Stroke is a generic term that describes
the clinical event of a sudden onset of neurologic deficit secondary to
cerebrovascular disease.
Stroke has 4 main etiologies, including
cerebral infarction (80%),
intraparenchymal hemorrhage (15%),
nontraumatic subarachnoid hemorrhage (5%),
venous infarction (approximately 1%).
Clinically, ischemic infarction is the
most common etiology and will be the main topic of this introduction.
The principal cause of cerebral
infarction is atherosclerosis and its sequelae.
Ischemic
Infarction
There are 3 major clinical ischemic
stroke subtypes based
upon the
classification from a multicenter clinical trial (trial of
drug ORG
10172 in acute stoke treatment [TOAST]).
These 3 subtypes include
large artery/atherosclerotic
infarctions,
cardioembolic infarctions,
small vessel
occlusion (lacunar)
infarctions.
Large artery/atherosclerotic strokes
represent approximately 40%
of strokes and can arise from thrombosis at the
site of a plaque or from emboli produced at the plaque that lodge
downstream.
The most common site of
atherosclerotic plaque
is at the carotid bifurcation with involvement of
the distal common carotid artery and the 1st 2 cm of the internal carotid artery.
The most frequently occluded intracranial
vessel is the middle cerebral artery (MCA).
Other common
locations for atherosclerotic plaque include the
carotid siphon and proximal anterior and middle cerebral arteries.
The vertebral and basilar arteries are also
commonly involved
by atherosclerosis.
.
Cardioembolic
disease
accounts for
15-25% of ischemic
strokes.
Risk factors include myocardial
infarction, ventricular
aneurysm,
atrial fibrillation or flutter, cardiomyopathy, and valvular heart
disease.
Lacunar infarcts
are small in size (< 15 mm),
typically in the
basal ganglia
and thalamus, and account for 15-30% of all strokes.
They are often multiple and are due to embolic,
atheromatous, or
thrombotic lesions in the single penetrating end arterioles that supply the deep
gray nuclei, including the
lenticulostriate and thalamoperforating
arteries.
Other common locations
for lacunar infarcts include the internal capsule,
pons, and corona radiata.
Intraparenchymal
Hemorrhage
Intraparenchymal hemorrhage
represents ~ 15% of all strokes and includes multiple etiologies.
Hypertensive hemorrhage is the most
common etiology, representing ~ 40-60% of all primarily intracranial
hemorrhages.
Other etiologies include amyloid angiopathy in
elderly patients, as well as vascular malformations, vasculitis, drugs, and
bleeding diathesis.
Risk factors for hemorrhagic stroke
include increasing age,
hypertension,
smoking, excessive alcohol
consumption,
prior
ischemic stroke,
abnormal cholesterol, and anticoagulant medications.
Although the
MR physics related to hemorrhage are complex, the stages
are generally accepted as
hyperacute,
acute, early
subacute,
late subacute, and
chronic.
Nontraumatic Subarachnoid Hemorrhage
Nontraumatic
subarachnoid hemorrhage is typically related to an aneurysm
(75%) or a vascular malformation, such as an arteriovenous malformation
or cavernous angioma
Nonaneurysmal "perimesencephalic"
subarachnoid hemorrhage is uncommon.
Venous Infarction
Dural sinus or cerebral vein occlusion is
rare, representing less than 1% of strokes.
Venous thrombosis risk factors include
pregnancy, trauma, dehydration, infection, oral contraceptives, coagulopathies,
malignancies, collagen vascular diseases, and protein C and S deficiencies.
Venous infarcts occur in only ~ 50% of
venous thrombosis cases, and can be differentiated from arterial infarcts by
the location of
the
ischemia.
Superior sagittal sinus thrombosis
typically results in T2/FLAIR hyperintense parasagittal lesions, while thrombosis of the transverse sinus often
results in T2/FLAIR hyperintensities in the posterior temporal lobe.
Additionally, venous infarcts more
commonly present with associated hemorrhage.
Contrast-enhanced CT is useful to
identify the "empty-δ" sign representing thrombus within a major dural sinus, typically the superior sagittal or
transverse sinus.
Approach
to Stroke Imaging
Cerebral ischemia
results from significantly decreased blood flow to
selected areas or the entire brain.
Stroke progresses
in
stages from
ischemia to actual infarction.
In the most common
situation,
MCA occlusion, there is a densely ischemic central core and a
less densely ischemic "penumbra."
The central core
is usually
irreversibly damaged unless reperfusion is quickly established,
whereas the cells within the penumbra may remain viable
but at risk for several hours.
Current stroke therapies attempt
to rescue the "at-risk" cells.
Currently, acute stroke protocols
vary among different
institutions.
The exact protocol is often based on the
availability of
CT vs. MR, technology/software, time of stroke,
physician expertise, and the
possibility of neurointervention.
Typically, stroke neurologists work
with neuroradiologists to
devise a
plan that best serves the patient's needs.
Most stroke protocols begin with a noncontrast head CT to evaluate for hemorrhage or mass, which directly affects treatment decisions. Additionally, > 1/3 MCA territory hypodensity at presentation is considered by most to be a contraindication to thrombolysis, as it is associated with a greater risk of fatal hemorrhage.
CTA is useful to evaluate for
large vessel
occlusion.
When available, CT perfusion is an
excellent way
to evaluate for large vessel ischemia.
MR with diffusion-weighted imaging
(DWI) is particularly
useful for
acute ischemia when CT perfusion is negative and the clinical
suspicion for stroke remains.
MR is also the primary
imaging tool
when the clinical question includes a posterior fossa or
brainstem lesion.
MR with perfusion imaging (PWI)
has been
found extremely helpful in guiding therapy when available.
Most stroke protocols use 3-hour and
6-hour windows for
treatment of
nonhemorrhagic
ischemic stroke.
If the patient presents within
6 hours after the initial onset of symptoms, an unenhanced CT is
typically the initial study of choice to exclude a
mass or hemorrhage.
If there is a hemorrhage or
mass,
no thrombolytic therapy is initiated.
If there is no hemorrhage or mass
and the patient is within 3 hours after onset of symptoms, the patient is
eligible for intravenous (IV) thrombolysis.
If the patient is between 3 and 6
hours of onset,
either a
CTA with CT perfusion or an MR with DWI and PWI is performed to
determine if they are eligible for treatment.
If the patient has an intracranial
thrombus with a penumbra intraarterial
(IA) thrombolysis or IA
thrombectomy is
recommended.
If there is no penumbra, IA therapy
may notbenefit the
patient, so each case is evaluated individually.
The effective therapeutic window
for the posterior circulation
is thought
to be longer than the 3-6-hour window, but the exact time
is variable and depends on collateral circulation.
Therefore, patients with vertebrobasilar
thrombosis are
evaluated individually
for risk vs. benefit of IA thrombolysis or thrombectomy.
Ischemic Penumbra
Ischemic stroke results in a core of
tissue that has undergone irreversible injury.
The ischemic penumbra is the area of
brain that may be salvageable with appropriate therapy.
The penumbra typically surrounds the
ischemic core and is supported by collateral circulation.
The ischemic penumbra can be identified
by a combination of MR diffusion (DWI) and perfusion imaging (PWI).
DWI is the most reliable estimate of the
ischemic core and generally correlates with irreversible injury. However, with
early reperfusion following thrombolysis, some reversal of DWI can be observed.
PWI evaluates the presence of a penumbra.
With MR, the mismatch between the DWI and
PWI defines the penumbra.
This model provides a practical means to
estimate the ischemic penumbra.
In general, if there is no
diffusion/perfusion mismatch, therapy may be ineffective.
With the newer CT perfusion
techniques, an ischemic
penumbra may
also be measured with CT.
With the urgency of acute stroke,
MR may be impractical.
However, with new faster MR
protocols and the superiority of MR to CT in detecting small vessel
ischemia and brainstem
ischemia,
MR may be a preferred technique.
CT
Perfusion (pCT)
Cerebral perfusion refers to the
tissue-level blood flow in the brain.
This flow is evaluated by 3 main
parameters at pCT:
Cerebral blood flow (CBF),
cerebral blood
volume (CBV),
mean transit time (MTT).
CBF is defined as the volume of blood
moving through a given
unit volume
of brain per unit time.
CBF uses units of milliliters
of blood
per 100 g of brain tissue per minute.
Studies suggest that CBF
is a reasonable marker for the ischemic penumbra.
CBV is defined as the total volume
of blood in a given unit
volume of
brain.
This includes blood in the tissues as
well as
blood in
the large-capacitance vessels, such as arteries, arterioles,
capillaries, venules, and
veins.
CBV uses units of
milliliters of
blood per 100 g of brain tissue.
Some studies suggest that
CT perfusion-acquired CBV is a reasonably reliable marker
of the ischemic core.
MTT is defined as the average of the
transit time of blood through a given brain region. The transit time of blood
through the brain parenchyma varies depending on the distance traveled between
arterial inflow and venous outflow.
MTT equals CBV/CBF.
CBF/CBV mismatch correlates with stroke
enlargement in untreated or unsuccessfully treated patients.
Those patients with a CBF/CBV match or
those with early complete recanalization do not exhibit progression of the
ischemic stroke.
The general treatment guidelines for pCT are as follows.
If there is a CBF/CBV mismatch, with a
larger CBF suggesting an ischemic penumbra, the patient is likely a good
candidate for therapy.
Many treatment guidelines suggest that a
≥ 20% CBF/CBV mismatch should be present to consider thrombolysis.
Some authors propose that if there is no
mismatch between CBV and CBF, treatment is unlikely to benefit the patient.
CT
Perfusion Interpretation Pearls
The MTT is the most sensitive parameter
for perfusion
deficits.
Although it is
generally elevated due to a thromboembolic process,
it may be elevated in a patient with
significant arterial
atherosclerotic narrowing.
In early ischemia,
MTT is
elevated and CBF is decreased. However, the CBV can be preserved
or even
elevated due
to capillary bed dilatation
in very
early ischemia.
Once a CBF threshold is reached, CBV
starts to
decline.
This results in the ischemic core, which
has a
matched decrease
in CBF and CBV, whereas a mismatch
between CBF and CBV suggests a
penumbra.
Differential
Diagnosis
When considering stroke in a child or
young adult, several
possible etiologies
should be addressed, including arterial dissection,
vascular malformation with hemorrhage, drug abuse, or
clotting disorder.
In young children, other
possibilities include
congenital heart disease with emboli and idiopathic progressive
arteriopathy of
childhood (moyamoya
disease).
In a middle-aged or older adult,
the typical stroke etiologies
include arterial
thromboembolism, hypertensive hemorrhage, and cerebral
amyloid angiopathy.
When evaluating a hemorrhagic
stroke, etiologies in children
include vascular
lesions, hematologic disorder, vasculopathy, and
venous
infarct.
In a young adult, considerations include
vascular malformations,
drug abuse, and less commonly
venous occlusions
or vasculitis.
In older adults, common
considerations for
intracranial hemorrhage include
hypertensive hemorrhage,
neoplasm, cerebral amyloid
angiopathy,
and, less commonly, dural
sinus/cerebral venous
occlusion and
coagulopathy.
Imaging gallery
Axial DWI MR shows diffusion restriction in the left ACA distribution within the medial parafalcine frontal lobe.
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Axial DWI MR shows diffusion restriction in the occipital lobe related to PCA ischemia. DWI is the most sensitive MR sequence for acute ischemia.
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Axial DWI MR shows diffusion restriction related to acute ischemia in a pontineperforating artery distribution.
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Axial T2WI MR shows hyperintensity in the right inferior cerebellum and lateral medulla related to a PICA infarct from a vertebral artery embolus.
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Axial T2WI MR shows hyperintensity and local mass effect in the right superior cerebellum related to an acute SCA infarct. SCA infarcts may involve the superior cerebellum and the upper lateral pons. |
Axial DWI MR shows restriction in left MCA territory with preservation of the basal ganglia.
The MCA territory is the most common location for ischemic stroke.
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Axial CT perfusion CBF color map shows a large area of decreased blood flow in the left hemisphere related to hyperacute MCA ischemia. |
Lateral gross pathology shows a chronic MCA infarct with hemorrhage and encephalomalacia in the frontal operculum and temporal lobe .
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Axial FLAIR MR shows hyperintensity in the bilateral medial thalami related to an acute artery of Percheron infarct.Extension to the medial midbrain is often present.
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Axial CT shows a classic thalamic hypertensive hemorrhage, the 2nd most common cause of stroke.
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Axial SWI MR image in an elderly patient shows extensive susceptibility artifact related microhemorrhages in the bilateral hemispheres. Pattern is typical of cerebral amyloid angiopathy.
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