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Show Superior Oblique Myokymia Following Endoscopic Arterial Ligation for Epistaxis Ligation of the anterior ethmoidal and sphenopalatine arteries is a common surgery for control of intractable epistaxis. Injury to the extraocular muscles and transient diplopia are potential complications of this procedure (1), and several cases of superior oblique palsy (SOP) have been reported (2-4). Transient superior oblique muscle dys-function may be masked by decreased visual acuity in the setting of postoperative swelling (3). We report a case of superior oblique myokymia (SOM) occurring shortly after endoscopic arterial ligation for epistaxis, speculating that it shares a common ischemic pathogenesis with SOP. A 38-year-old man who underwent endoscopic ligation of the right sphenopalatine and anterior ethmoidal arteries for recurrent epistaxis complained of ‘‘jumping'' of his right eye starting within a month after the surgery. He described countless daily episodes of vertical oscillopsia in the right eye lasting seconds and accompanied by binocular vertical diplopia. Brain/orbit MRI and MRA were normal. When his symptoms persisted, he consulted us 16 months post-operatively. We noted a prominent torsional microtremor of the right eye consistent with SOMas the only abnormality. Given the temporal correlation between the endoscopic surgery and onset of symptoms, we believe that the surgery was a contributing if not causative factor of SOM in this case. Several mechanisms have been proposed regarding the etiology of SOP following anterior ethmoidal and internal maxillary artery ligation for epistaxis. Couch et al (2) reported 2 cases of SOP, attributing it either to hematoma leading to periosteal elevation and trochlear displacement, posterior orbital hematoma causing compression of the fourth cranial nerve, or superior oblique muscle ischemia. Jacobson and Pesicka (3) reported a case of SOP following ligation of the internal maxillary, anterior ethmoidal, and posterior eth-moidal arteries. The palsy resolved within 5 months, and they suggested ligation-induced muscle ischemia as the cause. Lee (5) reported 2 cases of SOM preceded by SOP, speculating that the SOM represented a postdenervation phenomenon of the superior oblique muscle or aberrant nerve regeneration following a fourth cranial nerve lesion. We believe that our patient developed permanent SOM following arterial ligation as a consequence of ischemia to the fourth cranial nerve at the orbital level. The SOM in this case may have represented a milder form of ischemic injury than that resulting in SOP. Clifford Meyers, BA Division of Ophthalmology, The Warren Alpert Medical School of Brown University, Providence, Rhode Island Marjorie A. Murphy, MD Division of Ophthalmology, The Warren Alpert Medical School of Brown University, Providence, Rhode Island margiemurphy@cox.net REFERENCES 1. Kirchner JA. Current concepts in otolaryngology. New Engl J Med. 1982;307:1126-1128. 2. Couch JM, Somers ME, Gonzalez C. Superior oblique muscle dysfunction following anterior ethmoidal artery ligation for epistaxis. Arch Ophthalmol. 1990;108:1110-1113. 3. Jacobson DM, Pesicka GA. Transient superior oblique palsy following arterial ligation for epistaxis. Arch Ophthalmol. 1991;109:320-321. 4. Christmann LM, Wolin MJ. Superior oblique palsy as a complication of anterior ethmoidal artery ligation. Arch Ophthalmol. 1991;109:767. 5. Lee JP. Superior oblique myokymia: a possible etiologic factor. Arch Ophthalmol. 1984;102:1178-1179. Meyers and Murphy: J Neuro-Ophthalmol 2010; 30: 169 169 Clinical Observation Copyright © North American Neuro-ophthalmology Society.Unauthorized reproduction of this article is prohibited. |
