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REVIEW

Acute Stroke Imaging: What Clinicians Need to Know


Rihan Khan, MD, Kambiz Nael, MD, William Erly, MD
Department of Medical Imaging, Division of Neuroradiology, University of Arizona Medical Center, Tucson.

ABSTRACT
Advances in technology and software applications have contributed to new imaging modalities and
strategies in the evaluation of patients with suspected acute cerebral infarction. Routine computed
tomography (CT) and magnetic resonance imaging (MRI) have been the standard studies in stroke
imaging, which have been complemented by CT and MR angiography, diffusion-weighted MR imaging,
and cerebral perfusion studies, while conventional angiography is typically reserved for intra-arterial
therapy. The purpose of this article is to review the variety of imaging studies available in the acute stroke
setting, and to discuss the utility of each and the pertinent associated main findings. The appropriateness
of which study and when each should be ordered is also discussed. At the conclusion of this article, the
reader should have a more clear understanding of the neuroimaging modalities available for acute stroke
imaging.
2013 Elsevier Inc. All rights reserved. The American Journal of Medicine (2013) 126, 379-386
KEYWORDS: Acute stroke; CT stroke; MRI stroke; Stroke; Stroke imaging

Advances in technology and neuroscience have contributed


to new neuroimaging modalities and strategies in the evaluation of patients with suspected acute cerebral infarction.
Diffusion-weighted magnetic resonance imaging (MRI), cerebral perfusion, and noninvasive angiography using both
computed tomography (CT) and MR are widely available to
supplement standard imaging techniques of MRI and CT.
While beneficial to patient evaluation and management,
when caring for a patient with a potential acute cerebral
infarction, the multitude of diagnostic options may complicate the patients imaging evaluation. This article will describe the basics of imaging studies that may be performed
for a patient with a potential cerebral infarction, explain
their utility, and discuss the significance of the imaging
findings.

NONCONTRAST HEAD CT
Due to its broad availability and speed, noncontrast brain
CT is considered the first line of imaging of patients with
Funding: None.
Conflict of Interest: None.
Authorship: All authors had a role in writing the manuscript.
Requests for reprints should be addressed to Rihan Khan, MD, Department of Medical Imaging, Division of Neuroradiology, University of
Arizona Medical Center, 1501 North Campbell Avenue, Tucson, AZ
85724.
E-mail address: rkhan@radiology.arizona.edu

0002-9343/$ -see front matter 2013 Elsevier Inc. All rights reserved.
http://dx.doi.org/10.1016/j.amjmed.2012.11.014

suspected acute stroke in many centers across the country.


Because intravenous tissue plasminogen activator (tPA) is
the first-line therapy for acute ischemic infarction, potential
clinical mimics of ischemia must be excluded before instituting therapy.
To this end, a noncontrast CT scan of the brain is performed to look for other causes of the new focal neurologic
deficit besides ischemic disease and for any contraindications to therapy. The goal is to start intravenous thrombolytic therapy in patients with clinical suspicion of cerebral
ischemia without any contraindication. MRI is a more sensitive imaging modality than a noncontrast CT scan for the
detection of early infarction; however, because a CT scan is
quicker and much more readily available, CT is considered
the first study in most centers.
The CT scan is done without contrast, because a small
enhancing lesion may be mistaken for an intracranial hemorrhage. On CT, the denser the material is, the whiter it
appears (eg, bone or calcium), while less dense material is
darker (eg, air in the sinuses). Acute blood has the fortunate
imaging property of being higher density than normal brain,
so it is very conspicuous on the noncontrast CT. Incidental
calcifications that may be mistaken for hemorrhage may
occur in the globus pallidus, pineal gland, and the choroid
plexus.
If the patient presents with a new-onset focal neurologic
deficit, and the CT reveals an intracranial hemorrhage, ob-

380
viously they are not a candidate for thrombolysis. If no
blood is seen on the noncontrast CT, an intracranial hemorrhage is excluded, but ischemic disease is still in the
differential diagnosis. Early on in the course of an ischemic
infarct, the head CT scan may look normal. Signs of early
infarction that may indicate an
early ischemic stroke include:

The American Journal of Medicine, Vol 126, No 5, May 2013

sufficiently sensitive to exclude a proximal thrombus if


the dense vessel is not seen.
After around 6 hours, ischemic tissue becomes more
reliably visibly evident as the affected tissue becomes more
edematous. Studies have shown that the area of hypodensity
seen on noncontrast CT correlates
with infarcted tissue. When evaluating the CT scan at presentation,
the insular ribbon sign;
CLINICAL SIGNIFICANCE
when an MCA territory infarction
the basal ganglia sign;
is suspected, it is important to ob In acute stroke, first exclude intracra global loss of gray-white differserve how much of the territory is
nial hemorrhage, a contraindication to
entiation;
involved, as involvement of 1/3
thrombolysis.
mild sulcal effacement; and
of the MCA territory is associated
the dense middle cerebral artery
Cervical and cerebral arteries can be
with an increased risk of bleed
(MCA) or dense basilar artery
evaluated with computed tomography
with thrombolysis,3 while insign.
volvement of 1/2 of the MCA
(CT) or magnetic resonance (MR) anA brief digression into the
territory is associated with brain
giography to look for clot, significant
physical principles that are reherniation.4 Hence, there is the constenosis, dissection, arterial occlusion,
sponsible for the changes in the
traindication to tPA when more than
and other vascular abnormalities.
CT scan as a result of ischemic
1/3 of the MCA territory is involved
Perfusion studies can be performed with
disease will make understanding
on noncontrast CT.
either CT or MR to assess for ischemic
the signs of early infarction easier.
Mass effect from an infarction
penumbra and core infarct.
One of the first concepts to retypically peaks around 3-5 days.
member is that water (serum) is
Acute infarcts also may undergo
Conventional angiography is typically
less dense than cellular material
hemorrhagic conversion, which is
reserved for intra-arterial therapy.
readily confirmed comparing the
commonly thought to represent
cerebrospinal fluid (CSF) in the
reperfusion injury into severely
ischemic tissue via recanalized arventricles to the surrounding
teries
or
via
collateral
flow.
Lastly, after weeks to months,
brain. As a result of hypoperfusion, cellular oxidative mean
infarct
evolves
to
its
chronic
state (Figure 1D), when
tabolism decreases or completely stops, rendering the cell
edema
is
long
gone
and
volume
loss is clearly evident
unable to produce adenosine triphosphate (ATP). ATP-de(encephalomalacia).
pendent membrane transport terminates and the net effect is
water being drawn into and becoming trapped within the
cell. As the cellular water content increases, the CT density
CT ANGIOGRAPHY OF THE HEAD AND NECK
of the affected tissues decreases, in a type of visual averIf cerebral ischemia is suspected after the initial CT scan,
aging of the normal brain parenchyma with the black CSF.
evaluation of the status of the neck and brain arterial vasThe insular ribbon sign (Figure 1A) results from edema
culature is recommended. CT angiography (CTA) is much
causing a loss of gray-white differentiation within the insumore readily available than magnetic resonance angiogralar cortex. This region is sensitive to early ischemic disease.
phy (MRA), with diagnostic accuracy approaching that of
Analogous to the insular ribbon sign is the basal ganglia
conventional angiography. A relatively small bolus of insign (Figure 1B) in which there is edema of the globus
travenous contrast is given, and with modern CT scanners,
pallidus, putamen, or caudate nucleus, and a loss of visuala combined CTA of the head and neck can be performed
ization of these structures. In the case of a large or slightly
with one contrast injection.
older infarction, one may see a loss of gray-white differenSignificant findings on the CTA of the neck include
tiation throughout the affected area (Figure 1C). This is
high-grade arterial stenosis (Figure 2B), occlusion, or disfrequently associated with effacement of the adjacent sulci,
section. Plaque ulceration also may be seen from a ruptured
which is reflective of the cellular edema and development of
plaque. In the intracranial vasculature, areas of stenosis and
mild regional mass effect.
occlusion also may be seen, and sometimes the clinical
In contrast to the decreased density of the affected
presentation points to an area of high clinical suspicion in a
areas of the brain described previously, the dense MCA
particular vascular territory. Focal areas of intraluminal clot
(Figure 2A) or dense basilar artery signs are areas of
can be seen outlined by contrast, in the form of either
abnormal increased density within the vessel lumen. The
arterial stenosis or complete occlusion (Figure 2C). CTA
high density corresponds to thrombus lodged within the
has been shown to be sensitive for detection of intracranial
artery and has been shown to occur in up to one third to
thrombus in the large arteries, but not for the more distal,
one half of patients with angiographically proven thromsmaller branches.4 Once identified, proximal branch occlu1,2
sions may lead to intra-arterial thrombolytic therapy or
bosis. It is therefore useful when seen, but CT is not

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381

Figure 1 Signs of early infarct compared with chronic infarct: (A) Insular ribbon sign.
Notice the small focal area of low density in the anterior portion of the insular gray matter
relative to the posterior aspect (arrows). (B) Basal ganglia sign. Notice the subtle uniform
low density throughout the right basal ganglia (small arrows), while the gray nuclei of the
left basal ganglia maintain their normal higher density (large arrows). (C) Acute large
infarct, left middle cerebral artery territory. Note subtle loss of gray white differentiation
with well-delineated borders. In this case, notice how the insular ribbon is involved, but the
basal ganglia are not. (D) Chronic infarct in left parietal lobe (arrow). Note the low density
from cerebrospinal fluid replacing the infarcted brain and dilation of the ipsilateral lateral
ventricle. An acute to subacute ischemic infarct that underwent hemorrhagic conversion
also is seen on the right side.

mechanical thrombectomy, as opposed to intravenous


thrombolysis, given that intra-arterial thrombolysis may be
more efficacious in treating proximal large vessel occlusion
compared with intravenous thrombolysis.5 The time from
onset of symptoms to initiation of treatment also is a major
factor, as intra-arterial thrombolysis and mechanical thrombectomy have longer window periods for treatment than
does intravenous thrombolysis. Less commonly, multifocal
areas of arterial narrowing may suggest vasculitis, but this

diagnosis can be more sensitively assessed in the clinical


context of systemic disease.
Besides visualizing the arterial vasculature, the CTA
source images (CTA-SI) are very useful as they reflect
blood volume.5 With contrast, normal brain tissue will enhance while areas of infarction will not, thus making the
infarcted tissue more apparent, even more than on the concurrent noncontrast head CT. Size of the infarct as demonstrated on CTA-SI has been shown to closely parallel the

382

The American Journal of Medicine, Vol 126, No 5, May 2013

Figure 2 Vascular abnormalities to look for: (A) Dense middle cerebral artery sign. High density is present in the proximal right M1
segment related to clot. This density was focal and significantly brighter than the other arteries. Also note the areas of right frontal and
temporal subacute infarct. (B) Severe stenosis. Computed tomography angiography (CTA) coronal reformatted image shows a severe
stenosis at the origin of the left internal carotid artery related to atherosclerotic plaque build-up (arrow). (C) Arterial occlusion. Coronal
reformatted image from head CTA shows an abrupt cutoff of the mid to distal left M1 segment (arrow). Contrast opacification of the
more distal branches is related to collateral flow.

size of infarct on follow-up CT.4 CTA-SI has been shown to


be comparable to diffusion-weighted imaging (DWI) in the
detection of ischemic regions, with DWI better at detecting
small infarcts and those in the brainstem and posterior
fossa.6,7
Pitfalls to watch for include a suboptimal contrast bolus,
which may warrant a repeat examination, and significant
venous contamination. Also remember that vascular contrast may have a nephrotoxic effect. Radiology departments
should have a protocol in place for how to deal with contrast
administration in the setting of poor renal function. Alternatively a noncontrast MRA could be performed to evaluate
the head and neck, or an ultrasound examination to evaluate
the carotid bifurcations.

CT PERFUSION
A CT perfusion study can be performed to look for ischemia
or infarct, as the clinical neurologic examination cannot
differentiate the nonfunctioning reversibly ischemic tissue
from irreversibly infarcted tissue. This can be done at the
same time as a CTA study by adding a second contrast bolus
and repeating the scan, tracking changes in cerebral enhancement over time. This allows for assessment of the
ischemic penumbra, which is the area of potentially salvageable tissue ischemia surrounding an area of core infarct.
Although more maps are now available, the key basic
perfusion maps to focus on are: cerebral blood volume
(CBV), cerebral blood flow (CBF), and mean transit time
(MTT). The key to understanding these maps is an understanding of the physiologic principals of ischemia and in-

farction. Ischemic brain has reduced blood flow and therefore it takes longer for the blood to get through the affected
brain (Figure 3), resulting in decreased CBF and increased
MTT. CBV remains near normal in ischemic brain because
it still has some blood flowing through it, which is enough
to keep the tissue alive but not enough for normal function.
Like ischemic brain, the infarcted brain will have an
elevated MTT and decreased CBF. The distinguishing feature that allows differentiation of ischemic brain from infarcted brain is the CBV: there is no blood volume in the
infarcted brain.
The color assignments regarding increased and decreased flow vary from center to center. A color scale is
printed along the side of the images to indicate what colors
represent increased or decreased flow, transit time, or volume. Symmetry is key to interpretationif the examination
is symmetric on all 3 maps, either the examination is normal, or there are bilateral symmetric areas of ischemia or
infarction.
A major pitfall with CT perfusion with most current CT
scanners is that the entire brain is not scanned during the
study. Even with a 64-slice CT scanner, only 4 or 5 slices
are typically obtained, centered at the level of the basal
ganglia where the anterior, middle, and posterior cerebral
vascular territories can be assessed. If a small infarct is
present in an area of the brain that was not imaged, it will
be missed. Some people therefore advocate repeating the
study at a different location. Alternatively, techniques have
been devised to move the table back and forth during the
scan, which helps to increase coverage. Some of the newest

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Figure 3 Computed tomography perfusion ischemia. Cerebral blood volume (CBV) map (A) is normal. Cerebral blood flow (CBF)
is decreased in a wedge-shaped area that is more blue in the left frontal region (B) with corresponding prolongation of mean transit time
(MTT) in the same area that is more red and yellow (C). Note the respective color scales to the side of each image, where blue represents
zero and red represents the maximum value of the scale. If this were infarct, the CBV map would show a similar abnormal wedge-shaped
area as in the CBF and MTT maps.

CT scanners can scan the entire brain without moving the


table (320 slices), but they are not yet prevalent. Consideration also must be given to patients with preexisting disease
(old infarct, brain tumor); the perfusion study will be altered
and one must take care to consider this when evaluating the
maps. As with CTA, because contrast is given, renal function should be considered.

MRI
MRI may be performed after any of the previously discussed CT scans, and in some instances may be the first
imaging test performed. In evaluation of suspected cerebral
infarction, the key sequence to be familiar with is DWI.
Because this image set is a map of water motion, when the
ATP-dependent membrane pumps stop working in infarcted
brain, water becomes trapped within the cell, resulting in
much higher signal than from the background tissues.
Sometimes, areas that are bright on T2-weighted images
with normal diffusion properties will show up as relatively
high signal areas on the DWI (a phenomenon known as T2
shine-through). The high signal area on the DWI must be
correlated with the finding on the apparent diffusion coefficient (ADC) map. Acute infarct will appear dark on the
ADC map, confirming restricted diffusion. So the overall
pattern to look for is: bright on DWI, dark on ADC (Figure
4A, B). It also is important to remember that not everything
that shows restricted diffusion represents acute infarction.
For example, pyogenic abscesses and highly cellular neoplasms also may show restricted diffusion, so the clinical
context and the remainder of the imaging study need to be
scrutinized.
Because the ATP-dependent membrane pumps stop
working nearly immediately, acute infarction will show

Figure 4 Magnetic resonance image (MRI) of acute infarct.


(A) Bright signal on diffusion weighted imaging (DWI) with
corresponding matching low signal on the apparent diffusion
coefficient (ADC) map (B) indicates restricted diffusion from
acute infarct. This is the MRI that corresponds to the computed
tomography (CT) scan in Figure 1C. (C) Coronal gadoliniumenhanced magnetic resonance angiogram from aortic arch to
just above the circle of Willis shows a proximal left middle
cerebral artery occlusion (arrow). (D) Infarct underwent hemorrhagic conversion by day 2 as shown on head CT scan.

384
restricted diffusion within 30 minutes of the initial event.
The practical implication of this is that by the time any
patient gets to the emergency department and placed in the
scanner, virtually everyone with an acute infarct should
show changes on the DWI sequence. Why not go to MRI
first? Some large institutions that have their MRI scanner
close to the emergency department and have 24/7 in-house
MR technician coverage may do that to simply answer if
there is an infarct or not. However, often a noncontrast CT
scan is still performed to rule out a bleed because the high
density of blood makes its presence very recognizable on
CT, and detecting acute hemorrhage on MRI can be
difficult.
Infarcts will vary in shape and size, depending on the
degree of arterial involvement. Proximal branch occlusions, such as the M1 segment of the MCA, can cause
infarction of the entire MCA territory if there is not
adequate collateral circulation. Smaller, more downstream branch occlusions will cause subterritorial infarcts, while tiny clots (as with embolic disease) will
cause terminal branch occlusions and small associated
infarcts. Embolic infarcts are suspected when infarcts
occur in more than one vascular territory: MCA, anterior
cerebral artery, or posterior cerebral artery. Ultimately,
when an infarct has evolved to the chronic stage, just as
on CT, there will be volume loss and encephalomalacia.
After infarcted tissue is resorbed, CSF fills in the cavitated area that follows fluid signal intensity on MRI.
Regarding the exclusion of intracranial hemorrhage in
the hyperacute stroke patient, MRI appears to be at least
equal to CT. Gradient-recalled-echo images can detect
microhemorrhages, both old and new, better than CT, and
in particular, 5 microhemorrhages have not been shown
to be a contraindication to thrombolysis. The fluid-attenuated inversion recovery sequence can be used to detect
subarachnoid hemorrhage, but may be associated with
artifacts at the skull base that mimic subarachnoid
blood.5 Hyperoxygenation also can cause high signal
intensity in the CSF spaces that mimics subarachnoid
blood.8
Some contraindications to MRI include cardiac pacemaker, metal in the eye, inability to fit in the scanner, and an
inability to stay still. The latter is particularly problematic in
the patient with acute mental status change. Contrast is not
necessary for this part of the examination to rule out acute
infarct.

MRA HEAD AND NECK


In many institutions, MRA is more often done in the
subacute setting, after the initial stroke work-up is complete and the tPA window has passed. This is simply
because MRI is usually not as readily available and has
historically taken longer than CT, although new MR
stroke protocols performed at certain acute stroke centers
are approaching CT in regards to time. Nevertheless, as
with CT, the arteries are assessed for significant stenosis,

The American Journal of Medicine, Vol 126, No 5, May 2013


occlusion, and dissection. Noncontrast (2-dimensional
time of flight, 3-dimensional time of flight) or contrastenhanced MRA techniques can be performed, and which
is utilized typically depends on local radiologist preference. However, contrast-enhanced MRA is thought to be
more accurate in imaging extracranial stenosis and vessel
morphology than nonenhanced MRA techniques, and
shows general agreement with conventional angiography
in 85%-90% of cases, as does CTA.5 For intracranial
stenosis, CTA and conventional angiography have been
felt to be more accurate than MRA.5 Due to advances in
MRI, contrast-enhanced MRA of the supra-aortic arteries
including the neck and brain can be obtained with isotropic submillimeter voxel size with high diagnostic
quality and excellent intermodality agreement with other
cross-sectional techniques such as CTA and time-offlight MRA.9,10 In addition to depiction of the cervical
vasculature, the large, proximal intracranial vessels are
well seen, which is of particular use in the acute stroke
setting. Interventionalists look for thrombus in these
large vessels when considering intra-arterial therapy
(Figure 4C), not in the smaller more distal vessels, which
are not as well resolved.

MR PERFUSION
MR perfusion has been incorporated into acute stroke imaging in many large stroke centers where interventional
treatment options such as intra-arterial tPA and clot retrieval
are available.11,12 The goal of MR perfusion is to detect
perfusion-diffusion mismatch with the implication of salvageable tissue that can benefit from further therapeutic
options. Over the last decade, several clinical trials have
suggested that patients with a mismatch between their infarction volume and the volume of hypoperfused tissue may
respond to reperfusion therapies.11-13
Commonly used MR perfusion techniques, including arterial spin labeling and dynamic susceptibility contrast perfusion, have been long used for evaluation of cerebral perfusion in patients with stroke, each with different strengths
and limitations.14,15 Faster image acquisition and the ability
to generate perfusion maps in a few minutes have made
dynamic susceptibility contrast a more robust and widely
accepted technique to measure cerebral perfusion in patients
with acute stroke.
Although the technique is significantly different, the basic premise of MR perfusion is similar to CT perfusion:
ischemic brain has increased MTT, decreased CBF, and
normal CBV; infarcted brain has increased MTT, decreased
CBF, and markedly decreased to no CBV. As in CT perfusion, in MR perfusion it is the presence or absence of blood
in the brain parenchyma (CBV) that allows one to differentiate ischemic from infarcted brain. DWI is used to assess
the core area of infarct (similar to CBV), while specific
perfusion-weighted images (ie, MTT, CBF) represent the
area of ischemia. When there is an abnormal area of perfu-

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Acute Stroke Imaging

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Stroke
*

CT without contrast

MRI without contrast

(most instuons)

(some instuons with MRI and tech


coverage readily available 24/7)

CTA Head & Neck

MRA Head & Neck

**
CT Perfusion of Head

MR Perfusion of Head
(includes DWI if not already done)

Convenonal Angiogram
(usually reserved for therapeucs)
*many radiologists feel more condent excluding blood based on CT and will then use the MR paradigm
**for those radiologists who prefer CTA to MRA but want to ulize MR Perfusion

Figure 5 Suggested acute stroke imaging flow chart. CT computed tomography;


MRI magnetic resonance imaging; CTA CT angiography; MRA MR angiography.

sion that is greater than the area of abnormal diffusion


(DWI), there is an ischemic penumbra.

CONVENTIONAL ANGIOGRAPHY (AKA, DIGITAL


SUBTRACTION ANGIOGRAPHY)
Conventional angiography is still considered the gold standard for the detection of cervical and cerebrovascular disease and is particularly important when considering invasive therapies. It also can provide valuable information
about collateral flow, perfusion status, and may detect other
occult vascular lesions. The resolution, sensitivity, and
specificity of conventional angiography is equal to or
greater than that of noninvasive techniques.6 Although relatively safe, there is a chance of permanent neurological
deficit, including death, due to the presence of the catheter
in the carotid artery. In experienced hands, this is 1%. In
part because of this and the ready availability and relative
ease of use of the noninvasive techniques, conventional
angiography is typically reserved for cases that may require
intra-arterial treatment.

CONCLUSION
This article reviewed the many imaging studies available in
the acute stroke setting. The utility of each study and the
pertinent main findings associated with each were reviewed,
as was the appropriateness of which study and when each
should be ordered. A suggested imaging algorithm for acute
stroke patients also is presented (Figure 5). The authors
hope that our readers have a more clear understanding of

stroke imaging that will translate into a tailored imaging


workup.

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