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Isolated Superior Rectus Palsy Due to Contralateral Midbrain Infarction

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Isolated Superior Rectus Palsy Due to Contralateral Midbrain Infarction OBSERVATION Isolated Superior Rectus Palsy Due to Contralateral Midbrain Infarction Jee-Hyun Kwon, MD; Sun U. Kwon, MD; Hyo-Sook Ahn, MD; Ki-Bum Sung, MD; Jong S. Kim, MD Background: Isolated superior rectus palsy due imaging showed a tiny infarct at the area of the oculo- to a contralateral midbrain lesion has not been re- motor nucleus on the contralateral side. ported. Conclusion: Isolated superior rectus palsy may be caused by a contralateral midbrain lesion that selec- Case Description: A 71-year-old woman suddenly tively involves crossing superior rectus nerve fibers. developed diplopia. Examination showed that she had isolated superior rectus paresis. Magnetic resonance Arch Neurol. 2003;60:1633-1635 IDBRAIN INFARCTS may the red glass test, maximally separated im- produce ocular motor ages were present on the right, upward paresis without other gaze when the red image was present su- neurological signs.1 perior to the white one. Weakness of a single Although the palpebral fissure in the Mextraocular muscle has also been re- right eye appeared slightly narrow as com- ported to be caused by a small midbrain pared with the left one, the patient and her infarction.1 However, to our knowledge, relatives stated that this had been present isolated contralateral superior rectus palsy long before hospital admission. A fundus ex- had not been reported to be caused by mid- amination showed extorsion of the right eye brain lesions. without a torsional component in the left eye (Figure 1B). Diplopia test findings with REPORT OF A CASE the Hess chart were consistent with the su- perior rectus palsy in the right eye. Mag- A 71-year-old woman with diabetes melli- netic resonance imaging showed a discrete tus and hypertension suddenly devel- infarction in the midbrain anterolateral to oped vertigo and vertical diplopia. On hos- the cerebral aqueduct at the superior col- pital admission 1 day later, neurologic liculi level (Figure 2). Magnetic reso- examination results revealed no extrem- nance angiography findings were normal. ity weakness, sensory changes, dysmet- Over the next few weeks, the patient’s ver- ria, or gait disturbances. There was no an- tical diplopia gradually resolved. isocoria or anhidrosis. Head tilting was not observed. On ocular examination, the pupil size COMMENT was equal and nystagmus was absent in both eyes. On forward gaze, there was Our patient had vertical diplopia and lim- From the Departments of slight hypotropia in the right eye. Supra- ited supraduction of the right eye due to Neurology (Drs J. Kwon, duction of the right eye was significantly a tiny infarction in the contralateral mid- S. U. Kwon, and Kim) and limited, while abduction, adduction, and brain. There were no other neurologic Ophthalmology (Dr Ahn), infraduction movements were within nor- signs except for a slightly narrowed right College of Medicine, University Figure 1A of Ulsan, Asan Medical Center, mal limits ( ). The limitation palpebral fissure, which probably had been and the Department of of supraduction was also observed dur- present before the onset of stroke. Neurology, College of Medicine, ing tests of the Bell phenomenon and ocu- These findings should be differenti- Soonchunhyang University locephalic reflexes. Eyeball movements of ated from ocular tilt reaction, which may (Dr Sung), Seoul, Korea. the left eye were considered normal. On result in vertical diplopia in patients with (REPRINTED) ARCH NEUROL / VOL 60, NOV 2003 WWW.ARCHNEUROL.COM 1633 ©2003 American Medical Association. All rights reserved. Downloaded From: https://jamanetwork.com/ on 09/28/2021 A B Right Eye Left Eye Figure 1. A, Extraocular movements in 9 cardinal positions. Right eye showed supraduction deficit and hypotropia. B, Dysconjugate ocular torsion in fundus photography. There was excyclotorsion in the right eye without incyclotorsion of the left eye. the patient. Second, ocular torsion due to midbrain le- sions should be conjugate, but only the torsion of the right eye was observed in the patient (Figure 1B). Finally, up- ward eyeball movements were absent during tests of the Bell phenomenon and oculocephalic reflexes.2 Al- though extratorsion of the right eye may also be caused by a fourth nerve palsy, red glass examination and Hess test findings were not consistent with the superior ob- lique paresis. Therefore, we considered that the patient had iso- lated superior rectus palsy caused by a contralateral mid- brain lesion, which was probably due to an involvement of the oculomotor nucleus complex. In the midbrain, the oculomotor nuclei extend rostrocaudally at the supe- rior colliculi level, ventral to the cerebral aqueduct. The rostrocaudal length of the complex has been shown to be 6.1 mm in humans.3 The subnucleus subserving the superior rectus is located in the caudal two thirds of the oculomotor nucleus on the contralateral side. Because the decussation of fibers to the superior rectus takes place within the oculomotor nuclear complex, the lesions af- Figure 2. T2-weighted magnetic resonance imaging shows a discrete infarct fecting the nucleus may simultaneously involve the ip- in the left midbrain (arrow). silateral superior rectus subnucleus, as well as the cross- ing fibers, resulting in bilateral superior rectus palsy.4,5 brainstem stroke. The tilting in ocular tilt reaction is con- However, isolated contralateral superior rectus palsy has traversive in patients with pontomesencephalic brain- been reported with concomitant paralysis of some of the stem lesions involving the rostral medial longitudinal fas- ipsilateral extraocular muscles, such as the inferior rec- ciculus or the interstitial nucleus of Cajal, while it is tus or the medial rectus.6-8 ipsiversive in patients with medullary lesions.2 Ocular tilt It has been shown that the crossing nerve fibers reaction was ruled out in the patient because of the fol- subserving the contralateral superior rectus arise mainly lowing observations. First, there was no head tilting in in the dorsoventral area of the caudal one third to one (REPRINTED) ARCH NEUROL / VOL 60, NOV 2003 WWW.ARCHNEUROL.COM 1634 ©2003 American Medical Association. All rights reserved. Downloaded From: https://jamanetwork.com/ on 09/28/2021 9 half of the nucleus. On the other hand, no crossing REFERENCES fibers are seen in the rostral half of the nucleus.9 There- fore, we speculate that a lesion localized at the caudal one third to one half of the oculomotor nucleus may 1. Kim JS, Kang JK, Lee SA, Lee MC. Isolated or predominant ocular motor nerve have selectively involved the crossing fibers toward the palsy as a manifestation of brain stem stroke. Stroke. 1993;24:581-586. contralateral superior rectus, causing isolated superior 2. Brandt T, Dieterich M. Vestibular syndromes in the roll plane: topographic diag- nosis from brainstem to cortex. Ann Neurol. 1994;36:337-347. rectus palsy on the side contralateral to the lesion. 3. Marinkovic S, Marinkovic Z, Filipovic B. The oculomotor nuclear complex in hu- mans: microanatomy and clinical significance. Neurologija. 1989;38:135-146. Accepted for publication July 21, 2003. 4. Brazis PW. Localization of lesions of the oculomotor nerve: recent concepts. Mayo Author contributions: Study concept and design (Drs Clin Proc. 1991;66:1029-1035. 5. Warwick R. Representation of the extra-ocular muscles in the oculomotor nu- Sung and Kim); acquisition of data (Drs Jee-Hyun Kwon, clei of the monkey. J Comp Neurol. 1953;98:449-503. Sun U. Kwon, and Ahn); drafting of the manuscript (Drs 6. Warren W, Burde RM, Klingele TG, Roper-Hall G. Atypical oculomotor paresis. Jee-Hyun Kwon, Sun U. Kwon, Ahn, Sung, and Kim); criti- J Clin Neuroophthalmol. 1982;2:13-18. cal revision of the manuscript for important intellectual con- 7. Eustace P. Partial nuclear third nerve palsies. Neuro-ophthalmology. 1985;5: tent (Dr Kim); study supervision (Dr Kim). 259-262. 8. Dehaene I, Marchau M, Vanhooren G. Nuclear oculomotor nerve paralysis. Neuro- Corresponding author: Jong S. Kim, MD, Department ophthalmology. 1987;7:219-222. of Neurology, Asan Medical Center, Song-Pa PO Box 145, 9. Bienfang DC. Crossing axons in the third nerve nucleus. Invest Ophthalmol. 1975; Seoul 138-600, Korea (e-mail: [email protected]). 14:927-931. Call for Papers ARCHIVES Express The ARCHIVES launched a new ARCHIVES Express section in the September 2000 issue. This section will enable the editors to publish highly selected papers within approxi- mately 2 months of acceptance. We will consider only the most significant research, the top 1% of accepted pa- pers, on new important insights into the pathogenesis of disease, brain function, and therapy. We encourage authors to send their most exceptional clinical or basic research, designating in the cover letter a request for ex- pedited ARCHIVES Express review. We look foward to pub- lishing your important new research in this accelerated manner. Roger N. Rosenberg, MD Editor (REPRINTED) ARCH NEUROL / VOL 60, NOV 2003 WWW.ARCHNEUROL.COM 1635 ©2003 American Medical Association. All rights reserved. Downloaded From: https://jamanetwork.com/ on 09/28/2021.
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