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Circle

Of Willis Vertebrobasilar
Carotid System
System

Cardiovascular Disease Blood Supply to


Spinal Cord

Cerebrovascular
Blood Supply System Venous Drainage
To Brain

Oxygen Demands
And Metabolism Perfusion Territories

Patient
Cases
Map of Essential
Concepts DM McKeough
© 2008
The Cerebrovascular System
 Oxygen demands and metabolism
 Cerebrovascular disease
 Blood supply to the brain
 Carotid system
 Stroke effects

 Vertebrobasilar system
 Stroke effects

 Circle of Willis
 Perfusion Territories
 Venous drainage
 Blood supply to the spinal cord
 Patient cases

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Oxygen Demands 1/2
 The CNS (brain and spinal cord) is the best
protected organ in the human body including
mechanisms to protect its blood supply.
 At approximately 3 pounds, the brain accounts for
about 2% of body mass.
 Consumes 17% of cardiac output.
 Responsible for 20% of oxygen consumption at
rest.
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Metabolism 2/2
 Brain’s sole source of energy is aerobic or oxidative
metabolism.

 Therefore, the brain requires a constant supply of


O2 and glucose, 24 hours a day.

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Cerebrovascular Disease
 While the blood supply to the brain is highly
protected, cerebrovascular disease is the third
leading cause of death in American adults and the
number one cause of chronic functional disability
requiring rehabilitative intervention.

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Blood Supply to the Brain 1/6
 Approximately 1,000 ml/min
delivered via two systems.
 Anterior (Carotid) system:
 70% of supply (35% from
each internal carotid artery)
 Supplies the superior 2/3 of
the brain
 Posterior (Vertebrobasilar)
system:
 30% of supply

 Supplies the inferior 1/3 of the


brain and brainstem
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Blood Supply to the Brain 2/6

Carotid
Perfusion
Territory
(Superior 2/3)

Verterbo-
Basilar
Perfusion
Territory
(Inferior 1/3)
A.

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Carotid System 3/6

 Anterior (Carotid)
system:
 70% of supply (35%
from each internal
carotid artery)
 Supplies the superior
2/3 of the brain

Click to animate

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Vertebrobasilar 4/6
System
 Posterior

(Vertebrobasilar)
system:
 30% of supply
 Supplies the inferior 1/3

of the brain and


brainstem

Click
Click to
to animate
animate

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Blood Supply 5/6

to the Brain

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Blood Supply to the Brain 6/6

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Carotid System 1/12
Anterior cerebral a.
 Anterior (Carotid)
Anterior communicating a.
system:
Middle cerebral a.
 70% of supply (35%
from each internal
Internal carotid a.
carotid artery)
 Supplies the superior
2/3 of the brain

Click to Animate
Click to Animate

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Carotid System 2/12
 Bilateral system, each hemisphere
has its own carotid artery.
 Supplies the superior two thirds of
the brain.
 Derived from: aorta, common
carotid, internal carotid, carotid
foramen (adjacent to optic chiasm)
 Anterior cerebral artery (ACA)

 Middle cerebral artery (MCA)

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Carotid System 3/12

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Carotid System 4/12

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Carotid System 5/12

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Anterior Cerebral Artery 6/12

ADAM

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Middle Cerebral Artery 7/12

ADAM

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Carotid System 8/12

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Middle Cerebral Artery 9/12

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Carotid System 10/12
Perfusion territory by artery

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11/12
Stroke Effects
S&S of ACA occlusion
Distribution
Contralateral leg
Precentral gyrus
Paresis/ paralysis
Postcentral gyrus
Sensory impairment

S&S of MCA occlusion


Distribution
Contralateral face & arm
Precentral gyrus
Paresis/ paralysis
Postcentral gyrus
Sensory impairment

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Middle Cerebral Artery Occlusion 12/12
 Most common stroke
 L MCA
 Most common effects
 Right hemiplegia Face & UE > LE

 If MCA perfuses lateral aspect of


hemisphere, how is the LE
affected?
 Occlusion occurs in the internal
capsule

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Vertebrobasilar System 1/11
 Supplies the inferior one third of the
brain; inferior surface of the temporal
and occipital lobes and brainstem.
 Derived from: subclavian, vertebral,
foramen magnum, anterior spinal,
posterior inferior cerebellar, basilar,
anterior inferior cerebellar, internal
auditory, superior cerebellar,
posterior cerebral artery

Click to animate

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Vertebrobasilar System 2/11

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Vertebrobasilar System 3/11

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Vertebrobasilar System 4/11

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Vertebrobasilar System 5/11

Basilar a.

Vertebral a.

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Vertebrobasilar System 6/11

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Posterior Cerebral Artery 7/11

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Posterior Cerebral Artery 8/11

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Posterior Cerebral Artery 9/11

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3 Cerebellar Arteries 10/11
Superior cerebellar a.

Pons

Anterior inferior cerebellar a.

Medulla

Posterior inferior cerebellar a.


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Stroke Effects 11/11
 S&S of vertebrobasilar occlusion (brainstem stroke)
 Impaired life support systems (HR, RR, BP, consciousness)
 S&S of basilar artery occlusion
 Impaired CN functions
 Impaired long tract functions (motor/ sensory)

 S&S of PICA occlusion


 Impaired pain sensation in ipsilateral face and contralateral body

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Circle of
Willis

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Perfusion Territories
Watershed Territory

Primary Artery Territory

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Venous Drainage 1/2

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Venous Drainage 2/2

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1/2
Blood
Supply
to the
Spinal
Cord

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Spinal Arteries 2/2
Anterior Posterior

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Patient Cases
 Sudden inability to speak
 Left leg weakness
 Worst headache of life
 Decreased vision in one eye
 Left neglect
 Anterior cord syndrome

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Minicase
Sudden Inability to Speak 1/5
While standing in the check-out line at the store, 55 year-old
retired nurse realized she was suddenly unable to speak.
Consciousness, attention, voluntary movement, and the ability
to understand speech were all unaffected. Incredulous, but
believing she knew what is happening to her. She left the
store and drove herself directly to the emergency room. In the
ER she communicated to doctors what she thought was
occurring. With difficulty she uttered two words: “stroke” and
“speech”.

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Minicase
Sudden Inability to Speak 2/5
 Her past medical history was notable for overweight,
hypertension and type II diabetes.
 Examination revealed loss of the nasal-labial fold on the left
and weakness in the left cheek and jaw.
 Her jaw-jerk reflex was hyperactive.
 All other movement, sensation, and reflexes were within
normal limits.

 Where is the lesion causing these symptoms?

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Minicase Follow-Up
Sudden Inability to Speak 3/5
 As confirmed by CT image, this woman was having a
stroke.

 The occlusion involved a deep penetrating branch of the


middle cerebral artery supplying the inferior frontal gyrus on
the left causing weakness in the lower part of the right face
and tongue and Broca’s aphasia.

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Productive (Broca’s) Aphasia 4/5
 Produced by a lesion of
the inferior frontal gyrus of
the dominant hemisphere.

 Play recording

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Minicase Follow-Up
Sudden Inability to Speak 5/5

The key signs and symptoms in this case are:


 Suddenly unable to speak

 Consciousness, attention, voluntary movement, and the

ability to understand speech were all unaffected


 Loss of the nasal-labial fold on the left and weakness in the

left cheek and jaw


 Her jaw-jerk reflex was hyperactive

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Minicase
Left Leg Weakness 1/5
On attempting to stand after finishing breakfast, a 67-
year-old woman fell to the ground, hitting the table on
the way down, because she was unable to support
her body weight on her left leg. She called for help
from her husband who was unable to get her off the
floor and called for emergency assistance.

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Minicase
Left Leg Weakness 2/5
 Her past history was positive for obesity, hypertension, peripheral
vascular disease, and smoking one pack per day for 52 years.
 She had hyperactive deep tendon reflexes in her left knee and ankle,
and a positive Babinski sign in her left foot.
 The left leg was flaccid and she had no voluntary control of
movement.
 She had mild impairment of light touch, pain, and temperature
sensation in her left leg.
 Voluntary movement, reflexes, and sensation were intact in all other
regions of the body.

 Where is the lesion causing these symptoms?

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Minicase Follow-Up
Left Leg Weakness 3/5
 A head CT scan was done and the results
suggested a probable right anterior cerebral artery
infarct.
 Follow-up hear CT scan one month later confirmed
the presence of a hypodense area on the anterior
medial aspect of the right hemisphere consistent
with a right anterior cerebral artery infarct

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Minicase Follow-Up
Left Leg Weakness 4/5

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Minicase Follow-Up
Left Leg Weakness 5/5
The key signs and symptoms in this case are:
 Unable to support her body weight on her left leg

 Hyperactive deep tendon reflexes in her left knee and ankle, and a

positive Babinski sign in her left foot


 The left leg was flaccid and she had no voluntary control of
movement
 She had mild impairment of light touch, pain, and temperature
sensation in her left leg
 Voluntary movement, reflexes, and sensation were intact in all other

regions of the body

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Minicase
Sudden-onset Worst Headache of Life 1/7
A 68-year-old man suddenly developed “the worst of my
life.” On the morning of admission he was sitting watching
TV when at 9:00 am he suddenly developed an explosive
headache worse than anything he had ever experienced.
The headache began in the bifrontal area and over the next
few minutes all over the head and down the neck. He
denied loss of consciousness, nausea, vomiting or vision
changes.

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Minicase
Sudden-onset Worst Headache of Life 2/7
 History was positive for severe diffuse
atherosclerosis, including coronary disease and
peripheral vascular disease requiring multiple
bypass surgeries.
 He was obese and smoked two packs a day for 43
years.
 Examination was unremarkable except for mild
nuchal rigidity.

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Minicase Follow-Up
Sudden-onset Worst Headache of Life 3/7

 Nuchal rigidity is often a sign of meningeal


irritation caused by inflammation, infection, or
hemorrhage in the subarachnoid space.

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Minicase Follow-Up
Sudden-onset Worst Headache of Life 4/7

 The man underwent emergency head CT which


demonstrated regions of hyperdensity in the subarachnoid
space consistent with subarachnoid hemorrhage layering
in the medial longitudinal fissure, lateral fissure, and
around the brainstem.
 Next he was taken for an angiogram which clearly
revealed an aneurysm arising from the region of the
anterior communicating artery.

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Berry Aneurysm 5/7
The circle of Willis has been
dissected, and three berry
aneurysms are seen.
Multiple aneurysms are
seen in about 20-30% of
cases of berry aneurysm.
Such aneurysms are
"congenital" in the sense
that the defect in the arterial
wall is present from birth,
but the actual aneurysm
takes years to develop, so
that rupture is most likely to
occur in young to middle
age adults.
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Berry Aneurysm 6/7

The white arrow on the black card marks the site of a ruptured berry aneurysm
in the circle of Willis. This is a major cause for subarachnoid hemorrhage.

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Minicase Follow-Up
Sudden-onset Worst Headache of Life 7/7

The key signs and symptoms in this case are:


 Suddenly developed “the worst of my life”

 Headache began in the bifrontal area and over the next few

minutes was all over the head and down the neck
 Examination was unremarkable except for mild nuchal

rigidity

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Minicase
Decreased Vision in One Eye 1/8
 A 63-year-old woman went to an ophthalmologist
complaining of episodes of decreased vision in her
“right eye” over the past several weeks.

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Minicase
Decreased Vision in One Eye 2/8
 Her medical history was notable for type II diabetes,
hypercholesterolemia, and coronary artery disease.
 About 5-6 weeks ago the patient began having “episodes of
sudden blurry wavy” appearance of her vision.
 She believed this was mostly in the right eye but never tried
looking with only one eye at a time.

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Minicase
Decreased Vision in One Eye 3/8
 Episodes would last for 15-20 minutes, resolved with no
visual impairment, repeated 3-4 times per week, and were
never accompanied by pain.
 Previously she was able to recognize faces during the
episodes but was unable to read.
 The current episode, that began two days ago, has resulted
in persistent decreased vision on the right.

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Minicase
Decreased Vision in One Eye 4/8
 Neurologic examination revealed fluent speech.
 Pupils 3 mm, constricting to 2 mm bilaterally.
 Normal fundi. Visual acuity 20/30 right and 20/25 left.
 Visual field testing revealed a right homonymous hemianopia.
 Extraocular movements intact.
 Facial sensation intact to light touch and pinprick.
 Face symmetrical. Normal palate elevation.
 Normal shoulder shrug. Tongue midline.

 Where is the lesion causing these symptoms?

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Minicase Follow-Up
Decreased Vision in One Eye 5/8
 The transient episodes of 15-20 minutes of decreased
right-sided vision occurring over several weeks, followed
by a sudden-onset persistent deficit is suggestive of TIAs
preceding a cerebral infarct.
 A right homonymous hemianopia can be caused by a
lesion in the left hemisphere visual pathway anywhere
from the left optic tract to the primary visual cortex.
 The patient’s age and past medical history raise the
suspicion of cerebrovascular disease of the cause.

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Minicase Follow-Up
Decreased Vision in One Eye 6/8
 The patient was sent to the hospital where an initial CT scan
suggested a left posterior cerebral artery infarct, and a follow-up MRI
confirmed the presence of a left PCS infarct involving the left primary
visual cortex.
 An magnetic resonance angiogram (MRA) revealed several stenoses
of the cerebral vessels compatible with diffuse intracranial
atherosclerotic disease.
 She was treated with long-term oral anticoagulation.
 Her right hemianopia did not improve, but over time she learned to
adapt to her visual deficit.

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Minicase Follow-Up
Decreased Vision in One Eye 7/8

MRI axial T2 weighted


image of left posterior
cerebral artery (PCA)
infarction

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Minicase Follow-Up
Decreased Vision in One Eye 8/8
The key signs and symptoms in this case are:
 Episodes of sudden “blurry/ wavy” appearance of her vision

in her “right eye” over the past several weeks


 Right homonymous hemianopia

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Minicase
Left Neglect 1/5
 A 61-year-old right-handed man was witnessed
slumping to the floor in the grocery store.

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Minicase
Left Neglect 2/5
 On examination in the hospital he denied anything was wrong but
said, “They called an ambulance because they said I had a stroke.”
 He was unaware of having any impairment and wanted to go home.
 He had profound left visual field neglect , no blink to threat on the left,
and no voluntary gaze to the left past midline.
 When trying to right, he moved the pen in the air off to the right of the
page.
 When shown his left hand and asked what it was, he replied
“Someone’s hand.”

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Minicase
Left Neglect 3/5
 When asked who’s hand it was he replied, “The doctor’s.”
 He had a marked right gaze preference.
 He had marked weakness in the lower portion of the left
face.
 Strength was 0/5 in the left arm and leg, the left plantar
response was upgoing, and there was no response to
pinprick on the left side.

 What lesion is causing this man’s symptoms?

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Minicase Follow-Up
Left Neglect 4/5
 The patient exhibits several forms of neglect.
 In addition to anosognosia, he has left sensory neglect, to visual
and tactile stimuli, as well as left motor neglect.
 These signs and symptoms are most commonly seen in patients
with nondominant (usually right) parietal lobe lesions.
 Given the sudden onset of the deficits, involvement of the left arm
and leg, the presence of sensory and motor deficits, and the
patient’s age, the most likely cause is ischemic infarction of the
right internal carotid artery.

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Minicase Follow-Up
Left Neglect 5/5
The key signs and symptoms in this case are:
 Anosognosia

 Left face, arm and leg plegia with positive Babinski’s sign

 No blink to threat on the left

 No voluntary gaze to the left past midline

 No response to pinprick on the left

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Occlusion of the anterior spinal artery (anterior cord
syndrome) in the cervical region would produce
what impairments? 1/2
Click for answer

The anterior spinal artery perfuses the anterior 2/3 of the


spinal cord including the ventral horns as well as all tracts in
the lateral and anterior columns, bilaterally. Damage to the
lateral corticospinal tracts cause upper motor neuron signs,
bilaterally, below the lesion level. Damage to lower motor
neurons in the ventral horns cause lower motor neuron
signs, bilaterally, at the lesion level. Damage to the lateral
spinothalamic tracts cause absence of pain and temperature
sensation, bilaterally, below the lesion level. Sparing of the
dorsal columns leaves light touch, vibration, and position
sense intact throughout.
Click for explanation
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Anterior Cord Syndrome 2/2
UMN UMN
Click to animate

DRG
DRG

R L

Anterior cord lesion


Common
causes include Lateral corticospinal tract lesion
anterior spinal Ipsilateral upper motor neurons signs
artery infarct,
Lateral spinothalamic tract lesion
trauma, and Contralateral loss of pain and
MS. temperature sense

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The End

© DM McKeough 2008

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