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Divisional oculomotor nerve paresis caused by intrinsic brainstem disease.

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Divisional Oculomotor Nerve Paresis
Caused by Intrinsic Brainstem Disease
Susan M. Ksiazek, MD," Michael X. Repka, MD," Albert Maguire, MD,T Robert C. Harbour, MD,f
Peter J. Savino, MD," Neil R. Miller, MD,? Robert C. Sergott, MD," and Thomas M. Bosley, MD"
Two patients with findings ascribable to superior branch oculomotor nerve paresis and one patient with findings
ascribable to an inferior branch paresis are described. I n each patient the paresis was caused by an intra-axial midbrain
lesion. These patients represent the first described cases of divisional oculomotor nerve paresis caused by intrinsic
brainstem disease.
Ksiazek SM, Repka MX, Maguire A, Harbour RC, Savino PJ, Miller NR, Sergott RC, Bosley TM.
Divisional oculomotor nerve paresis caused by intrinsic brainstem disease. Ann Neurol 1989;26:714-718
The oculomotor nerve divides into superior and inferior divisions in the cavernous sinus. Divisional pareses are, therefore, classically localized either in the
anterior cavernous sinus or in the posterior orbit.
Nevertheless, divisional oculomotor paresis has been
described in patients with lesions affecting the subarachnoid portion of the oculornotor nerve {I).
We report 3 patients in whom ocular misalignment
patterns of a divisional oculomotor nerve paresis resulted from damage to the fascicular portion of the
oculomotor nerve in the midbrain.
Case Reports
Patient 1
A 66-year-old woman began to experience intermittent dizziness. Three days later she developed a mild rght upper lid
ptosis. One day after the ptosis began, she suddenly developed binocular vertical diplopia associated with an unsteady
gait.
Visual acuity was 617.5 in each eye (OU). Pupils were 5
mm each and briskly reactive to light and near stimulants.
There was no relative afferent pupillary defect (RAPD).
There was 4 mm of right upper lid ptosis. The right eye had
reduced sursumduction, but otherwise had normal ductions.
There was a 25 prism diopter (PD) right hypotropia in primary position. The hypotropia increased to 40 PD in attempted upward gaze (Fig 1).
Neurological examination demonstrated increased tone of
the left leg with an equivocal left Babinski's reflex and a brisk
left knee jerk. There was mild dysmetria of the left side. The
patient's gait was wide based, and she was unable to perform
tandem walking. Cognitive function, speech, strength, reflexes, and sensation were otherwise normal.
Magnetic resonance imaging (MRI) with a 1.5-Tesla Gen-
From the *Neuro-Ophthalmology Service, the Wills Eye Hospital,
Philadelphia, PA; the tWilmer Ophthalmological Institute, Johns
MD; and the
Of
Hopkins
Georgia, Augusta, GA.
eral Electric Signa Unit showed changes consistent with ischemia on long repetition time (TRj and short echo time (TE)
as well as long TR and long TE images in the central tegmentum at the mesencephalic-pontine junction and in the middle
and lateral third of the right cerebral peduncle (Fig 2). The
patient was stable at 2 weeks and subsequently was lost to
follow-up.
Patient 2
A 30-year-old previously healthy man underwent uncomplicated extraction of several impacted teeth after anesthesia
using local injection of 2% xylocaine. Postoperatively, he
had a dull headache and mouth pain for which he was given
oxycodone hydrochloride. Four days later, he awoke with
painless vertical diplopia
In the emergency room of the Wilmer Eye Institute he
had visual acuity of 6/6 OU with normal color perception
using Hardy-Rand-Rittler pseudoisochromatic plates. Visual
fields were full. The right pupil measured 5 mm in dim light
and was sluggishly (1 +) reactive to direct and consensual
light. The left pupil measured 3 mm in dim light and was
briskly (4 +) reactive to direct and consensual light.
There was no RAPD. There was no ptosis or proptosis.
The right eye had limitation of adduction and depression.
Abduction and elevation were normal (Fig 3). The left eye
had full extraocular movements. Forced ductions were normal. There was a dysconjugate, torsional jerk nystagmus with
the larger amplitude in the right eye. The fast phase of the
nystagmus was counterclockwise. Corneal and facial sensation were normal and symmetrical bilaterally. Ophthalmoscopic findings were normal bilaterally. The remainder of the
neurological examination was unremarkable.
A computed tomographic (CT) scan showed a density
compatible with hemorrhage in the mesencephalon (Fig 4Aj.
The lesion seemed to be in the midline or slightly to the
Received Jan 12, 1989, and in revised form Mar 20 and Apr 19.
Accepted for publication Apr 20, 1989.
Address correspondence to Dr Savino, Neuro-Ophthdmology Service, Wills Eye Hospital, Ninth and Walnut Streets, Philadelphia,
PA 19107.
714 Copyright 0 1989 by the American Neurological Association
A
B
Fig 1. Right superior division III nerve paresis.
right. The results of an MRI scan confirmed the CT findings
(Fig 4B). Although cerebral arteriography showed no evidence of an arteriovenous malformation or other vascular
anomaly, the patient was thought to have bled from a cryptic
arteriovenous malformation that damaged the interstitial nucleus of Cajal and the portion of the right oculomotor nerve
fascicle destined to become the inferior division of the
oculomotor nerve. The patient’s diplopia cleared completely
in 6 weeks.
Patient 3
A 25-year-old woman experienced the acute onset of
binocular vertical diplopia and drooping of the right upper
Fig 2. Ischemia-right superior division 111 nerve paresis. (A)
Axialproton denrity (Tr = 3,000 msec; TE = 30 msec) image
shows an iwegular zone of increased signal intensity (arrow)
consistent with infarction within midbrain. This abnormality
lies somewhat more posteriorly and kzterally within the midbrain
tegmentum in the proximal course of nervefibers subtending the
medial and central subnuclei of the oculomotor nucleus. (B) T2weighted image (TR = 3,000 msec; TE = 80 msec) shows
hyperintensity at the same locus.
eyelid. The past medical history was remarkable for an episode of left retrobulbar optic neuritis 1 year earlier.
Visual acuity was (26 OU with normal color vision using
Ishihara color plates. The pupils were equal and briskly reactive to light without an RAPD. There was 4 mm of right
upper lid ptosis in primary position. Ductions revealed decreased elevation of the rght eye, greatest in abduction. Depression, adduction, and abduction were otherwise normal
Ksiazek et al: Division I11 Nerve Paresis 715
A
Fig 3. Right infevor division 111 nerve paresis.
Fig 4. Occult vascular malfrmation-right inferior division 111
nerve paresis. (A) Axial noncontrast computed tomographic scan
shows focal blood in the midbrainjust to the right of midline.
(B) Axial T 1-weighted fast magnetic resonance scan (TR =
150 msec; TE = IS msec;fEip angle = 50 degrees) shows hypointentity e f f t at the site ofpresumed blood on computed tomography, consistent with old blood breakdown products (hemosiderinj. This might befound with occult vascular malformations.
The lack of evidence for enlarged blood vessels at the site excludes
a nonoccult arteriwenous vascular malformution. This abnormality Iies centrally in the midbrain tegmentum involving
oculomotor nervejbers arisingfmm the lateral subnucleus of the
ocnlomotor nucleus.
B
716 Annals of Neurology Vol 26 No 6 December 1989
Fig 6. Multiple sclerosis-superior division III nerve paresis.
Magnetic wsonance axial proton density (TR = 2,000 msec; TE
= 40 mec) image shows high signal intensity area (arrow)
consistent with a zone of demyelination in the mdial aspect of
the right cerebral peduncle. This abnormality lies anterior in the
tegmentum of the midbrain, most likely affecting oculomotor nerve
fiberssubtending medial and central subnuclei of the oculomotor
nucleus just proximal to their joining with other elements t o
form cranial nerve III within the interpeduncular cistern.
vealed a high-intensity signal in the right anterior mesencephalon adjacent to the interpeduncular cistern (Fig 6). Multiple high-intensity periventricular signals were also present.
The diagnosis of multiple sclerosis with mesencephalic involvement was made. Both the upper eyelid ptosis and elevation deficit resolved uneventfully over 3 weeks.
Fig 5. Right superior division III nerve paresis.
(Fig 5). Maddox rod testing revealed an 8-PD right hypotropia that increased in elevation and right gaze, decreased in
left gaze, and cleared in depression. The left eye had full
ductions. Mild bilateral optic disk pallor was noted, but visual
field tested with a Goldmann perimeter were full. A general
neurological examination was normal.
CT scan of the head was normal. Complete blood count,
chemistry profile, erythrocyte sedimentation rate, and antinuclear antibody level were all normal. A pattern-reversal
visual-evoked potential revealed bilateral prolonged latency.
Lumbar puncture produced clear cerebrospinal fluid with 2
leukocytes and 1 erythrocyte per cubic millimeter. The
spinal fluid protein was 46 mgldl and glucose was 52 mgidl.
Immunoglobulin G was 4.5 mddl (normal 2.1-4.5 mgldl),
and several oligoclonal bands were present. Myelin basic
protein measured 0.9 ngldl (normal 0-4.0 ng/ml). MRI re-
Discussion
The oculomotor nucleus extends through the entire
dorsal portion of the midbrain. Nerve fibers that supply the levator palpebrae superioris divide into right
and left bundles from one central caudal nucleus. The
other nuclei are represented bilaterally, with the superior rectus being the only subnucleus with conualateral
representation. This subnucleus is located in the more
caudal portion of the nuclear complex. These fibers
cross intraparenchymally, and all fibers run ventrally
and slightly rostrally to exit through the interpeduncular fossa. The oculomotor nerve then courses anteriorly within the subarachnoid space until it pierces the
dura covering the roof of the cavernous sinus. In the
anterior cavernous sinus the oculomotor nerve divides
into superior and inferior divisions. The superior division innervates the levator palpebrae superioris and
the superior rectus muscles, whereas the inferior division innervates the inferior and medial rectus muscles,
the inferior oblique muscle, and the iris sphincter 121.
Ksiazek et al: Division I11 Nerve Paresis 717
Traditionally, divisional oculomotor pareses are localized to the anterior cavernous sinus or posterior
orbit. Aneurysms of the internal carotid artery, diabetes mellitus, enlargement of the third ventricle, and
presumed viral syndromes have all been reported to
cause superior division paresis [3-71. Inferior division
third nerve palsies have been ascribed to viral disorders, trauma, or local orbital disease {8-10].
More recently, 5 cases of superior division oculomotor nerve paresis caused by disease in the subarachnoid space have been described. Guy and colleagues
El} postulated that segregation of fibers occurred
before the anatomical division in the cavernous sinus.
Our 3 cases illustrate that intrinsic brainstem disease
can also produce ocular misalignment identical to a
divisional third nerve paresis. Two of the three patients had other signs suggesting a brainstem process.
The lesion was confirmed in all 3 patients by neuroimaging studies. These cases demonstrate that the
functional separation of the oculomotor nerve into
superior and inferior divisions occurs within the brainstem in the fascicular portion of the nerve.
Each patient had a different process causing the divisional oculomotor nerve paresis: a presumed infarct,
demyelination secondary to multiple sclerosis, and
bleeding from a probable cryptic arteriovenous malformation. The presence of findings consistent with a divi-
sional oculomotor nerve paresis requires imaging of
the entire course of the oculomotor nerve.
It is thus clear that ocular misalignment in a divisional oculomotor nerve pattern may result from damage at any location along the course of the nerve from
the fascicle to the orbit.
References
1. Guy J, Savino PJ, Schatz NJ, et al. Superior division paresis of
the oculomotor nerve. Ophthalmology 1985;92:777-784
2. Warwick R Representation of the extra-ocular muscles in the
oculomotor nuclei of the monkey. J Comp Neurol 1953;98:
449-504
3. Derakhshan I. Superior branch palsy of the oculomotor nerve
with spontaneous recovery. Ann Neurol 1978;4:478-479
4. Feder R. Camp A. Superior branch palsy of oculomotor nerve
and pupillary constriction caused by intracranial carotid artery
aneurysm. Ann Neurol 1979;5:493-495
5. Masucci EF, Kurtzke JF. Diabetic superior branch palsy of the
oculomotor nerve. Ann Neurol 1980;7:493
6. Osher RH, Corbett JJ, Schatz NJ, et al. Neuro-ophthalmologic
complications of enlargement of the third ventricle. Br J Ophthalmol 1978;62:5 36-542
7 . Trobe JD, Glaser JS, Post JD. Meningiomas and aneurysms of
the cavernous sinus. Arch Ophthalmol 1978;96:457-467
8. Cross AG. The ocular sequelae of head injury. Ann R Coll Surg
Engl 1948;2:233-240
9. Susac JO, Hoyt WF. Inferior branch palsy of the oculornotor
nerve. Ann Neurol 1977;2:336-339
10. Walsh FB, Hoyt WF. Clinical Neuro-ophthalmology, vol 1. 3rd
ed. Baltimore: Williams & W i h , 1969:256
718 Annals of Neurology Vol 26 No 6 December 1989
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