Eye-Movement Disorders in
Brain-Stem and Cerebellar Stroke
Julien Bogousslavsky, MD, Otmar Meienberg,
\s=b\ Vertebrobasilar strokes can yield
varied disturbances of eye movements,
by affecting specific centers and path-
ways contained in the brain stem and
cerebellum. Unique disorders combining
supranuclear, nuclear, and infranuclear-
syndromes may occur. Some eye-move-
ment abnormalities are useful localizing
signs (eg, gaze palsies, rotatory nystag-
mus, and ipsilateral saccadic bias), but
many others are not. The use of tech-
niques such as magnetic resonance imag-
ing may provide new insights in
clinicotopographic correlations in pa-
tients with good recovery, in the absence
of pathologic verification.
(Arch Neurol 1987;44:141-148)
T~)isorders
common
of
in
eye movements
vertebrobasilar
are
strokes because the brain stem and
cerebellum contain a large number of
structures belonging to the oculomo¬
tor system. Since many of these struc¬
tures have specific functions and are
relatively small, careful clinical anal¬
ysis of eye movements often allows
exact conclusions about the localiza¬
tion and size of a lesion. Such a precise
topographic diagnosis is particularly
useful in the early stage of a stroke,
when computed tomography usually
yields normal results, and it also con-
Accepted publication Aug 4,1986.
for
From the Department of Neurology, Centre
Hospitalier Universitaire Vaudois, Lausanne,
Switzerland (Dr Bogousslavsky) and the Depart-
ment of Neurology, Kantonsspital, Basel, Swit-
zerland (Dr Meienberg).
Reprint requests to the Department of Neurol-
ogy, Centre Hospitalier Universitaire Vaudois,
1011 Lausanne, Switzerland (Dr Bogousslav-
sky).
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MD
stitutes a solid basis for monitoring
the clinical course of the stroke. An
overview of the most important struc¬
tures of the brain-stem ocular motor
system is given in Fig 1. The physio¬
logic correlates of the anatomic struc¬
tures will not be discussed here, as
extensive reviews can be found else¬
where.1"4 The scheme (Fig 1) is con¬
fined to those structures the lesion of
which produces characteristic eye-
movement disorders of high-localiz¬
ing value. Although nystagmus fre¬
quently occurs in acute vascular
lesions of the brain stem or cerebel¬
lum, its localizing value is generally
limited.
In the brain stem, the following
three different levels of involvement
can be defined: the supranuclear,
nuclear, and infranuclear levels.1'4 At
the supranuclear level, the ocular
motor subsystems (pursuit, saccadic,
vestibular, and vergence) can be selec¬
tively affected. For example, in verti¬
cal gaze palsy, voluntary upgaze can
be abolished, while the eyes can be
fully moved upward by the vestibulo-
ocular reflex (elicited by a fast down¬
ward movement of the head), or, in
internuclear ophthalmoplegia (INO),
the affected eye cannot adduct during
lateral gaze, while it can normally
adduct during convergence. Intranu¬
clear ophthalmoplegia, which is, in
fact, a disorder of the internuclear
gaze pathways, is the result of a lesion
of the medial longitudinal fasciculus
(MLF). Lesions of the paramedian
pontine reticular formation (PPRF)
lead to palsies of ipsilateral conjugate
gaze. Lesions that simultaneously
affect the PPRF and the ipsilateral
MLF produce a so-called one-and-a-
half syndrome.5 In partial PPRF
lesions, there can be only a slowing of
the ipsilateral saccades and, some¬
times, a "gaze paretic" nystagmus
with an exponentially decreasing
velocity of the centripetal slow phase.
Conjugate palsies of vertical gaze are
either due to bilateral lesions of the
mesencephalic reticular formation, or
to a lesion of the posterior commis¬
sure. Nuclear lesions differ from
lesions of the corresponding cranial
nerve, since the motoneurons for the
individual eye muscles may be specifi¬
cally grouped, as in the third-nerve
nucleus6 (Fig 1), or since the motoneu¬
rons are intermingled with interneu-
rons, as in the sixth-nerve nucleus. A
caudal lesion of the third-nerve nucle¬
us, for example, can cause a complete
bilateral ptosis with sparing of all
other extraocular muscles. A lesion of
the sixth nerve nucleus produces an
ipsilateral gaze palsy. Infranuclear
lesions affect the fasciculi of the
third, fourth, or sixth nerves before
they leave the brain stem, and lead to
the same eye movement disorder as a
peripheral lesion. Therefore, a dis¬
tinction between a fascicular and a
peripheral lesion is only possible in
the presence of additional brain-stem
signs.
MESENCEPHALON
The arterial territories of the upper
and lower midbrain are schematized
in Fig 2, top and bottom left. The
upper midbrain and the thalamome-
sencephalic junction are supplied
mainly by the posterior thalamosub-
thalamic paramedian branches of the
P, segment of the posterior cerebral
artery,78 but the anterior choroidal

Fig 1.—Schematic view of paramedian brain-stem structures involved in horizontal and vertical
(inset) gaze. Fourth-nerve fibers come from contralateral fourth-nerve nucleus, and MLF comes
from contralateral sixth-nerve nucleus. MLF indicates median longitudinal fasciculus; riMLF,
rostral interstitial nucleus of the MLF; PPRF, paramedian pontine reticular formation; and 2 A
through D refer to sections discussed in Fig 2.
artery occasionally contributes to this
supply.9 In the lower midbrain, the
following five main territories have
been found: the median territory
(third-nerve nucleus, part of MLF),
supplied by direct twigs coming off
the basilar tip, the paramedian (third
intra-axial fibers), intermediolateral
(part of MLF), and lateral (brachium
conjunctivum) territories supplied by
the short circumferential branches of
P„ and the superior or collicular terri¬
tory supplied by the quadrigeminal
(long circumferential) branches of the
superior cerebellar artery (SCA) and
of ,.'·8
Thalamomesencephalic
Junction Syndromes
Small infarcts (due to emboli from
the heart or to basilar occlusion10) or
hemorrhages limited to the region of
the mesencephalic reticular forma¬
tion (MRF, Fig 1) and posterior com¬
missure give rise to rather specific
oculomotor disturbances, with major
involvement of vertical gaze. Upgaze
palsy, downgaze palsy, and complete
vertical gaze palsy are usually related
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to bilateral lesions involving the
region of the rostral interstitial nucle¬
us of the MLF11 (riMLF, Fig 1) and
posterior commissure.6 Selective
downgaze palsy seems to be related to
bilateral involvement of the medio-
caudal region of the riMLF.12 On the
other hand, selective upgaze palsy and
combined downgaze and upgaze palsy
may occasionally be due to a unilater¬
al iesion of the MRF involving the
laterally spreading fibers of the poste¬
rior commissure11·1314; at least ten such
pathologically studied cases have been
reported.1113 In upgaze palsy due to
involvement of the posterior commis¬
sure, upward vestibulo-ocular re¬
sponses are preserved because no ves-
tibulo-oculomotor fibers travel in the
posterior commissure.1214 Rarely, dis¬
sociation of voluntary, pursuit, and
reflex movements involvement has
been reported in downgaze palsy.12·14·15
Sustained upgaze in downgaze palsy
and sustained downgaze in upgaze
palsy are uncommon13·1416; distur¬
bances of vestibular mechanisms by
involvement of the nucleus of Cajal
may be critical for the development of
these phenomena.17 Other distur¬
bances of vertical eye movements may
occur, but are usually much less local¬
izing, for example, skew deviation
with usually the ipsilateral eye up,15
seesaw nystagmus,18 palpebrai nys¬
tagmus of Pick, and retraction of the
upper lid or blepharospasm.4·19 A head
tilt may occur if the region of the
contralateral nucleus of Cajal is
involved4 and may incorrectly suggest
a fourth nerve palsy.
Disturbances of horizontal eye
movements may occur, with decrease
of the contralateral saccades, possibly
from involvement of the anterior cor-
ticopontine pathway before its decus-
sation.20·21 The pseudo-sixth-nerve
palsy corresponds to a slow abducting
movement during the horizontal
refixation,22·23 perhaps from an excess
of convergence tone; convergence-
retractory nystagmus is common412;
organic convergence spasm and paral¬
ysis of convergence or divergence have
also occasionally been reported.4
The pupils may also be abnormal,
according to Fisher,5 a moderate dila¬
tation (4 to 6 mm) suggests a large
lesion involving the sympathetic as
well as the parasympathetic fibers,
whereas a huge dilatation (7 to 10
mm) suggests selective parasympa¬
thetic involvement; dissociation of the
light-near reflex is a classic finding.
While ectopie pupils (corectopia) may
be suggestive of a midbrain stroke,24
oval pupils typically correspond to a
transient phase in progressive injury
to the oculomotor complex that occurs
in more diffuse brain damage.25
In this region, there is very little to
allow the clinician to differentiate a
small hemorrhage from a small
infarct. In hemorrhages with a con¬
spicuous thalamic involvement, conju¬
gate eye deviation opposite to the
lesion (wrong-way eyes) may occur.5
Also, in hemorrhages, sustained
downgaze may be related to secondary
hydrocephalus, not to primary dam¬
age due to the MRF.26
Mesencephalic Syndromes
Acute vascular lesions limited to
the midbrain are more often infarcts
than hemorrhages. These infarcts are
frequently embolie from the heart.27·28
They may involve selective arterial
territories (Fig 2, top and bottom
right) and give rise to oculomotor
syndromes, which can be supranu¬
clear (prenuclear), nuclear, and post-
nuclear (fascicular), with regard to
the oculomotor complex nucleus.
Nuclear lesions of the fourth-nerve
nucleus or intra-axial fibers are usu¬
ally associated with third-nerve
 involvement or more extensive pon-
tomesencephalic strokes.29·31
Prenuclear Syndromes of the Third
Nerve.—These are related to small
infarcts in the most caudal territory
of the posterior thalamo-subthalamic
paramedian arteries or of the anterior
choroidal artery, when this artery
contributes to the blood supply of the
midbrain.9 Typically, a monocular
paresis of elevation of the eye contra-
lateral to the infarct is produced, by
involvement of the fibers traveling
from the upper midbrain to the ipsi¬
lateral subnucleus, which innervates
the contralateral superior rectus.3234
Internuclear ophthalmoplegia is fre¬
quent, because of involvement of the
MLF just before it reaches the oculo¬
motor complex nucleus.33 Bilateral
ptosis can occur and is probably relat¬
ed to partial damage to the central
caudal nucleus.33 In rare cases, the
aspect of a "vertical one-and-a-half
syndrome" may be produced when the
lesion extends toward the upper mid¬
brain, with upgaze palsy and monocu¬
lar downgaze palsy, or downgaze palsy
and monocular upgaze palsy.32·35 A
monocular paresis of elevation has
been reported in an ipsilateral infarct
of the anterior choroidal artery terri¬
tory,9 but the explanation for that is
obscure.
Nuclear Syndrome of the Third
Nerve.—This is produced by an infarct
in the median mesencephalic territo¬
ry7 and has the very characteristic
disturbance of a more or less complete
ipsilateral third-nerve palsy associ¬
ated with a paresis of elevation in the
contralateral eye, due to involvement
of the subnucleus, which innervates
mainly the contralateral superior rec¬
tus.20·21 The primary position of the
eyes is highly suggestive, with ipsilat¬
eral exotropia and contralateral
hypotropia. This paresis of elevation
in both eyes has been called pseudo-
Parinaud's syndrome,20 and must be
differentiated from upgaze palsy due
to supranuclear lesions. Bilateral
mydriasis and bilateral ptosis may
sometimes occur.21 Associated neuro¬
logic disturbances are usually scarce
(eg, somnolence and mild ataxia),
because of the localization of the
infarct.
Associated Supranuclear and Nuclear
Disturbances.—These may occur in
various combinations,27·28 usually in
larger and bilateral mesencephalic
infarcts. Other neurologic distur¬
bances are usually prominent, some¬
times with a mesencephalic "locked-
in" syndrome.36
Bilateral Infarcts or Hemorrhages of
the Periaqueductal Gray Matter.—These
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have been recently reported in
patients showing selective downgaze
or upgaze palsy,17·37 in the absence of
rostral MRF involvement. Involve¬
ment of periaqueductal neurones or of
fibers descending from the MRF
toward the third and fourth nerve
nuclei has been implicated.
Isolated Mesencephalic Hemor¬
rhages.—These are very uncommon.
They usually produce combined
supranuclear and nuclear distur¬
bances of eye movements.38 40 They are
probably due to hypertension or relat¬
ed to small vascular malformations.
Fascicular Syndromes of the Third
Nerve.—These are related to more
ventrolateral infarcts. The third-
nerve palsy may be incomplete, with
pupillary sparing38 and even miosis,
when the descending sympathetic
pathway is involved.21 Associated neu¬
rologic impairment is prominent with
either contralateral hemiplegia (para¬
median territory: syndrome of Weber)
or contralateral ataxia (intermediola-
teral territory: Claude-Nothnagel's
syndrome).21·34·41
PONS
There are two main arterial pontine
networks.42·43 One is formed by direct
paramedian branches off the basilar
artery and indirect intermediate
branches off the short circumferential
arteries. The other network is formed
by lateral branches coming from two
(one on each side) long circumferen¬
tial arteries, the anterior inferior cer¬
ebellar artery (AICA) and the SCA
(Fig 2, top right).
Paramedian Pontine Syndromes
Pontine eye-movement disorders
due to small ischemie paramedian
lesions are common, particularly in
hypertensive patients. The most often
encountered syndrome is INO.44·45
When due to a stroke, INO is general¬
ly of sudden onset and unilateral,
although bilateral INO of vascular
origin is not uncommon.46 Besides a
restriction of adduction with pre¬
served convergence, there is often a
dissociated nystagmus with larger
amplitude in the abducting eye and a
nystagmus evoked by vertical gaze. In
bilateral INO, reflex (vestibular) ver¬
tical eye movements may be abol¬
ished, due to involvement of the ves-
tibulo-oculomotor fibers that travel in
the MLF en route toward the oculo¬
motor and trochlear nuclei.47·48 Some¬
times a skew deviation44·49 is present.
When skew deviation is due to inter¬
nuclear ophthalmoplegia, the eye ipsi¬
lateral to the lesion is usually hyper-
tropic.49 However, this rule is not
absolute,4 and skew deviation by itself
has little localizing value, since it is
also found in pontine lesions sparing
the MLF. Actually, lesions limited to
the midbrain or medulla can produce
a skew deviation.49 Horizontal gaze
palsies can be due to a lesion of the
ipsilateral PPRF or of the abducens
nucleus.48·50"52 In acute vascular lesions,
conjugate deviation of the eyes con¬
tralateral to the lesion may be
present.3·48 In a pure PPRF lesion, the
eyes can still be moved to the paretic
side with vestibular stimuli, which is
not possible in a lesion of the sixth-
nerve nucleus.48·51 In addition, the lat¬
ter is usually accompanied by a
peripheral facial palsy because of the
close vicinity of the facial nerve
knee.53 Isolated vascular lesions of the
abducens nucleus and facial nerve
knee should not be too rare, since one
of us (O.M.) has seen three such cases
within a relatively short time. Partial
lesions of the PPRF do not produce a
gaze palsy, but considerably slow all
ipsilaterally directed saccades.3·54 In
bilateral destruction of the caudal
PPRF, some reports have suggested
that, in addition to horizontal gaze
palsy, there is also vertical gaze palsy,
because of involvement of inputs to
the mesencephalic reticular forma¬
tion52·55; however, the occurrence of
complete ophthalmoplegia from a
lesion limited to the pons remains
controversial. Often, vascular lesions
involve the PPRF or abducens nucleus
together with the ipsilateral MLF (af¬
ter it has crossed the midline coming
from the contralateral abducens
nucleus). The clinical result is a one-
and-a-half syndrome.5·48·51·56 In a
review of the literature, 24 of 49 one-
and-a-half syndromes were of vascu¬
lar origin; 16 one-and-a-half syn¬
dromes were due to an infarct, and
eight of them, to a hemorrhage.56 In
the acute phase, exotropia of the eye
opposite to the lesion may occur (par¬
alytic pontine exotropia)54·57; this is
due to the fact that contralateral ocu¬
lar deviation due to acute paramedian
pontine involvement cannot occur in
the ipsilateral eye, because of INO,
and is, therefore, limited to the con¬
tralateral eye. In the locked-in syn-
drome,42'58-59 tetraplegia and paralysis
of all lower cranial nerves is due to a
mainly ventral pontine lesion; the
patient is fully conscious and typically
can perform only lid and vertical eye
movements, since the patient also has
bilateral horizontal gaze palsy. When
one side of the pontine tegmentum is
spared, such patients can demonstrate
a one-and-a-half syndrome.48 Ocular

bobbing consists of intermittent
downward jerks of the eyes followed
by a slow return to the midposition.60
In the majority of cases, the patients
are comatose, quadriplegic, and have
bilateral gaze palsy due to extensive
intrapontine hemorrhage or infarc¬
tion. However, this clinical picture
may be mimicked by a cerebellar hem¬
orrhage without intrapontine lesion.61
Rarely, typical bobbing may be inter¬
polated with reverse bobbing (rapid
upward movement followed by a slow
return to the midposition).62 A typical
bobbing with preserved consciousness
and less-marked neurologic deficits
has been observed in small hemato¬
mas of the pons63 and in brain-stem
compression from a cerebellar hemor¬
rhage.62 Lesions of the abducens nerve
fascicle within the pons may be asso¬
ciated with contralateral brachiocru-
ral hemiplegia (Millard-Gubler syn¬
drome).64 In the recovery of paramed¬
ian pontine hematomas sparing the
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midbrain, involuntary vergence move¬
ments induced by voluntary horizon¬
tal or conjugate gaze attempts may
develop (convergence and divergence
synkinesis)55; these synkineses may
occur when pontine centers of gaze
are involved, together with sparing of
brain stem association pathways. In
vascular pontine syndromes, the
pupils may be small and reactive,
when the descending sympathetic
pathways are involved.5
Lateral Pontine Syndrome
Hemorrhages limited to the lateral
tegmentum of the pons produce a rel¬
atively consistent syndrome with con¬
tralateral hemiplegia and sensory
loss, ipsilateral limb ataxia, Horner's
syndrome, and marked eye-movement
disorders.43-51·63 Most of these patients
have an ipsilateral one-and-a-half
syndrome, some have an ipsilateral
fascicular sixth-nerve palsy, and, in
the acute stage, some have ocular bob-
Fig 2.—Schematic transverse cuts from mid¬
brain to medulla with arterial territories. Top
left, Level of third-nerve nucleus; bottom left,
level of fourth-nerve nucleus; top right, level of
sixth-nerve nucleus; bottom right, level of
eighth- (vestibular), tenth-, and twelfth-nerve
bing that is occasionally asymmetric.
A similar syndrome should also occur
after occlusion of lateral penetrating
branches of the SCA with infarction
of the lateral brain stem, but infarcts
in the distribution of the SCA involve
mainly the superior part of the cere¬
bellum, and brain-stem signs are
often not prominent.65 In caudolateral
pontine infarcts, corresponding to the
distribution of the AICA, oculomotor
signs are either absent or suggest
vestibular involvement.66
CEREBELLUM
The main supply of the cerebellum
comes from the SCA (upper surface of
the vermis and hemisphere) and the
 nuclei MLF and PPRF as in Fig 1. PCA
indicates posterior cerebral artery; SCA,
superior cerebellar artery; AICA, anterior infe¬
rior cerebellar artery; and PICA, posterior
inferior cerebellar artery.
posteroinferior cerebellar artery
(PICA) (inferior part of the cerebel¬
lum).65·67 When the PICA is not well
developed, the supply is taken over by
the AICA, and vice versa. The overlap
of branches in the arterial system of
the cerebellum is important and also
includes branches from the contralat¬
eral hemisphere. Location and size of
infarcts, therefore, are quite variable.
For example, in some cases, unilateral
occlusion of a cerebellar artery gives
rise to a large bilateral infarct, but, in
other cases, it causes only a small
unilateral infarct. Furthermore, oc¬
clusion of the vessels supplying the
cerebellum often produces associated
brain-stem infarction, making diffi-
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cult a precise clinical localization of a
lesion.
Although a number of cerebellar
eye signs have been described,68 only a
few of them can be observed clinically
in acute vascular lesions of the cere¬
bellum. Horizontal pursuit move¬
ments may become superimposed
with microsaccades (Cogwheel pur¬
suit).4·69 When infarction in the PICA
territory is confined to the posteroin¬
ferior part of a cerebellar hemisphere,
the patient presents with vertigo,
vomiting, and ataxia.70 74 In such situa¬
tions, the mistaken diagnosis of an
acute peripheral vestibular disorder
might be made. The key differential
points are the findings of prominent
ipsilateral cerebellar signs together
with horizontal nystagmus in both
directions of gaze with larger ampli¬
tude toward the ipsilateral side of the
lesion. By contrast, in an acute
peripheral vestibular disorder, the
nystagmus would be unidirectional
and beat toward the contralateral
side.
Compared with infarction in the
PICA distribution, cerebellar infarc¬
tion in the SCA territory is much
rarer. Such patients, in addition to an
acute ataxia of gait, sometimes have
an upbeating nystagmus present on
gaze straight ahead, due to involve¬
ment of the superior vermis.65·75
Hypermetria of the contralateral sac-
cades (saccadic lateropulsion) with
hypometria of the ipsilateral saccades
is just the opposite phenomenon from
what is seen in PICA-territory
infarcts involving the lateral medul¬
la.76 In cerebellar hemorrhage, com¬
mon eye-movement disorders include
gaze palsy (54%), nystagmus (51%),
abducens palsy (28%), and skew devi¬
ation (20% ),77 which are more sugges¬
tive of brain-stem than cerebellar
dysfunction.
The presence of these brain-stem
oculomotor disturbances and other
 disorders in a cerebellar stroke do not
necessarily indicate an associated
brain-stem infarction, but can also be
the consequence of brain-stem com¬
pression by a large cerebellar hemor¬
rhage or infarction.67·77"80 A reliable
clinical distinction between the two
conditions is generally not possible.
MEDULLA
The arterial supply to the medulla
can be divided into three or four terri¬
tories81 (Fig 2, bottom right) as fol¬
lows: the dorsal and lateral aspects of
the medulla are supplied by the med¬
ullary branches of the PICA, and the
medial territory is fed by branches of
the anterior spinal artery; the olivary
territory is situated between the lat¬
eral and the medial territories and is
inconstant.82
Lateral Medullary Infarcts
Infarcts in the lateral medullary
territory are due to occlusion of the
vertebral artery in 75% of these cases,
whereas isolated occlusion of the
PICA is found in less than 15% of
these cases.83 When the infarct is
related to vertebral artery occlusion,
associated pontine involvement may
be found, which does not occur in
cases with isolated PICA occlusion.83
Cerebellar infarction is frequently
associated with the medullary infarct,
and it may be difficult to establish
which of the oculomotor disturbances
are related to medullary or to cerebel¬
lar involvement. Magnetic resonance
imaging is able to visualize medullary
infarcts without cerebellar involve¬
ment and may be of considerable help
in clinicotopographic studies.84
The lateral medullary syndrome
(Wallenberg's syndrome) is one of the
most typical clinical syndromes found
in neurologic practice. However, eye-
movement disturbances may be very
complex and are often not well as¬
sessed. Various subjective complaints
may be encountered.85 Vertical or
oblique diplopia corresponds to skew
deviation, and fluctuating vertical
diplopia occurs when monocular
downward-beating nystagmus ap¬
pears in the ipsilateral eye during
gaze toward the affected side.85 Diplo¬
pia may also increase markedly dur¬
ing gaze toward the nonaffected side,
a phenomenon that is called crossed
diplopia." Also, tilting of the head to
the nonaffected side typically worsens
diplopia and oscillopsia. Oscillopsia is
predominantly in the horizontal plane
and tends to subside within the weeks
following the stroke. Blurred vision,
which can be monocular or binocular,
has been reported in the absence of
nystagmus; it could be related to
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impairment of fixation.85 A tilt (either
(90° or 180°) of the visual field may
occur and is very suggestive of lateral
medullary infarct8586; sometimes, an
oblique torsion of the visual field may
be limited to the ipsilateral eye.85
Occasionally, forced tonic deviation of
the eyes toward the affected side may
be one of the patient's complaints.
Various objective disturbances may
be found, but are frequently over¬
looked if the oculomotor examination
is not performed carefully. Most signs
can be readily elicited at bedside, and
the interest of electro-oculography is
mainly in quantification of the abnor¬
malities. Skew deviation (vertical
divergence of Hertwig-Magendie)
may be related to damage to otolith-
oculomotor pathways.49·87 The ipsilat¬
eral eye is typically down in skew
deviation due to lateral medullary
infarct. It is typically increased by
head tilt toward the lesion.85·87 Rotato¬
ry or horizontorotatory nystagmus on
gaze straight ahead (primary position
nystagmus) is closely allied to vertigo
and imbalance and is typically related
to large lateral medullary infarcts.88
However, it may occur without com¬
plete destruction of the vestibular
nuclei.83 In left-sided infarcts, the
rotatory component of the nystagmus
is clockwise for the examiner, and, in
right-sided infarcts, it is counter¬
clockwise.88 The quick phase of the
horizontal component is opposite to
the lesion, but the direction may
reverse with the eyes closed.89 Ipsilat¬
eral gaze increases the nystagmus,
which often becomes predominant in
the ipsilateral eye.88 In rare cases, the
nystagmus may be replaced after a
few weeks by irregular multidirection
movements close to opsoclonus.88 A
downward-beating component limited
to the ipsilateral eye may sometimes
appear during gaze toward the af¬
fected side.84·85 Bilateral gaze-evoked
nystagmus has also been reported,90
but it may have been related to associ¬
ated cerebellar involvement. Palpe¬
brai nystagmus synchronous with the
fast phase of horizontal nystagmus
(Popper-type of lid nystagmus) has
been reported in lateral medullary
infarct, and is a more accurate localiz¬
ing sign than the Pick-type of lid
nystagmus, which is triggered by con¬
vergence and can occur in various
brain-stem and cerebellar lesions.91
One of the most constant oculomotor
abnormalities of lateral medullary
syndrome is hypermetric saccades
toward the affected side with hypo-
metric saccades toward the opposite
side.86·90 It may correspond to isolation
of the vestibular nuclei from the floe-
culus due to lesion of the restiform
body,86 or to otolith imbalance.4 This
ipsilateral bias of ocular movements90
also explains the frequent tonic conju¬
gate deviation of the eyes toward the
affected side (ocular lateropulsion of
Barré92'95); this lateropulsion may
sometimes be seen with the patient's
eyes open, but, more often, it is inhib¬
ited by fixation and is observed only
when the eyes that have been previ¬
ously closed are quickly opened by the
examiner; examination with a Frenzel
prism may also help elicit this sign.
Sometimes a deviation of the corneal
protuberance can be palpated under
the lids. The ipsilateral pupil is miot-
ic, in relation to Homer's syndrome,
due to disruption of the discending
sympathetic fibers.
In large infarcts, all of these oculo¬
motor disturbances may persist indef¬
initely, although some degree of func¬
tional adaptation is usually seen, with
subjective improvement.88
Medial Medullary Infarcts
These infarcts are usually related to
occlusion of the anterior spinal artery;
their rarity may be due to the usually
bilateral origin of the anterior spinal
artery96; however, they are still very
uncommon in bilateral distal occlu¬
sion of the vertebral artery.97·98 The
medial territory is usually involved
bilaterally.99
Oculomotor anomalies are infre¬
quent and are mainly limited to
upbeat nystagmus, the amplitude of
which may increase during upward
gaze.96-99 Dorsal extension of the
infarct toward the MLF seems to cor¬
relate with occurrence of this type of
nystagmus.96·99 A rotatory nystagmus
has been reported in one case,84 but
the finding of an occlusion of the
ipsilateral vertebral artery suggests
that the lateral territory was initially
involved as well.
In the very uncommon hemimedul-
lary infarcts, oculomotor abnormali¬
ties due to lateral medullary involve¬
ment usually coexist.
Medullary Hemorrhages
Hemorrhages limited to the medul¬
la are extremely uncommon, and their
origins are not well established. Ocu¬
lomotor disturbances may mimic
those of lateral medullary in¬
farcts100·101 but may also be absent102 or
suggest a pontine lesion.103
COMBINED SYNDROMES
In basilar artery occlusion, it is not
uncommon to have extensive infarc¬
tion of the brain stem, from the lower
pons up to the upper midbrain; the
 deep and superficial territory of the
posterior cerebral artery (PCA) is
also commonly involved.22·29 These
facts explain why combined oculomo¬
tor abnormalities are frequently
present in this condition.29·30 Midlower
pons syndromes or upper midbrain
syndromes usually predominate, ac¬
cording to the level of the occlusion.
Embolie occlusion of the basilar
artery mostly occurs at the distal
bifurcation of this artery, and typical¬
ly produces upper midbrain and PCA
syndromes.22 Atherosclerotic occlu¬
sion of the basilar artery usually orig¬
inates more proximally and pontine
syndromes may predominate, in asso¬
ciation with usually extensive neuro¬
logic deficits (locked-in syndrome).29·48
Very often, supranuclear, nuclear, and
infranuclear disturbances are associ¬
ated,28 but, sometimes, isolated su¬
pranuclear21 or infranuclear30 eye
movement disorders may also be
found.
In vertebral artery occlusion, the
eye movement disturbances due to
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B\l=u"\ttner-EnneverJA, B\l=u"\ttnerU, Cohen B,
11.
et al: Vertical gaze palsy and the rostral intersti-
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J Neurol Neurosurg Psychiatry 1986;49:686-694.
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lateral medullary involvement domi¬
nate the oculomotor picture, but signs
of lower pontine involvement may
sometimes occur, as sixth-nerve pal¬
sy.83 More distal involvement occurs
much more uncommonly than in basi¬
lar artery occlusion.55·56 Cerebellar
infarction in the distribution of the
PICA territory may be extensive, with
prominent cerebellar oculomotor dis¬
turbances or secondary pontine dys¬
function due to compression; in these
cases, primary lateral medullary
involvement may not be recognized.
Large brain-stem hemorrhages
usually originate in the pons, with
prominent pontine oculomotor distur¬
bances in a usually deeply comatose
patient.104
COMMENT
Few oculomotor disturbances are
specific for vertebrobasilar stroke,
and it is their association with other
signs and their pattern of develop¬
ment that may suggest a cerebrovas¬
cular event.105 Indeed, only acute
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