| OCR Text |
Show Photo and Video Essay Section Editors: Melissa W. Ko, MD Dean M. Cestari, MD Peter Quiros, MD Isolated Oculomotor Neuritis After Dengue Fever Manjushree Bhate, MD, Sandeep Ponnaganti, MD FIG. 1. Clinical photograph in primary position at presentation showing deviation and ptosis of the left side and subsequent improvement on follow-up. Abstract: We report a rare case of isolated partial left III cranial nerve palsy due to inflammatory oculomotor neuritis after dengue fever with unique neuro-imaging findings of enhancement seen along the entire course of the oculomotor nerve. Journal of Neuro-Ophthalmology 2021;41:e369–371 doi: 10.1097/WNO.0000000000001223 © 2021 by North American Neuro-Ophthalmology Society A 35-year-old otherwise healthy male patient presented to the neuro-ophthalmology clinic at the L.V.Prasad Eye Institute Hyderabad with complaints of horizontal double vision since 2 weeks. He presented with a background of high-grade fever since 2 weeks with severe thrombocytopenia and was diagnosed as a case of dengue hemorrhagic fever Strabismus, Pediatric and Neuro-Ophthalmology Services (MB), Jasti V Ramanamma Children’s Eye Care Centre, L. V. Prasad Eye Institute, Hyderabad, India; and Department of Neuroradiology (SP), Citi Neuro Centre, Hyderabad, India. The authors report no conflicts of interest. Address correspondence to Manjushree Bhate, MD; E-mail: manjubhate@lvpei.org Bhate and Ponnaganti: J Neuro-Ophthalmol 2021; 41: e369-e371 by his treating physician for which he was admitted and treated with 4 units of platelet transfusion elsewhere. On presentation, his best-corrected visual acuity was 20/20 in each eye. An abnormal head posture with a 15° right face turn and a mild chin down head position was noted. He presented with a primary position exotropia and hypotropia with mild-to-moderate ptosis of the left eye. The ocular motility of the left eye revealed a limitation of adduction of 24 and limitation of elevation and depression of 23. Abduction was noted to be full. The prism cover test for distance revealed an exotropia of 30 Δ with a left hypotropia of 8 Δ, and for near, an exotropia of 35 Δ with a left hypotropia of 6 Δ was observed. A 3-mm ptosis of the left upper eyelid was noted (Fig. 1). The pupil on the left was dilated and nonreactive to light and accommodation. An anisocoria of 2 mm was documented. The left eye anterior and posterior segment examination was normal, and the right eye examination was unremarkable. A working diagnosis of left pupil involving partial III cranial nerve palsy was made, and the patient was advised an urgent MRI with contrast and a MRA to rule out sinister causes such as a posterior communicating artery aneurysm. e369 Copyright © North American Neuro-Ophthalmology Society. Unauthorized reproduction of this article is prohibited. Photo and Video Essay FIG. 2.P recontrast and postcontrast fat-suppressed T1 sagittal and axial images show enhancement of the cisternal, cavernous, and intraorbital segments of the left oculomotor nerve. Precontrast and postcontrast fat-suppressed T1 MRI revealed thickening, signal changes, and enhancement of the left oculomotor nerve from its origin and extending along its entire course in the cisternal and cavernous portion up to its division at the orbital apex and beyond involving individual branches to the superior rectus, medial rectus, and inferior rectus muscles. (Fig. 2A–D). The MRA study of intracranial arterial system was normal, and the rest of the brain study was unremarkable. The patient underwent a complete blood profile, inflammatory markers, and blood glucose levels and tested for HIV, HbsAg, sarcoidosis, tuberculosis, and syphilis that were reported as negative. A physician clearance was obtained and the patient was administered IV methylprednisolone 1 g daily for 3 days, followed by oral steroids of 1 mg/kg body weight that were tapered over a period of 10 weeks. An improvement was noted in the strabismus, range of ocular motility, and ptosis of the left eye on follow-up visits. On 2 months follow-up, a resolution of the diplopia in primary gaze and a full range of ocular motility with residual exotropia of 10 Δ and no ptosis were noted. DISCUSSION Few case reports from the Indian and Southeast Asian subcontinents describe dengue fever-related mononeuropathies or encephalitis. Isolated infective or inflammatory oculomotor neuritis is rare; the unique appearance of the oculomotor nerve after dengue fever on the MRI has not been previously reported. e370 Kapoor et al described ocular manifestations of dengue fever in admitted patients during an epidemic in East India (1). They reported petechial conjunctival hemorrhages and superficial retinal hemorrhages; however, no neuro-ophthalmic complications were noted in their cases. Dengue fever-related encephalitis and isolated abducens nerve palsy in a 20-year-old patient were reported by Mitrakrishnan et al (2). Based on a study conducted by Carod-Artal, the pathogenesis in denguerelated neuro-ophthalmic complications was believed to be immune mediated, although the exact mechanism is not clearly understood (3). The delayed onset of visual symptoms up to 1 week after dengue infection favors the immune-mediated theory (2,3). The spectrum of neuroophthalmic manifestations after dengue fever has been reported to include encephalitis and encephalopathy, as well as myelitis, cerebellitis, mononeuropathies, and Gullian–Barre syndrome (GBS). GBS and variants have been reported to occur as immune-mediated complications, 1 or more weeks after the acute infection (3– 5). However, more recently de Silva et al (6) reported Miller Fisher syndrome in a 70-year-old adult presenting in the acute phase of dengue fever and suggested that Miller Fisher syndrome may be the result of direct neurotrophic effect of the dengue virus. There is limited anecdotal evidence on the use of highdose corticosteroids in postinfectious mononeuropathies, and we cannot be certain if the improved clinical picture in our patient was posttreatment or otherwise spontaneous. Further evidence in such cases with or without treatment may prove beneficial to ascertain the role of corticosteroids. Bhate and Ponnaganti: J Neuro-Ophthalmol 2021; 41: e369-e371 Copyright © North American Neuro-Ophthalmology Society. Unauthorized reproduction of this article is prohibited. Photo and Video Essay STATEMENT OF AUTHORSHIP Category 1: a. Conception and design: M. Bhate and S. Poonaganti; b. Acquisition of data: M. Bhate and S. Poonaganti; c. Analysis and interpretation of data: M. Bhate and S. Poonaganti. Category 2: a. Drafting the manuscript: M. Bhate and S. Poonaganti; b. Revising it for intellectual content: M. Bhate and S. Poonaganti. Category 3: a. Final approval of the completed manuscript: M. Bhate and S. Poonaganti. REFERENCES 1. Harpreet KK, Bhai S, John M, Xavier Jai. Ocular manifestations of dengue in an east Indian epidemic can J Ophthalmol. 2006;41:741–746. Bhate and Ponnaganti: J Neuro-Ophthalmol 2021; 41: e369-e371 2. Shivnthan MC, Ratnayake EC, Wijesiriwardena BC, Somaratna KC, Gamagedara LK. Paralytic squint due to abducens nerve palsy: a rare consequence of Dengue fever. BMJ Infect Dis. 2012;12:156. 3. Carod-Artal FJ, Wichmann O, Farrar J, Gascón J. Neurological complications of Dengue virus infections. Lancet Neurol. 2013;12:906–919. 4. Verma R, Sahu R, Holla V. Neurological manifestations of dengue infection: a review. J Neurol Sci. 2014;346:26– 34. 5. Withana M, Rodrigo C, Chang T, Karunanayake P, Rajapakse S. Dengue fever presenting with acute cerebellitis: a case report. BMC Res Notes. 2014;7:125. 6. de Silva NL, Weeratunga P, Umapathi T. Miller Fisher syndrome developing as a parainfectious manifestation of dengue fever: a case report and review of the literature. J Med Case Rep. 2019 13:120. e371 Copyright © North American Neuro-Ophthalmology Society. Unauthorized reproduction of this article is prohibited. |
