR, Urry PA, Lee AJ. Giant cell arteritis with spinal cord infarction and basilar artery thrombosis. J Neurol Neurosurg Psychiatry. 1985;48:945-948. Letters to the Editor: J Neuro-Ophthalmol 2018; 38: 566-574 Copyright © North American Neuro-Ophthalmology Society. Unauthorized reproduction of this article is prohibited. |