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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
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
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:
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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.
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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.
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.
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
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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.
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-
Khan et al
385
Stroke
*
CT without contrast
(most instuons)
**
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
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
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