CASE REPORTJ Neurocrit Care 2011;4:11-13 ISSN 2005-0348

A Case of Internuclear Ophthalmoplegia with Transient Rotatory Nystagmus in Facial Colliculus Infarction

Sook Young Roh, MD1, Hyun Jeung Yu, MD1, Ku Eun Lee, MD1, Hyun Seok Kang, MD1, Hyun Kyung Kil, MD2 and Yoon Hee Kim, MD3

1Departments of Neurology, 2Opththalmology, 3Neuroradiology, Bundang Jesaeng General Hospital, Seongnam, Korea

Background: Although internuclear ophthalmoplegia (INO) is a definite sign of an intrapontine or mesencephalic lesion, INO is rarely as-sociated with rotatory nystagmus in pontine lesions. We experienced a case of INO with transient rotatory nystagmus in facial colliculus infarction. Case Report: An 83-year-old male patient was admitted for acute vertical diplopia. Neurological examination revealed bilateral INO with transient ipsiversive rotatory nystagmus and ipsilateral peripheral type facial palsy. Diffusion weighted image revealed focal in-farction in the right facial colliculus. Ocular symptoms were improved within one month. Conclusion: We report a case of bilateral INO with transient rotatory nystagmus in right facial colliculus infarction. J Neurocrit Care 2011;4:11-13

KEY WORDS: Internuclear ophthalmoplegia · Transient rotatory nystagmus · Facial colliculus infarction.

Copyright © 2011 The Korean Neurocritical Care Society 11

Address for correspondence: Sook Young Roh, MDDepartment of Neurology, Pundang Jesaeng General Hospital, 255-2 Seohyon-dong, Bundang-gu, Seongnam 463-050, KoreaTel: +82-31-779-0879, Fax: +82-31-779-0879E-mail: syrohnu@dmc.or.kr

Introduction

A lesion of the medial longitudinal fasciculus (MLF) re-sults in an ipsilateral adduction deficit, and a contralateral abducting nystagmus and is often called internuclear ophth-almoplegia (INO).1 The interneurons of the MLF are intermix-ed with the abducens neurons in the sixth-nerve nucleus, wh-ich lies dorsally in the pons near the genu of the seventh crani-al nerve. A lesion in the facial colliculus produces a combin-ation of INO and peripheral facial palsy. However, INO associated with rotatory nystagmus is rare in pontine lesions and only a few cases have been reported in the literature.2-5 Here we reported a case of INO with transient rotatory nys-tagmus accompanied by peripheral facial palsy in facial col-liculus infarction.

Case Report

An 83-year-old male patient with hypertension and diabe-tes mellitus was admitted to our neurology department due to vertical diplopia that had developed suddenly. His initial blo-od pressure was 145/65 mm Hg, blood glucose was 175 mg/

dL, and Hb A1c was 9.8%. Ocular examination showed bila-teral pupils of normal size with prompt direct light reflexes. But bilateral adduction palsy with normal convergence, right-ward gaze limitation with clockwise rotatory nystagmus in the right eye and horizontal nystagmus in the left eye on leftward gaze were observed (Fig. 1). Right peripheral type facial palsy was also present. No other neurologic abnormalities were not-ed, and skew deviation and head tilting were not observed. On the first day of admission, diffusion weighted image showed acute focal infarction in the right lower pons with restricted diffusion on the apparent diffusion coefficient map and cor-responding high signal intensity on T2 weighted image/fluid-attenuated inversion recovery imaging (Fig. 2). He was pre-scribed a regimen of aspirin and glimepiride. The bilateral INO with ipsiversive rotatory nystagmus had resolved on the sixth day after symptom onset. The ipsilateral lateral gaze limitation and peripheral facial palsy persisted for one month (Fig. 3).

Discussion

INO has diagnostic value in determining the site of the le-sion. The pontine center for lateral eye movement regulates lateral gaze via innervation of the ipsilesional lateral rectus muscle and the contralesional medial rectus through the MLF. Unilateral lesions of the MLF between the midpons and the oculomotor nucleus disconnect the ipsilateral medial rectus

online © ML Comm

J Neurocrit Care ▌ 2011;4:11-13

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subnucleus, causing adduction failure during horizontal gaze. These ocular findings associated with abduction nystagmus of the contralateral eye are collectively referred to as INO. INO is frequently accompanied by a variety of other neurologic de-ficits due to extension of the MLF lesion into adjacent brain-stem structures. A lesion that involves the sixth-nerve nucleus, facial nerve fibers and the interneurons of the MLF near the facial colliculus produces the combination of ipsilateral ad-duction palcy, abduction limitation and peripheral facial palsy in INO.6-8 However, INO is rarely associated with rotatory nys-tagmus.9 Lesions responsible for rotatory nystagmus with INO

are usually located in the MLF above the level of the abducens nucleus and below the level of the trochlear nucleus. An MLF lesion could inactivate the interstitial nucleus of Cajal (INC). The INC is the integrator for ipsiversive rotatory movements and is situated between the red nucleus and the superior collic-ulus. The INC receives excitatory inputs from the vertical semicircular canals of the contralateral labyrinth via the MLF. Projections from the vestibular nuclei or vestibulocerebellum to the INC coordinate torsional gaze. It has been suggested that INC inactivation produces contralesional torsional devia-tion and rotatory ipsilesional nystagmus.10 MRI of our patient revealed a focal infarction in the right dorsomedial portion of the pontine tegmentum. There were no lesions in the vestibu-lar nuclei or INC. His bilateral adduction gaze palsy and rota-tory nystagmus resolved within one week. We suspect that a small facial colliculus lesion involving the MLF may have been responsible for the inactivation of the ipsilateral vertical integrator (the INC), producing INO associated with a tran-sient ipsiversive rotatory nystagmus. In contrast, his ipsilateral lateral gaze limitation and peripheral facial palsy were re-mained for one month. It may result from involvement of the abducens nerve nucleus and facial nerve fibers.

FIGURE 1. Ocular examination sh-ows bilateral medial gaze limitations.

FIGURE 2. Brain MRI findings on the first day of admission. The axial diffusion weighted image and fluid-attenuated inversion recovery im-age shows focal high sinal intensity in the right facial colliculus (arrow).

FIGURE 3. Anatomic localization of the patient in axial section through the pons at the level of facial colliculus.

4th ventricle

Superior cerebellar peduncle

Reticular formation

Groove for basillar artery

MLFFacial colliculus

Vestibular nuclei

Inferior cerebellar peduncle

Medial leminiscus

Trapezoid body

Facial nerve (7)

Abducent nerve (6)

Spinal tract and nucleus of trigeminal nerve

Middle cerebellar peduncle

Transverse pontine fibers

Bundles of corticospinal and corticonucler fibers

A Case of Internuclear Ophthalmoplegia with Transient Rotatory Nystagmus in Facial Colliculus Infarction ▌ SY Roh, et al.

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6. Anderson CA, Sandberg E, Filley CM, Harris SL, Tyler KL. One and one-half syndrome with supranuclear facial weakness: magnetic res-onance imaging localization. Arch Neurol 1999;56:1509-11.

7. Jeong JL, Yi MJ, Kim YJ, Kim HS, Yang HD. Unilateral horizontal gaze paresis without facial palsy from a lesion of the abducens nucle-us. J Korean Neurol Assoc 2009;27:449.

8. Park SW. Medial longitudinal fasciculus syndrome with ipsilateral peripheral facial palsy:7 and 1/2 syndrome. Korean J Stroke 2010;12: 119-20.

9. Bae JS, Song HK, Kim CH, Choi IL, Lee JH, Lee BC. Fifteen-and-a-half syndrome?: one-and-a-half syndrome with facial diplopia. Kore-an J Stroke 2002;4:151-3.

10. Halmagyi GM, Aw ST, Dehaene I, Curthoys IS, Todd MJ. Jerk-wave-form see-saw nystagmus due to unilateral meso-diencephalic lesion. Brain 1994;117:789-803.

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