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CASE REPORT
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J 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
1
Departments 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 associated 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 infarction 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.
Introduction
A lesion of the medial longitudinal fasciculus (MLF) results in an ipsilateral adduction deficit, and a contralateral
abducting nystagmus and is often called internuclear ophthalmoplegia (INO).1 The interneurons of the MLF are intermixed with the abducens neurons in the sixth-nerve nucleus, which lies dorsally in the pons near the genu of the seventh cranial nerve. A lesion in the facial colliculus produces a combination 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 nystagmus accompanied by peripheral facial palsy in facial colliculus infarction.
Case Report
An 83-year-old male patient with hypertension and diabetes mellitus was admitted to our neurology department due to
vertical diplopia that had developed suddenly. His initial blood pressure was 145/65 mm Hg, blood glucose was 175 mg/
Address for correspondence: Sook Young Roh, MD
Department of Neurology, Pundang Jesaeng General Hospital, 255-2
Seohyon-dong, Bundang-gu, Seongnam 463-050, Korea
Tel: +82-31-779-0879, Fax: +82-31-779-0879
E-mail: [email protected]
dL, and Hb A1c was 9.8%. Ocular examination showed bilateral pupils of normal size with prompt direct light reflexes.
But bilateral adduction palsy with normal convergence, rightward 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 noted, 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 corresponding high signal intensity on T2 weighted image/fluidattenuated inversion recovery imaging (Fig. 2). He was prescribed 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 lesion. 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
Copyright © 2011 The Korean Neurocritical Care Society
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J Neurocrit Care ▌2011;4:11-13
FIGURE 1. Ocular examination shows bilateral medial gaze limitations.
MLF
Facial colliculus
Vestibular nuclei
Inferior cerebellar peduncle
4th ventricle
Superior cerebellar peduncle
Reticular formation
Middle cerebellar peduncle
Spinal tract and nucleus of
trigeminal nerve
Medial leminiscus
Transverse pontine fibers
Trapezoid body
Facial nerve (7)
Abducent nerve (6)
Bundles of corticospinal and
corticonucler fibers
Groove for basillar artery
FIGURE 2. Brain MRI findings on the first day of admission. The axial
diffusion weighted image and fluid-attenuated inversion recovery image shows focal high sinal intensity in the right facial colliculus (arrow).
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 deficits due to extension of the MLF lesion into adjacent brainstem 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 adduction palcy, abduction limitation and peripheral facial palsy
in INO.6-8 However, INO is rarely associated with rotatory nystagmus.9 Lesions responsible for rotatory nystagmus with INO
12
FIGURE 3. Anatomic localization of
the patient in axial section through
the pons at the level of facial colliculus. 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 colliculus. 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 deviation 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 vestibular nuclei or INC. His bilateral adduction gaze palsy and rotatory 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 transient ipsiversive rotatory nystagmus. In contrast, his ipsilateral
lateral gaze limitation and peripheral facial palsy were remained for one month. It may result from involvement of the
abducens nerve nucleus and facial nerve fibers.
A Case of Internuclear Ophthalmoplegia with Transient Rotatory Nystagmus in Facial Colliculus Infarction ▌SY Roh, et al.
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