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Observation
November 2003

Isolated Superior Rectus Palsy Due to Contralateral Midbrain Infarction

Author Affiliations

From the Departments of Neurology (Drs J. Kwon, S. U. Kwon, and Kim) and Ophthalmology (Dr Ahn), College of Medicine, University of Ulsan, Asan Medical Center, and the Department of Neurology, College of Medicine, Soonchunhyang University (Dr Sung), Seoul, Korea.

Arch Neurol. 2003;60(11):1633-1635. doi:10.1001/archneur.60.11.1633
Abstract

Background  Isolated superior rectus palsy due to a contralateral midbrain lesion has not been reported.

Case Description  A 71-year-old woman suddenly developed diplopia. Examination showed that she had isolated superior rectus paresis. Magnetic resonance imaging showed a tiny infarct at the area of the oculomotor nucleus on the contralateral side.

Conclusion  Isolated superior rectus palsy may be caused by a contralateral midbrain lesion that selectively involves crossing superior rectus nerve fibers.

MIDBRAIN INFARCTS may produce ocular motor paresis without other neurological signs.1 Weakness of a single extraocular muscle has also been reported to be caused by a small midbrain infarction.1 However, to our knowledge, isolated contralateral superior rectus palsy had not been reported to be caused by midbrain lesions.

REPORT OF A CASE

A 71-year-old woman with diabetes mellitus and hypertension suddenly developed vertigo and vertical diplopia. On hospital admission 1 day later, neurologic examination results revealed no extremity weakness, sensory changes, dysmetria, or gait disturbances. There was no anisocoria or anhidrosis. Head tilting was not observed.

On ocular examination, the pupil size was equal and nystagmus was absent in both eyes. On forward gaze, there was slight hypotropia in the right eye. Supraduction of the right eye was significantly limited, while abduction, adduction, and infraduction movements were within normal limits (Figure 1A). The limitation of supraduction was also observed during tests of the Bell phenomenon and oculocephalic reflexes. Eyeball movements of the left eye were considered normal. On the red glass test, maximally separated images were present on the right, upward gaze when the red image was present superior to the white one.

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.

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.

Although the palpebral fissure in the right eye appeared slightly narrow as compared with the left one, the patient and her relatives stated that this had been present long before hospital admission. A fundus examination showed extorsion of the right eye without a torsional component in the left eye (Figure 1B). Diplopia test findings with the Hess chart were consistent with the superior rectus palsy in the right eye. Magnetic resonance imaging showed a discrete infarction in the midbrain anterolateral to the cerebral aqueduct at the superior colliculi level (Figure 2). Magnetic resonance angiography findings were normal. Over the next few weeks, the patient's vertical diplopia gradually resolved.

Figure 2.
T2-weighted magnetic resonance imaging shows a discrete infarct in the left midbrain (arrow).

T2-weighted magnetic resonance imaging shows a discrete infarct in the left midbrain (arrow).

COMMENT

Our patient had vertical diplopia and limited supraduction of the right eye due to a tiny infarction in the contralateral midbrain. There were no other neurologic signs except for a slightly narrowed right palpebral fissure, which probably had been present before the onset of stroke.

These findings should be differentiated from ocular tilt reaction, which may result in vertical diplopia in patients with brainstem stroke. The tilting in ocular tilt reaction is contraversive in patients with pontomesencephalic brainstem lesions involving the rostral medial longitudinal fasciculus or the interstitial nucleus of Cajal, while it is ipsiversive in patients with medullary lesions.2 Ocular tilt reaction was ruled out in the patient because of the following observations. First, there was no head tilting in the patient. Second, ocular torsion due to midbrain lesions should be conjugate, but only the torsion of the right eye was observed in the patient (Figure 1B). Finally, upward eyeball movements were absent during tests of the Bell phenomenon and oculocephalic reflexes.2 Although 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 oblique paresis.

Therefore, we considered that the patient had isolated superior rectus palsy caused by a contralateral midbrain lesion, which was probably due to an involvement of the oculomotor nucleus complex. In the midbrain, the oculomotor nuclei extend rostrocaudally at the superior 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 affecting the nucleus may simultaneously involve the ipsilateral superior rectus subnucleus, as well as the crossing fibers, resulting in bilateral superior rectus palsy.4,5 However, isolated contralateral superior rectus palsy has been reported with concomitant paralysis of some of the ipsilateral extraocular muscles, such as the inferior rectus or the medial rectus.68

It has been shown that the crossing nerve fibers subserving the contralateral superior rectus arise mainly in the dorsoventral area of the caudal one third to one half of the nucleus.9 On the other hand, no crossing fibers are seen in the rostral half of the nucleus.9 Therefore, we speculate that a lesion localized at the caudal one third to one half of the oculomotor nucleus may have selectively involved the crossing fibers toward the contralateral superior rectus, causing isolated superior rectus palsy on the side contralateral to the lesion.

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Article Information

Corresponding author: Jong S. Kim, MD, Department of Neurology, Asan Medical Center, Song-Pa PO Box 145, Seoul 138-600, Korea (e-mail: jongskim@amc.seoul.kr).

Accepted for publication July 21, 2003.

Author contributions: Study concept and design (Drs Sung and Kim); acquisition of data (Drs Jee-Hyun Kwon, Sun U. Kwon, and Ahn); drafting of the manuscript (Drs Jee-Hyun Kwon, Sun U. Kwon, Ahn, Sung, and Kim); critical revision of the manuscript for important intellectual content (Dr Kim); study supervision (Dr Kim).

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