Posterior Circulation
Syndromes
The Non Focal Presentation
Victoria Parada MD
Valley Baptist Neuroscience Department
UTHSCSA RAHC Harlingen
2
Objectives
Recognize the most relevant clinical
findings consistent with posterior
circulation ischemic stroke syndromes
Understand the pertinent history, clinical
evaluation, and management.
3
Clinical manifestations
► Posterior
circulation infarcts comprise
approximately 20% to 25% of all ischemic
strokes (Kumral et al 2004)
► Vertebrobasilar ischemic stroke is not a
homogenous entity
 Duration of transient ischemic attacks varies
considerably
 Symptoms vary from mild to extreme
 Frequency may vary from a solitary attack to many
per day
Symptoms of vertebrobasilar transient
ischemic attacks are complex!
► Unilateral
or bilateral motor or sensory symptoms
involving the face or limbs and unilateral or bilateral
visual field defects
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Vertigo
Diplopia
Dysarthria, dyphagia
loss of balance
isolated sensory symptoms
► may
be considered as transient ischemic attacks
when occurring in combined fashion (simultaneously
or successively)
(Albucher et al 2005)
Clinical manifestations
► The
clinical manifestations of vertebral
basilar occlusive disease vary according to
the site and nature of vascular compromise
and the location of resultant neural
ischemia
4
Etiology
► In
situ atherosclerosis and cardioembolism
are the most common causes of basilar
artery strokes
► Less frequent etiologies include
cervicocephalic arterial dissection, migraine,
dolichoectasia, vasculitis, and paradoxical
embolism.
Clinical profiles may be
distinguished
Vignette 1
A 68-year-old woman with a history of atrial fibrillation
on chronic anticoagulation presented to the hospital
with acute behavioral changes, visual disturbances,
and right hemiparesis.
On examination, she was somnolent, had poor shortterm recollection, dense right hemianopia, mild right
hemiparesis, and profound right hypoesthesia.
5
6
POSTERIOR CEREBRAL ARTERY
OCCLUSION
MRI of her brain showed a large left PCA
infarction and MRA disclosed proximal
occlusion of this vessel.
Despite some functional recovery over the
following 6 months, her visual and cognitive
disturbances remained disabling
7
POSTERIOR CEREBRAL ARTERY
OCCLUSION
The PCAs supply the midbrain, thalami,
lateral geniculate bodies, posterior portion
of the choroid plexus, occipital lobes,
inferior and medial aspects of the temporal
lobes, and posterior-inferior areas of the
parietal lobes.
8
Proximal occlusion of a PCA may
produce:
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decreased level of consciousness
profound disturbances of visual perception
antegrade amnesia
ophthalmoparesis (from damage to the upper
midbrain)
hemiplegia (typically from peduncular ischemia)
hemihypoesthesia
hemianopia.
9
Patients with left PCA infarctions may
experience incapacitating neurocognitive
disorders:
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Alexia without agraphia (corpus callosum)
alexia with agraphia (corpus callosusm + angular
gyrus).
Anomic aphasia may be produced by left temporooccipital strokes.
Severe memory impairment can be caused by
ischemia of the mesial temporal structures or the
thalamus.
Left PCA stroke may be responsible for single
stroke dementia.
10
POSTERIOR CEREBRAL ARTERY
OCCLUSION
Midbrain ischemia may express with
ipsilateral or bilateral ophthalmoparesis (III
nerve palsy, abnormal vertical eye
movements).
Embolism from a cardiac or an arterial
(aortic arch, vertebral artery origin) source
is the most common mechanism of PCA
stroke.
11
Vignette 2
A 64-year-old woman was found unresponsive in her
bathroom by her husband.
She was intubated by EMS and transported to our
emergency department.
On arrival, she was comatose and breathing at a rate
of 40 to 45 per minute. She was tachycardic and
hypertensive. Her pupils were slightly anisocoric (3.5
mm on the left and 3 mm on the right), and responses
to light were minimal on the left and absent on the
right. Corneal and oculocephalic reflexes were
preserved. Best motor responses to pain were in the
form of withdrawal.
12
DWI showed
restricted diffusion in
the midcerebellum
and mesencephalon.
A hyperintense signal
in the basilar artery
indicative of acute
thrombosis was
visualized on FLAIR.
Conventional
angiography
confirmed occlusion of
the basilar trunk.
13
She underwent successful
basilar recanalization by
intra-arterial thrombolysis
combined with mechanical
disruption of the clot.
Despite reperfusion, the
patient failed to improve
neurologically.
Repeat MRI showed
established infarction
throughout the midbrain.
Patient expired shortly after
her family requested
withdrawal of artificial life
support.
14
VERTEBROBASILAR DISEASE
Occlusion of the basilar artery represents
the most dreaded form of ischemic stroke.
At its worst, it causes massive fatal
infarction involving the brainstem,
cerebellum, the occipital and posterior
temporal lobes, and the thalami.
Catastrophic results may at times be
avoided by prompt recognition of early signs
of vertebrobasilar ischemia.
15
16
VERTEBROBASILAR DISEASE
Infarctions at different levels are caused by
different mechanisms:

♦ Proximal territory infarctions (i.e., involving the medulla and
lower cerebellum) are caused by embolism from the heart or
atherosclerosis of the extracranial vertebral arteries or by
hypoperfusion related to severe intracranial vertebral occlusive
lesions.
♦ Middle territory infarctions (i.e., involving pons and
anterior cerebellum) are typically due to intrinsic basilar artery
disease.
♦ Distal territory infarctions (i.e., involving midbrain, superior
cerebellum and posterior cerebral artery territories) are mostly
embolic from cardiac or vertebral artery sources.
17
Dolichoectasia of the basilar artery
►
►
Basilar artery becomes markedly widened, elongated, and
tortuous
Compression due to mass effect may arise in addition to ischemic
syndromes
 Cranial nerve compressive signs are present in over half of symptomatic cases,
most often hemifacial spasm and trigeminal neuralgia
 Direct brainstem compression of the ventral pons may produce slowly
progressive ataxia and hemiparesis
 Hydrocephalus may arise and produce gait, bladder, and cognitive
abnormalities.
 Headaches occur in 15%
 Almost one half of reported symptomatic cases have coexisting or isolated
ischemic symptoms, affecting pontine, midbrain, cerebellar, thalamic, or
occipitotemporal regions
 Subarachnoid hemorrhage occurs infrequently
VERTEBROBASILAR DISEASE
Early signs of vertebrobasilar ischemia can
be subtle and possibly deceiving
Fluctuations with remissions and
relapses of symptoms may precede frank
progression and irreversible development of
severe deficits
Diagnostic imaging modalities other than
angiography have limited value in the acute
setting
18
The top of the basilar syndrome
sudden loss of
consciousness
sometimes
preceded by acute
vertigo
Ataxia
diplopia
19
Signs suspicious for basilar artery occlusion
Combination of ophthalmoplegia with motor,
sensory, or coordination deficits
Crossed motor or sensory findings
Acute ataxia with inability to walk
Sequential appearance of bilateral Babinski
signs
Sequential appearance of bilateral weakness
Acute reduction in the level of consciousness
20
Vignette 3
A 63-year-old man developed acute onset of slurred
speech, gait imbalance, left-sided weakness, and
horizontal diplopia.
On examination, he had mild dysarthria, right
abducens palsy, right facial weakness, left arm and
leg weakness, and mild axial and right appendicular
ataxia.
21
Pontine infarction
22
Pontine Infarctions
Clinical manifestations of pontine infarctions
include oculomotor palsy, contralateral motor
and sensory deficits, and ataxia.
Vestibular disorder ipsilateral to the infarction
may also occur.
Dysarthria may be extremely disabling.
23
Pontine Infarctions
Identification of paramedian
pontine infarctions should prompt
evaluation of the basilar artery,
because they are often caused by
atherothrombosis of this vessel.
24
Vignette 4
A 75-year-old man was admitted with sudden
onset of dysphagia, dysarthria, and gait
imbalance.
He had long-standing history of hypertension
and poorly controlled type 2 diabetes.
On examination, he had left miosis and ptosis,
dysarthria, difficulty swallowing his saliva, left
ataxia, and decreased sensation to pain and
temperature on the right side.
He developed uncontrollable hiccups in the
emergency department.
CT scan was not informative.
26
Wallenberg's Syndrome
DWI demonstrated a left lateral
medullary infarction with
associated ischemia of the left
cerebellum.
The PICA was not seen on
noninvasive angiogram and
considered to be occluded.
27
Wallenberg's Syndrome
The triad of Horner's syndrome, ipsilateral
ataxia, and contralateral hypolgesia
The ipsilateral vertebral artery must be
investigated because occlusion of this
vessel is often responsible for the infarction.
Vertebral atherothrombosis is by far the
most common mechanism.
Vertebral dissection has been found
responsible in some cases.
28
Vignette 5
• 32 year old male. Transient
tinnitus right ear, then 10
minutes of right sided
weakness. Resolved. CT
negative. BP 160/90.
• TIA ABCD2 score 3
32 year old male. Transient tinnitus right ear, then 10
minutes of right sided weakness. Resolved.
Cervical Artery Dissections
Dissections represent one of the most common
causes of ischemic stroke in the young (under
age 45)
They should be suspected in trauma patients
presenting with focal neurological symptoms or
Horner's sign
Majority are due occur with trivial activity
29
Differential Diagnosis
► Analysis
of clinical features of patients who
present with posterior circulation ischemic
disease or stroke show commonality with:
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unilateral limb weakness (81.9%)
central facial palsy (61.1%)
dysarthria (46.3%)
dizziness (33.8%) (Shi 2008).
►The
incidence of crossed paralysis was relatively low
(2.8%).
Differential Diagnosis
► Basilar
artery disease is most closely
mimicked by other illnesses that cause
acute pontine dysfunction
 brainstem encephalitis
 demyelinating disease
 central pontine myelinolysis (osmotic
demyelination syndrome)
 basilar-type migraine
Management VB ischemia
► General
precepts of acute stroke treatment
fully apply to basilar artery stroke
 IV rTPA for patients < 3 hours-4.5 hours
 For patients presenting within 3 hours who fail
to recanalize with intravenous tPA, rescue
endovascular embolectomy therapy should be
considered
Management of VB ischemia
► The
common occurrence of a slowly
progressive or stuttering course suggests
that borderline hypoperfusion is a frequent
feature of basilar artery ischemia
► Regulating intravascular volume and blood
pressure to maximize blood flow is an
accordingly critical aspect of acute care
The Basilar Artery International Cooperation Study
(BASICS)
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The largest prospective observational registry available to date
enrolled 592 patients with basilar artery occlusion confirmed by conventional angiography
619 patients entered in the registry of 27 patients who were excluded all had fatal outcomes
Exclusion was due to the lack of administration of any type of acute antithrombotic or thrombolytic
therapy
Severe deficit was defined as coma, tetraplegia, or locked-in state. Mild to moderate deficit was defined as
anything less than coma, tetraplegia, or locked-in-state. Poor outcome, evaluated at 1 month follow up,
was defined as a modified Rankin scale (mRS) score of 4 or higher.
Therapeutic interventions were divided into antithrombotic therapies (either aspirin or heparin), primarily
immediate intravenous thrombolysis, and immediate intraarterial thrombolysis. Intravenous thrombolysis
included patients treated with and without additional intraarterial thrombolysis. Intraarterial thrombolysis
comprised intraarterial tPA only, mechanical thrombectomy, stenting, or a combination of these
approaches
Thirty-one percent received antithrombotic therapy, 30% intravenous tPA only, 14% intravenous tPA only,
13% intra-arterial tPA and thrombectomy, 5% mechanical thrombectomy only, and 7% received intraarterial and intravenous r-tPA.
There was no statistically significant superiority among the different therapeutic interventions.
At one month follow up, one third of patients were dead and one third were dependent on activities of
daily living. Severe deficit at initial presentation predicted poor outcome. Patients with moderate deficits at
presentation had worse outcome after intraarterial thrombolysis as compared to intravenous thrombolysis
(adjusted RR 1.49, 1.00 to 2.23). Although the BASICS study does not confirm or reject one specific
therapeutic intervention, it questions the alleged superiority of interventional procedures over other
therapies. Randomized control trials comparing current guidelines of acute stroke management against
intraarterial thrombolysis in patients with basilar artery occlusion are necessary.
BASICS
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At one month follow up, one third of patients were dead and
one third were dependent on activities of daily living. Severe
deficit at initial presentation predicted poor outcome.
Patients with moderate deficits at presentation had worse
outcome after intraarterial thrombolysis as compared to
intravenous thrombolysis (adjusted RR 1.49, 1.00 to 2.23).
BASICS study does not confirm or reject one specific
therapeutic intervention
Randomized control trials comparing current guidelines of
acute stroke management against in patients with basilar
artery occlusion are necessary
Key points
►A
posterior circulation infarct may be
preceded by a transient ischemic attack in
one fourth of patients
► Same precepts of acute stroke treatment
fully apply to vertobro-basilar artery stroke
► Clinical suspicion is important to identify
these patients
Questions?