Case Study Pneumonia

2/25/2018 Posterior circulation cerebrovascular syndromes - UpToDate
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Posterior circulation cerebrovascular syndromes
Author: Louis R Caplan, MD

Section Editor: Jose Biller, MD, FACP, FAAN, FAHA
Deputy Editor: John F Dashe, MD, PhD
All topics are updated as new evidence becomes available and our peer review process is complete.
Literature review current through: Jan 2018. | This topic last updated: Jun 02, 2017.
INTRODUCTION — Twenty percent of ischemic events in the brain involve posterior circulation (vertebrobasilar)
structures. This topic will review the major clinical syndromes associated with posterior circulation ischemia
related to stenosis or occlusion of the large aortic arch, neck, and intracranial arteries. These arteries are the
innominate and subclavian arteries in the chest, the vertebral arteries in the neck, and the intracranial vertebral,
basilar, and posterior cerebral arteries.
The evaluation and management of acute ischemic stroke (including stroke involving the posterior circulation)
are discussed separately. (See "Initial assessment and management of acute stroke" and "Approach to
reperfusion therapy for acute ischemic stroke" and "Antithrombotic treatment of acute ischemic stroke and
transient ischemic attack".)
SOURCE OF ISCHEMIA — The most common causes of posterior circulation large artery ischemia are
atherosclerosis, embolism, and dissection. Dolichoectasia (elongation and tortuosity) of the vertebral and basilar
arteries is another occasional cause.
● About one-third of posterior circulation strokes are caused by occlusive disease within the large neck and
intracranial arteries, which are the vertebral arteries in the neck and the intracranial vertebral, basilar, and
posterior cerebral arteries [1-4].
● The proximal portion of the vertebral artery in the neck is the most common location of atherosclerotic
occlusive disease within the posterior circulation [1-5]. Atherosclerosis of the intracranial vertebral arteries
and of the basilar artery is also common. (See "Intracranial large artery atherosclerosis".)
● Dissection of the extracranial and intracranial vertebral arteries is another frequent cause of ischemia within
the posterior circulation.
● Unlike the vertebral and basilar arteries, atherosclerosis and dissection of the posterior cerebral arteries is
not common. Most infarcts in the posterior cerebral artery territory are due to embolism from the heart, aorta,
or vertebral arteries.
SUBCLAVIAN AND INNOMINATE ARTERIES — Atherostenotic lesions of the innominate and subclavian
arteries do cause arm ischemia and transient ischemic attacks (TIAs) but seldom cause strokes. Because the
vertebral arteries in the neck originate from the proximal subclavian arteries, disease of the subclavian or
innominate arteries proximal to the vertebral artery origin can cause reduction of vertebral artery flow.
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In the subclavian steal syndrome, obstruction of the proximal subclavian artery produces a low-pressure system
within the ipsilateral vertebral artery and in blood vessels of the ipsilateral upper extremity. Blood from a higher-
pressure system, the contralateral vertebral artery and basilar artery, is diverted and flows retrograde downward
into the ipsilateral vertebral artery into the arm. (See "Subclavian steal syndrome", section on 'Clinical
presentations' and "Subclavian steal syndrome", section on 'Upper extremity ischemia'.)
Most often, subclavian artery disease is detected when patients with coronary or peripheral vascular occlusive
disease are referred to ultrasound laboratories for noninvasive testing.
Most patients with subclavian artery disease are asymptomatic. The most frequent symptoms of subclavian
artery disease relate to the ipsilateral arm and hand. Coolness, weakness, and pain on use of the arm are
common.
Neurologic symptoms are uncommon unless there is accompanying carotid artery disease. Dizziness is by far
the most common neurologic symptom of the subclavian steal syndrome, and usually has a spinning or
vertiginous character. Diplopia, decreased vision, oscillopsia, and staggering all occur, but less frequently, often
accompanying the dizziness. Attacks are brief and occasionally are brought on by exercising the ischemic arm.
However, in most patients exercise of the ischemic limb does not provoke neurologic symptoms or signs. (See
"Subclavian steal syndrome", section on 'Clinical presentations' and "Subclavian steal syndrome", section on
'Upper extremity ischemia'.)
Innominate artery disease is much less common than subclavian artery disease [1,3,6]. When the innominate
artery becomes stenotic or occluded, signs and symptoms of decreased carotid artery flow may also develop.
Ipsilateral monocular visual loss, ipsilateral cerebral hemisphere ischemia in the territories of the anterior and
middle cerebral arteries, ipsilateral arm ischemia, and ischemic symptoms referable to the distal portion of the
posterior circulation and/or the cerebellum may be due to innominate artery disease.
Takayasu's disease and giant cell (temporal) arteritis can cause subclavian and innominate artery occlusive
disease. Young women who smoke cigarettes and take oral contraceptives may develop occlusive disease of the
aortic arch vessels that mimics Takayasu disease, except that it is not inflammatory. (See "Clinical features and
diagnosis of Takayasu arteritis" and "Clinical manifestations of giant cell (temporal) arteritis".)
EXTRACRANIAL VERTEBRAL ARTERIES — The vast majority of occlusive lesions of the proximal vertebral
arteries are atherosclerotic. Among a series of 100 patients with angiographically documented vertebral artery
lesions, 92 percent were atherosclerotic in origin [7]. The most common location of atherosclerotic occlusive
disease within the posterior circulation is the proximal portion of the vertebral artery in the neck [1-5].
Atherosclerotic plaques may begin in the subclavian artery and extend into the ostia of the proximal extracranial
vertebral arteries (ECVAs), or begin within the most proximal portion of the ECVAs. Occlusions most often occur
within the first inch (2 to 3 cm) of the ECVAs. In contrast, atherosclerotic disease rarely involves the more distal
ECVAs within the cervical spine or near the penetration of the arteries into the skull (figure 1).
Another common cause of posterior circulation stroke is arterial dissection, which usually involves the ECVA just
before it enters the foramen transversarium at C5 or C6, or in the very distal part of the artery in the neck before
it penetrates the dura mater to enter the cranial cavity.
CT angiography can show occlusive lesions at the origin of the vertebral arteries from the subclavian arteries as
well as dissections. MR angiography often does not show the origins of the vertebral arteries well.
Proximal vertebral artery disease can cause sudden-onset strokes or transient ischemic attacks (TIAs). The most
frequently reported symptom during TIAs is dizziness. These vertebral artery TIAs are indistinguishable from
those described by patients with subclavian steal, except that vertebral artery TIAs are not precipitated by effort
or by arm exertion.
Although dizziness is the most common symptom, it is seldom the only neurologic symptom. Usually, in at least
some attacks, dizziness is accompanied by other signs of hindbrain ischemia. Diplopia, oscillopsia, weakness of
both legs, hemiparesis, and numbness are often reported.
In patients with proximal ECVA disease, a bruit can often be heard over the supraclavicular region when
auscultation is performed by moving the stethoscope bell over the posterior cervical muscles and the mastoid.
Sometimes a bruit may be heard over the vertebral artery contralateral to the side of the stenotic vertebral artery
because of increased collateral blood flow.
Artery to artery embolism and low flow — Embolization of white platelet-fibrin and red erythrocyte-fibrin
thrombi from atherostenotic occlusive lesions is the most common presentation of ECVA origin disease [1-5,8].
The intraarterial emboli travel from the ECVA origin to reach the ipsilateral intracranial vertebral artery (ICVA),
and sometimes travel on to block the rostral basilar artery and/or its branches. In support of this observation,
patients presenting with ischemia in the distribution of the ICVA (the medulla and posterior inferior cerebellum) or
the distal basilar artery (superior cerebellum, occipital and temporal lobes in the territory of the posterior cerebral
arteries, or the thalamus or midbrain) show a high frequency of recent ECVA occlusions [1,3-5].
A situation analogous to that of ECVA origin disease is well known in the anterior circulation, where
atherosclerotic disease of the internal carotid artery origin can cause distal ischemia by artery to artery
embolization. As an example, it is not uncommon that a patient with a small, middle cerebral artery territory
infarct is found to have an occlusion at the internal carotid artery origin by ultrasound or angiography. In most of
these cases, it is likely that a recently formed occlusive thrombus in the internal carotid artery fragmented and
embolized distally, causing the middle cerebral artery territory stroke.
In patients with proximal ECVA stenosis, intraarterial (artery to artery) embolism is a much more frequent cause
of ischemia to the intracranial posterior circulation arteries than hemodynamic insufficiency (ie, low flow). This
point is illustrated by results from the New England Medical Center Posterior Circulation Registry, which
evaluated a series of 407 patients who had posterior circulation TIAs or strokes within the prior six months and
included 80 patients with severe stenosis or occlusion of the proximal ECVA [1]. In 45 (56 percent) of these 80
patients, embolization from the vertebral artery lesion was the most likely cause of brain ischemia [1]. Only 13
patients (16 percent) had hemodynamic-related TIAs, and 12 of these 13 had severe bilateral vertebral artery
occlusive disease. The only patient with unilateral vertebral artery disease had bilateral internal carotid artery
occlusions.
Dissection and other causes — Dissection of the ECVA usually involves the distal portion of the ECVA as it
winds around the upper cervical vertebrae [9]. Sometimes dissections involve the proximal ECVA between the
origin of the artery and its entry into the vertebral column, usually at C5 or C6. Pain in the neck and/or occiput
and TIAs or strokes involving the lateral medulla and cerebellum are the most common findings. (See
"Spontaneous cerebral and cervical artery dissection: Clinical features and diagnosis", section on 'Clinical
features'.)
Ischemic symptoms due to ECVA dissection are most often vestibulocerebellar and include dizziness, vertigo,
veering to one side, and loss of balance. When infarcts develop, they usually involve the inferior portion of the
cerebellum, causing gait ataxia. Less common, are emboli to the distal posterior circulation, especially the
posterior cerebral artery territories, causing a hemianopia. Occasionally cervical root pain and signs, and spinal
cord ischemia can develop.
In older patients, giant cell arteritis is an occasional cause of occlusive disease involving the distal extracranial
vertebral artery just before it penetrates the dura to become intracranial. (See "Clinical manifestations of giant
cell (temporal) arteritis".)
Rotational vertebral artery occlusion is an uncommon cause of transient posterior circulation ischemic symptoms,
mainly paroxysmal vertigo or nonspecific dizziness, which may be accompanied by nystagmus, tinnitus,
syncope, blurred vision, nausea, or vomiting [10,11]. The nystagmus typically has a prominent downbeat
component, but may also include torsional and horizontal components [12]. The symptoms are due to dynamic
compression of one (dominant) vertebral artery by bony elements of the cervical spine, triggered by head turning
to one side, or less often by head turning to both sides or head tilting [10,11]. In most reported cases, there is
associated hypoplasia or stenosis of the other vertebral artery. The symptoms are relieved by returning the head
to the neutral position. Few if any cases result in infarction with permanent neurologic deficits from this
mechanism. (See "Pathophysiology, etiology, and differential diagnosis of vertigo", section on 'Rotational
vertebral artery syndrome'.)
INTRACRANIAL VERTEBRAL ARTERIES — Atherostenotic disease can involve any portion of the intracranial
vertebral arteries (ICVA) (figure 2). The most common location of ICVA stenosis is the distal portion of the artery
at or near the vertebral-basilar artery junction. Another common site of ICVA stenosis is the proximal portion of
the vertebral artery just after dural penetration and before giving off the posterior inferior cerebellar artery (PICA)
branch. Dissection of the ICVA also occurs, and ischemic symptoms are usually accompanied by prominent
headache [13]. ICVA dissections often extend into the basilar artery.
Occlusive ICVA disease presents in a variety of different ways [4,14,15]:
● Asymptomatic occlusion
● Transient ischemic attacks (TIAs), usually including vestibulocerebellar symptoms or elements of the lateral
medullary syndrome
● Lateral medullary infarcts
● Medial medullary infarction
● Infarction of one-half of the medulla (hemimedullary infarction) including the lateral and medial medulla on
one side
● Cerebellar infarction in PICA territory
● Embolization of the ICVA thrombus to the distal basilar artery and its branches causing TIAs and/or strokes
● Propagation of the ICVA thrombus into the basilar artery causing a basilar artery syndrome
Lateral medullary infarction — Lateral medullary infarction (Wallenberg syndrome) is the most common and
important syndrome related to intracranial vertebral artery occlusion (figure 3) [4,15]. The diagnosis is often
missed by non-neurologists, and so the features are very important to know and understand.
Vestibulocerebellar symptoms and signs — Vestibulocerebellar symptoms and signs are nearly always
present in patients with lateral medullary infarcts [14]. These are related to involvement of the vestibular nuclei
and their connections, and to involvement of the inferior cerebellar peduncle (restiform body). Common
symptoms and signs are as follows:
● Feeling dizzy or off-balance, which may take a number of forms:
• Turning, rotating, whirling, or moving in relation to the environment
• Being pulled or falling towards one side, most often ipsilateral to the lesion
• Swaying or rolling as if moving from side to side
• Tilting or leaning
● Difficulty sitting upright without support. Patients topple, lean, or veer to the ipsilateral side when they sit or
stand. In many, standing or walking is impossible during the acute period without support. When they regain
the ability to walk, patients often feel as if they are being pulled to the side of the lesion. They veer, list, or
weave to the side, especially on turns.
● Hypotonia of the ipsilateral arm. This cerebellar sign can be demonstrated by having the patient quickly
lower or raise the outstretched hands together, braking the ascent and descent suddenly. The symptomatic
arm on the side ipsilateral to the infarct often overshoots and is not as quickly braked compared with the
normal contralateral arm. In some patients, the ipsilateral arm also makes a slower ascent or descent.
● Blurred vision or diplopia. Some also describe oscillopsia, which is the appearance that objects in the visual
field are in rhythmic motion or oscillation. Less common is tilting or inversion of the visual environment.
● Nystagmus. This is nearly always present, especially in patients who describe dizziness or vertigo. The
nystagmus usually has both horizontal and rotational components. The rapid phase of the rotatory
nystagmus usually moves the upper border of the iris towards the side of the lesion. Most often, larger
amplitude, slower nystagmus is present on gaze to the side of the lesion, while smaller amplitude, quick
nystagmus is found on gaze directed to the contralateral side.
● Ocular torsion. The eye and ear ipsilateral to the lateral medullary infarct may rest in a down position below
the contralateral eye and ear [16]. At times, ocular torsion is accompanied by a head tilt and skew deviation
with the ipsilateral eye positioned downward. This combination of findings is referred to as the ocular tilt
reaction [4,17,18].
● Limb ataxia ipsilateral to the lateral medullary infarct. Some patients cannot feed themselves using the
ataxic arm. They overshoot targets and have difficulty pointing accurately to moving targets.
Sensory symptoms and signs — Sensory symptoms and signs are common in patients with lateral
medullary infarcts.
● Pain or unpleasant feelings in the face are sometimes the earliest and most prominent feature of the lateral
medullary syndrome and are diagnostic of a lateral tegmental brainstem localization. These are related to
lesions of the spinal nucleus of V and the descending spinal tract of V. The facial pain is usually described
as sharp jolts or stabs of pain most often in the ipsilateral eye or face. Sometimes pain persists and is limited
to the forehead and frontal scalp region. At times, the abnormal sensation is described as hot, burning, or
scalding.
● Loss of pain and temperature sensation in the contralateral trunk and limbs is related to lesions of the lateral
medullary spinothalamic tract.
● The most common pattern of sensory abnormality with lateral medullary infarcts is loss of pain and
temperature sensation in the ipsilateral face and the contralateral trunk and limbs. The next most frequent
combination is hypalgesia in the ipsilateral face and contralateral face, trunk, and limbs. Less often, the
hypalgesia can be solely contralateral, involving the face, arm, and leg, or sometimes only the face and arm
[4,19]. The least common pattern of sensory loss is hypalgesia only involving the contralateral trunk, arm,
and leg or parts thereof.
● Examination usually shows ipsilateral decreased pain and temperature sensation in the face. The corneal
reflex is usually reduced in the ipsilateral eye. Although contralateral loss of pain and thermal sensation
involving the body and limbs is usually found on examination, most patients with contralateral hypalgesia are
unaware of their sensory loss until they are tested. However, some do notice loss of thermal sensation when
they touch hot or cold objects with their contralateral upper and/or lower limbs.
Bulbar muscle weakness — Weakness of bulbar muscles innervated by the lower cranial nerves is a very
prominent feature when lateral medullary infarcts extend medially. Usually, the abnormality is unilateral.
● Involvement of the nucleus ambiguus causes paralysis of the ipsilateral palate, pharynx, and larynx,
resulting in hoarseness and dysphagia. Oropharyngeal muscle paralysis results in food being trapped in the
piriform recess of the pharynx. Food and secretions have relatively free access into the air passages.
Patients try to extricate the food with a cough or throat-clearing maneuver, which makes a characteristic
crowing-like sound.
● Examination shows paralysis of the ipsilateral vocal cord and a lack of elevation of the ipsilateral palate on
phonation. The uvula often deviates to the side contralateral to the lateral medullary infarct. Dysarthria and
dysphonia are common. In some patients, dysphagia and aspiration are prominent.
● Aspiration and pneumonia are very important complications of abnormal pharyngeal function. Hiccups are
also a relatively common and annoying complaint.
Respiratory dysfunction — Respiratory dysfunction is an important feature of lateral medullary ischemia.

Control of inspiration and expiration and their automaticity lies within the ventrolateral medullary tegmentum and
the medullary reticular zone.
The most common abnormality described in patients with lateral tegmental caudal brainstem lesions is failure of
automatic respirations, a phenomenon especially apparent during sleep. This failure to initiate respiration has
been referred to as Ondine's curse. (See "Disorders of ventilatory control", section on 'Ondine's curse' and
"Congenital central hypoventilation syndrome and other causes of sleep-related hypoventilation in children",
section on 'Congenital central hypoventilation syndrome'.)
Autonomic dysfunction — Autonomic dysfunction may occur in lateral medullary infarction.
● The ipsilateral eye often shows features of Horner's syndrome due to lesions of the descending sympathetic
nervous system. (See "Horner syndrome".)
● Cardiovascular abnormalities include tachycardia, orthostatic hypotension without cardiac rate acceleration,
and intermittent bradycardia [4]. Some patients have labile blood pressures, tachycardia, unusual sweating,
and arrhythmias. The anatomic basis is thought to be involvement of the dorsal motor nucleus of the vagus
nerve.
Medial medullary infarction — The most consistent finding in patients with medial medullary ischemia is a
contralateral hemiparesis [4,20]. Usually the hemiparesis is complete and flaccid at onset. Later, increased tone
and spasticity develop. In approximately one-half of patients, the face is also involved. Facial weakness, when it
occurs, is usually slight and transient and rarely persists.
Sensory symptoms are related to ischemia of the medial lemniscus. Some patients report paresthesias or, less
commonly, dysesthesias in the contralateral lower limb and trunk. Less often, sensory symptoms occur in the
arm and hand. In many patients with sensory symptoms there are no objective signs of touch, vibration, or
position sense loss. Proprioceptive dysfunction, with slight loss of position and vibration sense in the
contralateral foot, is found in some patients.
Ipsilateral tongue paralysis is the least common but most topographically localizing sign of medial medullary
infarction, and is due to involvement of the hypoglossal nucleus. Tongue paresis causes slurring of speech,
especially of lingual consonants.
Hemimedullary infarction — Occasional patients have infarction that involves both the lateral and medial
medullary territories on one side (hemimedullary infarcts). Symptoms are identical to those found in patients with
lateral medullary ischemia with the addition of a hemiparesis contralateral to the lesion. The hemiparesis may
develop concurrently with lateral medullary symptoms and signs or can occur later. (See 'Lateral medullary
infarction' above and 'Medial medullary infarction' above.)
Cerebellar infarction — Cerebellar infarction in PICA distribution can involve just the vermis, or the lateral
surface, or the full PICA territory (figure 4). Full PICA territory infarcts are often accompanied by edema
formation and mass effect (so-called pseudotumoral cerebellar infarcts). (See 'Pseudotumoral cerebellar
infarction' below.)
Approximately one-fifth of PICA territory cerebellar infarcts are accompanied by infarction in the dorsal or
dorsolateral medulla [3,4]. The combination of lateral medullary and PICA cerebellar infarction occurs when the
ICVA is occluded and blocks the orifice of both PICA and the lateral medullary penetrators. Sometimes medial
PICA territory infarcts are accompanied by dorsal medullary infarcts since the medial PICA branch has some
supply to the dorsal medulla [4,21,22].
Infarcts limited to the medial vermis in medial PICA territory usually cause a vertiginous labyrinthian syndrome
that closely mimics a peripheral vestibulopathy. Severe vertigo and prominent nystagmus are the major findings.
Some patients also have truncal lateropulsion characterized by feelings of magnetic pulling of the trunk to the
ipsilateral side.
Lateral cerebellar hemisphere PICA territory infarcts are usually characterized by minor degrees of dizziness and
gait incoordination with veering to the side of the lesion. Minor limb hypotonia and incoordination are found. A
common syndrome is acute unsteadiness with ataxia but without vertigo or dysarthria. Body sway towards the
side of the lesion, ipsilateral limb ataxia, and abnormal rapid alternating movements are also common.
When the full PICA cerebellar territory is involved, headache is usually present in the occiput or high neck on the
ipsilateral side. The head may also be tilted with the occiput tending to tilt toward the ipsilateral side.
Vomiting, gait ataxia, truncal lateropulsion, and limb incoordination are other common findings. The truncal
dysfunction is similar to that found in the lateral medullary syndrome; the body is often tilted or pulled ipsilaterally
upon sitting or standing. The limb incoordination consists mostly of hypotonia rather than a rhythmic intention
tremor.
Pseudotumoral cerebellar infarction — The syndrome of pseudotumoral cerebellar infarction, with edema
formation and mass effect, is most often associated with large full PICA territory infarcts. After the first day or so,
patients with this form of cerebellar infarction typically develop increased headache, vomiting, and decreased
consciousness, with drowsiness followed by stupor. Bilateral Babinski signs are an early sign of cerebellar mass
effect.
Characteristic oculomotor abnormalities of large cerebellar space-taking infarcts can develop and include the
following features:
● Most common are a conjugate gaze paresis to the side of the lesion or a paresis of abduction limited to the
ipsilateral eye
● Bilateral sixth nerve paresis may occur
● Later bilateral horizontal gaze palsies may develop, often accompanied by ocular bobbing
These signs are due to compression of the pontine tegmentum by the swollen cerebellar infarct. Stupor is
followed by deep coma when the oculomotor abnormalities become bilateral.
Dolichoectasia — Dolichoectasia (dilatative arteriopathy) is a term that describes arterial elongation, widening,
and tortuosity [23-28]. The intracranial vertebral and basilar arteries are most often affected. Dolichoectatic
arteries are characterized by an abnormally large external diameter and a thin arterial wall that shows
degeneration of the internal elastic lamina, and multiple gaps in the internal elastica. The media of dilated
arteries becomes thin because of reticular fiber deficiency and smooth muscle atrophy.
The most important clinical presentations of dilatative arteriopathy are as follows:
● Acute brain ischemia
● A progressive course related to compression of cranial nerves, the brainstem, or the third ventricle
● A catastrophic outcome caused by vascular rupture
Flow in dilated arteries may become to-and-fro, causing reduced antegrade flow and thrombus formation.
Elongation and angulation of arteries can stretch and distort the orifices of arterial branches leading to decreased
blood flow, especially in penetrating branches. Dilated intracranial vertebral arteries can compress the medulla
leading to the gradual onset of hemiparesis [26].
Distinguishing vertigo of brainstem and cerebellar ischemia from peripheral causes — A composite three-
part test entitled HINTS (Head-Impulse-Nystagmus-Test of Skew) is useful for distinguishing brainstem and
cerebellar ischemia from vestibular neuritis or other peripheral causes of vertigo [29-32]. The test is most helpful
in patients who have had continuous feelings of vertigo or dizziness. It is not useful in patients with momentary
position-related transient vertigo (often benign positional vertigo) or those with TIAs who are not dizzy when
examined.
● Head Impulse – For the head impulse test, also called head thrust test (see "Evaluation of the patient with
vertigo", section on 'Other vestibular signs'), the patient is instructed to fix their gaze on a distant target while
wearing his or her usual prescription eyeglasses. The head is then turned quickly and unpredictably by the
examiner, about 15º; the starting position should be about 10º from straight ahead. The normal response is
that the eyes remain on the target (figure 5). The abnormal response is that the eyes are dragged off of the
target by the head turn (in one direction), followed by a saccade back to the target after the head turn; this
response indicates a deficient vestibulo-ocular on the side of the head turn, implying a peripheral vestibular
lesion (ie, the inner ear or vestibular nerve) on that side. This reflex is preserved in central lesions, except
when cranial nerve (CN) VIII fascicles are affected in the lateral pons.
● Nystagmus – Peripheral vestibular lesions often are accompanied by nystagmus that is always in the same
direction (see "Evaluation of the patient with vertigo", section on 'Nystagmus'), while brainstem and
cerebellar lesions are typically associated with nystagmus that changes direction with different positions of
gaze.
● Test for Skew – The test involves covering one eye and seeing if there is a vertical shift in the eye when
uncovered. Brainstem and cerebellar lesions sometimes cause a slight skew deviation.
Any of the following, whether present or untestable, suggest a brainstem or cerebellar lesion [29-32]:
● Normal head impulse test on both sides
● Direction-changing nystagmus
● Skew deviation
The presence of all of the following suggests a peripheral lesion [29-32]:
● An abnormal head impulse test on one side
● Unidirectional, horizontal, torsional nystagmus that increases in intensity with gaze toward the fast phase
● Absent skew
The importance of these oculomotor tests is that brain imaging with either CT or MRI may be normal during the
acute phase of ischemic symptoms. In this regard, the HINTS test appears to be more sensitive for the diagnosis
of acute stroke than even brain MRI within the first two days after symptom onset [32].
One caveat is that there are rare examples of inner ear infarction (usually due to occlusion of the internal
auditory artery, an anterior inferior cerebellar artery branch) causing an acute vestibular syndrome. These are
typically associated with new hearing loss on the side of the vestibular lesion, which may be the only clue that
the mechanism is stroke [31,32]. In such cases, the eye movements elicited on HINTS are indistinguishable from
peripheral vestibular causes.
BASILAR ARTERY — The basilar artery begins at the medullopontine junction and ends at the junction of the
pons and midbrain. Occlusive lesions may occur anywhere along the basilar artery [33]. In addition, thrombi
engrafted upon occlusive lesions within the distal intracranial vertebral artery (ICVA), for example, near or at the
ICVA-basilar artery junction, can extend into the proximal basilar artery.
Basilar artery occlusive disease most often presents as ischemia in the pons. The major burden of ischemia is in
the middle of the pons, mostly in the paramedian base, and often also in the paramedian tegmentum (picture 1).
The reasons for this localization are as follows:
● The largest penetrating arteries supply the paramedian pons (figure 6) and arise directly from the basilar
artery.
● The pontine tegmentum is supplied mostly by arteries that arise from the distal basilar artery. When the
distal basilar artery remains patent, the tegmentum is relatively spared.
● Collateral circulation comes mainly from the ICVAs through their posterior inferior cerebellar artery (PICA)
branches that anastomose with anterior inferior cerebellar artery (AICA) and superior cerebellar artery (SCA)
branches; these course around the lateral aspect of the pons, supplying the lateral tegmental and basal
structures in the pons (figure 4 and image 1).
The paramedian pontine base contains descending long motor tract and crossing cerebellar fibers. The
paramedian tegmentum contains mostly oculomotor fibers. As a result, the predominant symptoms and signs in
patients with basilar artery occlusive disease are motor and oculomotor. Sensory and vestibular nuclei and tracts
located in the lateral tegmentum are relatively spared.
Alteration in the level of consciousness is an important sign in patients with basilar artery occlusion. They may
present with coma when the bilateral medial pontine tegmentum is ischemic.
Motor symptoms and signs — Most patients with symptomatic basilar artery occlusive disease and pontine
ischemia have some transient or persistent degree of paresis and corticospinal tract abnormalities [3,4,14,34-37].
The initial motor weakness is often lateralized and has been referred to as the "herald hemiparesis" of basilar
artery occlusion.
Hemiparetic patients with basilar artery occlusion almost always show some motor or reflex abnormalities on the
nonhemiparetic side. As examples, slight weakness, hyperreflexia, an extensor plantar reflex, or abnormal
spontaneous movements such as shivering, twitching, shaking, or jerking may be present on the relatively
spared side. Asymmetry but bilaterality is the rule.
Adventitious movements of the arms and/or legs are occasionally seen and can be prominent. These
movements are variable and sometimes intermittent. Small movements may resemble fasciculations. Larger
movements may resemble shivering, shuddering, or jerking; another variant is that of tremulous shaking.
Voluntary or passive limb movements or painful stimuli may precipitate a flurry of abnormal movements. At times
there are large repetitive jerking and twitching movements, especially in limbs contralateral to a hemiparesis.
These movements are often misdiagnosed as seizures [38].
Incoordination of limb movements is another common motor finding. Ataxia is invariably combined with some
degree of weakness. Incoordination is usually more severe in the legs. Toe-to-object and heel-to-shin testing
usually shows clumsiness and diminished coordination due to cerebellar dysfunction. The ataxia is invariably
bilateral but may be asymmetric and more severe on the weaker side. Intention tremor is not common.
Bulbar involvement — Weakness of bulbar muscles is very common and is an important cause of morbidity
with pontine infarction due to basilar occlusive disease. Bulbar symptoms include facial weakness, dysphonia,
dysarthria, dysphagia, and limited jaw movements. The face, pharynx, larynx, and tongue are most often
involved. The pattern may be that of crossed motor loss, such as weakness involving one side of the face and
the contralateral body, but more often the bulbar muscle weakness is bilateral.
Some patients totally lose the ability to speak, open their mouth, protrude their tongue, swallow, or move their
face at will or on command. Secretions pool in the pharynx; and aspiration is an important and serious
complication. When all voluntary movements other than the eyes are lost but consciousness is retained, the
deficit is referred to as the "locked-in syndrome." (See "Locked-in syndrome".)
Patients with infarction of the pontine base frequently have exaggerated crying and laughing spells and are
hypersensitive to emotional stimulus, a condition known as pseudobulbar affect or emotional lability.
Despite the loss of volitional muscle movement, reflexes of the jaw, face, and pharynx may be exaggerated. In
addition, clonic jaw movements or clamping down on a tongue blade may occur as a response to attempts to pry
the mouth open and to insert a tongue blade.
Some patients with pontine ischemia develop palatal myoclonus (a rhythmic involuntary jerking movement of the
soft palate and pharyngopalatine arch) that can involve the diaphragm and larynx. This movement disorder
usually begins sometime after the brainstem infarct. The movements of the palate vary in rate between 40 and
200 beats per minute. The movements are readily seen by watching the palate and pharynx when the mouth is
open. The movements involve the eustachian tube and make a click that the patient and clinician can hear.
Oculomotor symptoms and signs — Oculomotor symptoms and signs are common with symptomatic basilar
artery occlusive disease and pontine ischemia, and few patients with this condition have normal eye movements.
Abnormalities include:
● Complete bilateral horizontal gaze palsy
● Unilateral horizontal conjugate gaze palsy
● Unilateral or bilateral internuclear ophthalmoplegia (INO)
● One-and-a-half syndrome (a conjugate gaze palsy combined with an INO)
Skew deviation of the eyes and ocular bobbing may also be present. Horizontal, gaze-paretic nystagmus is
common and, when asymmetric, usually is more prominent when gaze is directed to the side of a unilateral
pontine tegmental lesion. Dissociated nystagmus, that is nystagmus that is more severe in one eye and not
rhythmically concordant in the two eyes, and vertical nystagmus are found in patients with an INO. (See
"Internuclear ophthalmoparesis".) Ptosis of the upper eyelids is also very frequent.
https://www.uptodate.com/contents/posterior-circulation-cerebrovascular-syndromes/print?search=cerebellar%20infarct&sectionRank=1&usage_typ… 10/27
The pupils may remain normal or become small. In some patients, the pupils are bilaterally very small
("pinpoint"). Use of a magnifying glass can show that, despite their very small size, the pupillary response to light
is preserved, although the amplitude of the response is slight.
Sensory symptoms and signs — Somatosensory abnormalities are generally not prominent in patients with
basilar artery occlusions. Paresthesias on one side of the body and limbs reflect involvement of the contralateral
medial lemniscus in the paramedian dorsal portion of the basis pontis. Bilateral paramedian lesions that include
the medial lemnisci on both sides can cause bilateral paresthesias. Proprioceptive loss is usually minimal or
absent despite the paresthesias.
Some patients with basilar artery occlusive disease have unusual burning pain in the face usually located in the
center of the face near the midline. Tinnitus and hearing loss relate to involvement of the central auditory tracts
and nuclei (auditory nuclei, lateral lemnisci, trapezoid bodies, inferior colliculi) or to ischemia of the eighth nerves
or the cochlea.
ROSTRAL BRAINSTEM ISCHEMIA AND "TOP OF THE BASILAR" SYNDROME — Occlusion of the rostral
portion of the basilar artery (the "top of the basilar") can cause ischemia of the midbrain, thalami, and temporal
and occipital lobe hemispheral territories supplied by the posterior cerebral artery branches of the basilar artery.
In most patients, infarction in this region (the top of the basilar) is caused by embolism from a more proximal
source such as the heart, the aorta, the vertebral arteries in the neck, or the intracranial vertebral arteries. Less
commonly, the syndrome is caused by intrinsic occlusive disease of the rostral portion of the basilar artery. In
many patients infarction is limited to the rostral brainstem.
The major abnormalities associated with rostral brainstem infarction involve alertness, behavior, memory, and
oculomotor and pupillary functions.
Oculomotor and pupillary abnormalities — The most common abnormalities of eye position and movement
involve vertical gaze and convergence [3,39,40]. Some patients lose all voluntary and reflex vertical eye
movements. Reflex movements are sometimes preserved despite loss of voluntary vertical eye movements.
Either upgaze or downgaze can be selectively involved, but in most patients both directions of vertical gaze are
involved. Upgaze and vertical gaze palsies are more common than downgaze palsies.
Asymmetric or unilateral lesions in the midbrain tegmentum and posterior thalami can cause ocular tilt reactions
in which the contralateral eye and ear are down. Other abnormalities include skew deviation, ocular torsion, and
abnormal estimation of the visual vertical [17].
Convergence abnormalities are also very common. Usually one or both eyes are hyperconverged. One or both
eyes may rest inward or down and in at rest. On attempted upgaze, the eyes may show adductor contractions,
causing convergence movements.
A rostral mesencephalic lesion near the level of the posterior commissure can cause pathologic retraction of the
upper eyelid with widening of the palpebral fissure (Collier sign). In some patients, both lids are retracted but one
eye may have a normal lid position or ptosis.
Lesions in the rostral brainstem also often affect the pupillary light reflex so that the pupils react slowly and
incompletely, or not at all, to light. In patients with diencephalic lesions, the pupils are often small at rest, and
may be fixed and dilated if the lesions involve the third nerve Edinger-Westphal nuclei. A combination of
diencephalic and midbrain lesions may cause mid-position fixed pupils.
The constellation of neuroophthalmologic findings seen with midbrain (pretectal) lesions has been called
Parinaud syndrome (table 1).
Altered alertness, behavior, and memory — Abnormalities of alertness and behavior are common in patients
with rostral brainstem infarcts [14]. Hypersomnolence and abulia are common. Patients may answer queries with
replies that have no relation to reality. The patient may mislocate themselves in place, reporting that they are in a
distant geographical location, and in the personal time dimension, saying that they are presently performing
activities that they had actually done in childhood, adolescence, or much earlier in adult life.
Thalamic or midbrain injury that "straddles the peduncles" can lead to peduncular hallucinations. These are
predominantly visual, but there may be some minor tactile and auditory components. Visual hallucinations are
often quite vivid and contain colors, objects, and scenes. The hallucinations occur predominantly after sundown
[3,39]. (See "Approach to the patient with visual hallucinations", section on 'Peduncular hallucinosis'.)
Prominent and sometimes persistent memory deficits may develop with rostral brainstem infarcts that include the
thalamus. The amnesia involves both anterograde and retrograde memory and usually includes both verbal and
nonverbal memory.
Other findings — Sensory and motor abnormalities are usually absent in patients with top of the basilar
infarction. Movement disorders, especially hemiballism, have been described in some patients with small infarcts
and hemorrhages involving the subthalamic nuclei, but hemiballism is rare in patients with well-documented "top
of the basilar" infarcts.
The superior portion of the cerebellum may also be infarcted, since the superior cerebellar arteries branch from
the distal end of the basilar artery. Common symptoms are slight dizziness, vomiting, ipsilateral limb dysmetria,
gait ataxia, and dysarthria. Vertigo is usually not prominent. Limb incoordination, intention tremor, and dysarthria
are more common with superior cerebellar artery territory infarcts than with infarcts involving the territory of other
cerebellar arteries.
POSTERIOR CEREBRAL ARTERIES — Most posterior cerebral artery (PCA) territory infarcts are due to
embolism from the heart, aorta, or vertebral arteries. Atherosclerosis and dissection of the PCAs is not common.
Visual loss — The most frequent finding in patients with PCA territory infarction is a hemianopia [1-4,41-43]. At
times, the central or medial part of the field is spared, so-called macular sparing. A superior quadrant field defect
results if the infarct involves just the lower bank of the calcarine fissure (the lingual gyrus). An inferior
quadrantanopia results if the lesion affects the cuneus on the upper bank of the calcarine fissure. (See
"Homonymous hemianopia".)
When the full PCA territory is involved, visual neglect can accompany the hemianopia. However, patients are
aware of the visual defect when infarcts are restricted to the striate cortex and do not extend into the adjacent
parietal cortex. The visual defect is often described as a void, blackness, or a limitation of vision to one side, and
patients usually recognize that they must focus extra attention to the hemianopic field. When given written
material or pictures, patients with hemianopia due to occipital lobe infarction are able to see and interpret stimuli
normally, although it may take somewhat longer to explore the hemianopic visual field.
Clinicians can reliably map out the visual fields by confrontation in patients with occipital lobe infarcts.
Optokinetic nystagmus is preserved. Some patients, although they accurately report motion or the presence of
objects in their hemianopic field, cannot identify the nature, location, or color of those objects.
Sensory and motor abnormalities — In patients with PCA territory ischemia, lateral thalamic infarction is the
major reason for somatosensory symptoms and signs [44]. Patients describe paresthesias or numbness in the
face, limbs, and trunk. On examination, touch, pinprick, and position sense are reduced.
The combination of hemisensory loss and hemianopia without paralysis is virtually diagnostic of infarction in the
PCA territory. The occlusive lesion is within the PCA before the thalamogeniculate branches to the lateral
thalamus. Rarely, occlusion of the proximal portion of the PCA causes a hemiplegia, which is probably due to
infarction in the lateral midbrain [3,45-47]. Involvement of the corticospinal and/or corticobulbar tracts in the
cerebral peduncles is thought to cause hemiplegia in these cases.
Left PCA territory symptoms and signs — When the left PCA territory is infarcted, alexia without agraphia [48-
51], anomic aphasia or transcortical sensory aphasia [52], and Gerstmann syndrome (acalculia, agraphia, finger
agnosia, and right-left disorientation) may be found [3,48].
Defective acquisition of new memories is common when both medial temporal lobes are damaged but also
occurs in lesions limited to the left temporal lobe [3,48,53,54]. The memory deficit in patients with unilateral
lesions is usually not permanent but may last up to six months. Patients cannot recall what has happened
recently and, when given new information, they do not recall it moments later. They often repeat statements and
questions spoken only minutes before.
Some patients with left PCA territory infarction have difficulty in understanding the nature and use of objects
presented visually (associative visual agnosia) [48,51]. They can trace with their fingers and copy objects,
demonstrating that visual perception is preserved; they can name objects presented in their hand and explored
by touch or when verbally described.
Right PCA territory symptoms and signs — Infarcts of the right PCA territory are often accompanied by
prosopagnosia, which is difficulty in recognizing familiar faces [51,55]. Disorientation to place and an inability to
recall routes or to read or visualize the location of places on maps are also common [56]. Patients with right
occipitotemporal infarcts also may have difficulty visualizing what a given object or person look like. Dreams may
be devoid of visual imagery.
Visual neglect is much more common after lesions of the right than of the left PCA territory.
SUMMARY
● The most common causes of posterior circulation large artery ischemia are atherosclerosis, embolism, and
dissection. Dolichoectasia (elongation and tortuosity) of the vertebral and basilar arteries is another
occasional cause. (See 'Source of ischemia' above.)
● Atherostenotic lesions of the innominate and subclavian arteries cause arm ischemia and transient ischemic
attacks (TIAs) but seldom cause strokes. (See 'Subclavian and innominate arteries' above.)
● The vast majority of occlusive lesions of the proximal vertebral arteries are atherosclerotic. The most
common location of atherosclerotic occlusive disease within the posterior circulation is the proximal portion
of the vertebral artery in the neck (figure 1). In patients with proximal extracranial vertebral artery (ECVA)
stenosis, intraarterial (artery-to-artery) embolism to the intracranial posterior circulation is a much more
frequent cause of ischemia arteries than hemodynamic insufficiency (ie, low flow). The most frequently
reported symptom during TIAs is dizziness. Diplopia, oscillopsia, bilateral leg weakness, hemiparesis, and
numbness are often reported. Patients presenting with ischemia in the distribution of the intracranial
vertebral arteries (the medulla and posterior inferior cerebellum) or the distal basilar artery (superior
cerebellum, occipital and temporal lobes in the territory of the posterior cerebral arteries, or the thalamus or
midbrain) show a high frequency of recent ECVA occlusions. Dissection of the ECVA usually involves the
distal portion of the ECVA as it winds around the upper cervical vertebrae. (See 'Extracranial vertebral
arteries' above.)
● Atherostenotic disease can involve any portion of the intracranial vertebral arteries (ICVA) (figure 2).
Occlusive ICVA disease presents in a variety of different ways (see 'Intracranial vertebral arteries' above):
• Asymptomatic occlusion
• TIAs, usually including vestibulocerebellar symptoms or elements of the lateral medullary syndrome
• Lateral medullary infarcts (see 'Lateral medullary infarction' above)
• Medial medullary infarction (see 'Medial medullary infarction' above)
• Infarction of one-half of the medulla including the lateral and medial medulla on one side (see
'Hemimedullary infarction' above)
• Cerebellar infarction in posterior inferior cerebellar artery territory (see 'Cerebellar infarction' above)
• Embolization of the ICVA thrombus to the distal basilar artery and its branches causing TIAs and/or
strokes
• Propagation of the ICVA thrombus into the basilar artery causing a basilar artery syndrome
● Basilar artery occlusive disease most often presents as ischemia in the pons. The major burden of ischemia
is in the middle of the pons, mostly in the paramedian base, and often also in the paramedian tegmentum
(picture 1). Most patients with symptomatic basilar artery occlusive disease and pontine ischemia have
some transient or persistent degree of paresis and corticospinal tract abnormalities. Bulbar symptoms
include facial weakness, dysphonia, dysarthria, dysphagia, and limited jaw movements. Oculomotor
symptoms and signs are common. (See 'Basilar artery' above.)
● Occlusion of the rostral portion of the basilar artery (the "top of the basilar") can cause ischemia of the
midbrain, thalami, and temporal and occipital lobe hemispheral territories supplied by the posterior cerebral
artery branches of the basilar artery. Infarction in this region is typically caused by embolism from a more
proximal source such as the heart, the aorta, the vertebral arteries in the neck, or the intracranial vertebral
arteries. Less commonly, the syndrome is caused by intrinsic occlusive disease of the rostral portion of the
basilar artery. The major abnormalities associated with rostral brainstem infarction involve alertness,
behavior, memory, and oculomotor and pupillary functions. (See 'Rostral brainstem ischemia and "top of the
basilar" syndrome' above.)
● Most posterior cerebral artery (PCA) territory infarcts are due to embolism from the heart, aorta, or vertebral
arteries. Atherosclerosis and dissection of the PCAs is not common. The most frequent finding in patients
with PCA territory infarction is a hemianopia. Lateral thalamic infarction is the major reason for
somatosensory symptoms and signs. Additional neurologic syndromes found with infarction of the left PCA
territory include alexia without agraphia, anomic aphasia or transcortical sensory aphasia, and Gerstmann
syndrome (acalculia, agraphia, finger agnosia, and right-left disorientation). Syndromes observed with right
PCA territory infarction include prosopagnosia, which is difficulty in recognizing familiar faces, spatial
disorientation, and visual neglect. (See 'Posterior cerebral arteries' above.)
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Topic 1102 Version 13.0
GRAPHICS
Anatomy of extracranial vertebral arteries
Graphic 59642 Version 3.0
Posterior circulation to the brain
Medulla oblongata
The usual location of lateral medullary infarcts is hatch-marked in the upper right of the
figure. The anatomical structures are labeled on the diagram.
Major cerebellar arterial branches
The intracranial vertebral and basilar arteries are depicted with their major cerebellar arterial
branches, including PICA (posterior inferior and cerebellar artery), AICA (anterior inferior
cerebellar artery), and SCA (superior cerebellar artery).
Reproduced with permission from Caplan, LR. Posterior circulation disease. Clinical findings, diagnosis,
and management. Blackwell Science, Boston 1996. Copyright ©1996 Blackwell Science.
Head thrust test
At rest, the patient is asked to fixate on a distant target. The patient's head is rotated
rapidly by the examiner, first to the left (A to B), then to the right (C to D). In a normal
response, the eyes remain on target (B). In an abnormal response, the eyes are dragged
off target (D), followed by a saccade back to the target (E). This response implies a
peripheral vestibular lesion on the right.
Myelin stain of the pons at necropsy after stroke due to basilar

artery occlusive disease
A large infarct (shown in white) involves the bilateral basis pontis and extends into the
ventral portion of the pontine tegmentum.
Reproduced with permission from: Caplan LR. Posterior circulation disease. Clinical findings,
diagnosis, and management. Blackwell Science, Boston 1996. Copyright © 1996 Blackwell
Science.
Vascular supply of the pons
The major penetrating arteries from the basilar artery are depicted. A) Large paired
median arteries. B) Paramedian arteries lying slightly laterally. C) Arteries that branch at
a right angle from the long circumferential artery (the superior cerebellar artery) into the
lateral pontine tegmentum.
Science.
Collateral blood flow in a patient with a proximal basilar artery

occlusion
Vertebral artery angiogram, lateral view. The proximal portion of the basilar artery is
occluded. Blood flow is seen in the intracranial vertebral artery (A), which gives off the
posterior inferior cerebellar artery (PICA) (B), which in turn anastamoses with the
superior cerebellar artery (SCA) (C). From there, blood flows over the cerebellum to fill
the rostral portion of the basilar artery (D).
Science.
Ophthalmic findings in the Parinaud syndrome
Vertical gaze abnormalities, especially upgaze
Downward gaze preference or tonic downward deviation of the eyes ("setting-sun sign")
Primary position upbeat or downbeat nystagmus
Impaired convergence and divergence
Excessive convergence tone
Convergence-retraction nystagmus
Skew deviation, often with the higher eye on the side of the lesion
Alternating adduction hypertropia or alternating adduction hypotropia
Bilateral upper eyelid retraction (Collier "tucked-lid" sign)
Bilateral ptosis
Pupillary abnormalities (large with light-near dissociation)
Modified with permission from: Lee AG, Brazis PW. Clinical Pathways in Neuro-ophthalmology: An Evidence-based Approach,
Thieme, New York 1998.
Contributor Disclosures
Louis R Caplan, MD Nothing to disclose Jose Biller, MD, FACP, FAAN, FAHA Nothing to disclose John F
Dashe, MD, PhD Nothing to disclose
Contributor disclosures are reviewed for conflicts of interest by the editorial group. When found, these are
addressed by vetting through a multi-level review process, and through requirements for references to be
provided to support the content. Appropriately referenced content is required of all authors and must conform to
UpToDate standards of evidence.
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2/25/2018 Posterior circulation cerebrovascular syndromes - UpToDate

Official reprint from UpToDate®

Posterior circulation cerebrovascular syndromes

Author: Louis R Caplan, MD

Occlusive ICVA disease presents in a variety of different ways [4,14,15]:

● Lateral medullary infarcts

● Medial medullary infarction

● Cerebellar infarction in PICA territory

● Feeling dizzy or off-balance, which may take a number of forms:

• Turning, rotating, whirling, or moving in relation to the environment

• Swaying or rolling as if moving from side to side

Respiratory dysfunction — Respiratory dysfunction is an important feature of lateral medullary ischemia.

Autonomic dysfunction — Autonomic dysfunction may occur in lateral medullary infarction.

● Bilateral sixth nerve paresis may occur

The most important clinical presentations of dilatative arteriopathy are as follows:

● Acute brain ischemia

● A catastrophic outcome caused by vascular rupture

● Normal head impulse test on both sides

The presence of all of the following suggests a peripheral lesion [29-32]:

● An abnormal head impulse test on one side

● Complete bilateral horizontal gaze palsy

● Unilateral horizontal conjugate gaze palsy

● Unilateral or bilateral internuclear ophthalmoplegia (INO)

● One-and-a-half syndrome (a conjugate gaze palsy combined with an INO)

• Lateral medullary infarcts (see 'Lateral medullary infarction' above)

• Medial medullary infarction (see 'Medial medullary infarction' above)

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Topic 1102 Version 13.0

Graphic 59642 Version 3.0

Posterior circulation to the brain

Graphic 66585 Version 3.0

Graphic 62175 Version 1.0

Major cerebellar arterial branches

Graphic 73656 Version 1.0

Head thrust test

Graphic 52022 Version 4.0

Myelin stain of the pons at necropsy after stroke due to basilar

Graphic 81264 Version 5.0

Vascular supply of the pons

Graphic 69507 Version 3.0

Collateral blood flow in a patient with a proximal basilar artery

Graphic 61444 Version 4.0

Ophthalmic findings in the Parinaud syndrome

Vertical gaze abnormalities, especially upgaze

Primary position upbeat or downbeat nystagmus

Impaired convergence and divergence

Excessive convergence tone

Alternating adduction hypertropia or alternating adduction hypotropia

Bilateral upper eyelid retraction (Collier "tucked-lid" sign)

Pupillary abnormalities (large with light-near dissociation)

Graphic 81227 Version 4.0

Conflict of interest policy

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