For patients presenting with acute stroke, it is likely that there will only be time to perform one diagnostic imaging study in order to attempt to reverse ischemic injury. As MRI can accurately diagnose both hemorrhage and ischemia, it may become the modality of choice in this scenario. This paper focuses on the MR appearance of acute ischemic infarction, hemorrhage, and MR angiography of the head and neck as it would appear on both a conventional MR imager and on the newer, echo planar imaging (EPI) systems.
is Director of MRI at Long Beach Memorial Medical Center in Long
Beach, CA, and Professor of Radiology at the University of
California, Irvine, in Orange, CA.
"stroke" is defined as an acute neurologic event. Approximately 85%
of strokes are thromboembolic events,
most of which present with normal findings on CT in the first 6
hours. CT is performed in these patients not to confirm the
diagnosis of infarction but to exclude hemorrhage when symptoms are
still evolving and heparin treatment is planned. Hemorrhage (from a
ruptured aneurysm, an AVM, a tumor, or a hemorrhagic infarct) is a
contraindication for heparinization.
Following exclusion of hemorrhage, the carotid arteries usually
are evaluated with duplex Doppler ultrasonography. Subsequently,
MRI of the brain usually is performed, followed by MR angiography
(MRA) of the carotids. If a flow-limiting stenosis is not detected
in the carotid artery, MR angiography of the circle of Willis
usually is performed.
This paper focuses on the MR appearance of acute ischemic
infarction, hemorrhage, and MR angiography of the head and neck as
it would appear on both a conventional MR imager and on the newer,
echo planar imaging (EPI) systems.
The most common cause of ischemic infarction is vascular
occlusion due to an embolus or thrombosis. If the collateral blood
supply to a region is insufficient, the oxygen supply to that area
of the brain decreases. The normal blood supply to the brain is 50
ml/min/100 gm of brain.
When the blood supply drops to one-third of the normal level (17
ml/min/100 gm), neurons cease to function--i.e., symptoms and EEG
abnormalities appear, but no morphologic changes are seen on either
CT or MRI.
When the blood supply falls to approximately 20% of normal (10
ml/min/100 gm) the ATP levels fall, the sodium-potassium pump
fails, and water and sodium begin to enter the
cell, resulting in intracellular swelling (cytotoxic edema).
Whether or not this initially reversible ischemic injury continues
on to irreversible cell death depends on two factors: the degree
and the duration of reduced blood supply. Reversible cytotoxic
edema can be maintained for several days in the setting of
vasculopathy (e.g., lupus) without infarction. On the other hand,
complete anoxia for a few minutes will result in irreversible
infarction, blood brain barrier breakdown (BBBB), and vasogenic
During the first few hours, CT studies generally appear normal
in the setting of ischemic infarction. On conventional MR images,
mass effect is minimal during the cytotoxic phase. This is because
the water entering the swollen cells has merely been transferred
from the local extracellular space (i.e., there is no net increase
in water content per unit volume of brain). With increasing time
and the development of vasogenic edema due to BBBB from infarction,
there will be increased water content in the brain. This leads to
decreased signal on T1-weighted MR images and increased signal on
T2-weighted MR images, with associated mass effect (figure 1).
When this pattern is seen in a vascular territory, the diagnosis of
ischemic infarction can confidently be made. During this period, MR
contrast agents (gadolinium chelates) also can confirm the
diagnosis of acute vascular occlusion, demonstrating vascular
stasis and leptomeningeal collaterals to the infarcted region
With the newest generation of EPI-capable MRI units, the
diagnosis of ischemic infarction can be made with a great deal of
certainty in minutes rather than hours (figure 3).
These systems are characterized by strong, fast gradients which
allow echo planar images to be acquired in one-tenth of a second
(It should be noted that this is 10 times faster than even the
newest generation of spiral CT scanners, and is as fast as electron
By modifying the basic EPI pulsing sequence, it can be made to
be very sensitive to the diffusion of water. Such "EPI diffusion
images" highlight areas of restricted water diffusion, such as
those found on the inside of cells swollen with cytotoxic edema due
to acute ischemia.
This restricted motion of water leads to high signal on EPI
diffusion images (figure 3C), allowing the rapid diagnosis of acute
cerebral ischemia while it may still be reversible. EPI diffusion
images remain positive for about three weeks after infarction has
occurred, presumably representing a mixed population of infarcted
and cytotoxic cells.
If conventional T2*-weighted EPI images are acquired every
second for 40 seconds following an injection of gadolinium,
perfusion information can be obtained for the entire brain.
As the bolus of paramagnetic gadolinium passes through the
capillary circulation, it causes a temporary drop in signal
intensity due to T2*-shortening from magnetic susceptibility
effects. (When it is inside a magnetic field, the gadolinium in the
capillary gets more magnetized than the adjacent nonparamagnetic
tissues, leading to magnetic nonuniformity, T2*-shortening, and
signal loss.) If this signal loss is plotted over time, information
regarding the blood supply to a particular part of the brain can be
determined, including the relative cerebral blood volume (rCBV) and
the mean transit time (MTT).
The calculated rCBV and MTT values for each voxel in the brain can
then be presented as maps of brain anatomy illustrating these two
characteristics of brain perfusion.
MTT perfusion scans (figure 3D) tend to be positive at milder
levels of vascular compromise than diffusion scans. The mismatch
between the two abnormalities--the so-called "ischemic penumbra",
--is an indicator of the brain at risk for extension of the initial
infarction (figure 3E). This is the target area for many of the new
"neuroprotective" agents being developed. These drugs are designed
to protect the brain after the initial insult has occurred and to
limit further damage. However, recent studies have indicated that
administering thrombolytic agents intra-arterially (IA) within the
first three hours of stroke may still lead to hemorrhage if the
rCBV is reduced by more than two-thirds of the normal level.
On the other hand, IA thrombolysis can be performed as late as 10
hours post-ictus if the rCBV is at greater than half the normal
Thus, it is quite likely that EPI diffusion and perfusion imaging
will be used more and more in the future to guide stroke
Using EPI techniques, four categories of ischemia can be
distinguished: 1) reversible ischemia (cytotoxic edema) not
requiring further treatment; 2) completed infarction without
immediate risk of extension (no ischemic penumbra); 3) completed
infarction with likely extension (ischemic penumbra present); and
4) completed infarction with increased chance of bleeding with
thrombolysis (markedly reduced rCBV due to poor collaterals).
Having made the initial diagnosis of a transient ischemic attack
(TIA) or early infarct, the diagnostic work-up is then directed
towards the cause (i.e., a flow-limiting carotid stenosis, or a
of emboli). Unlike its catheter-based cousin, conventional MR
angiography is noninvasive. In approximately 15 minutes, most of
the common and internal carotid artery can be examined (figure 4A).
Many centers are now combining two noninvasive techniques, MRA and
duplex Doppler ultrasound, to evaluate the carotid arteries in the
setting of stroke or TIA symptoms.
If both indicate a 70% or greater stenosis, then an endarterectomy
can be performed without the need for a catheter study (catheter
studies are now used only when there is a discrepancy between the
ultrasound and MR angiographic results).
At our hospital, stroke is still worked up with an initial CT
scan (to exclude hemorrhage) and a duplex Doppler ultrasound.
Following that, MR angiography of the carotids is performed, as
well as MR imaging of the brain with EPI diffusion imaging to
confirm the clinical diagnosis of infarction. If a flow-limiting
stenosis is not identified in the carotid, intracranial MRA is
performed to examine the circle of Willis and its major branches.
This takes about 10 minutes with conventional MR technology.
With the recent gradient advances which led to clinical echo
planar imaging, faster imaging of the carotid arteries can now be
performed. For example, it is now possible to scan both carotid
arteries from origin to siphon in 10 seconds (figure 4B).
These contrast-enhanced first-pass MR angiographic (CE MRA)
techniques are not only faster, they also are much more accurate in
sizing stenoses than conventional MRA. In addition, the carotid and
vertebral origins and the carotid siphons are able to be visualized
90% of the time. The estimated degree of stenosis is always within
10% of that measured by catheter angiography for CE MRA, compared
to 50% of the time for conventional MRA. Thus it seems likely that
in the future contrast enhanced MRA will be the only imaging test
required to evaluate the carotid arteries in the setting of stroke
Fifteen percent of strokes are due to hemorrhage from ruptured
aneurysms, AVMs (figure 5), or tumors. In the imaging of
hemorrhage, MRI offers two advantages: 1) it can be detected
quickly, and 2) the time between the bleeding episode and scanning
can be assessed fairly accurately. While a complete discussion of
the MR appearance of hemorrhage is beyond the scope of this
article, suffice it to say that five stages of hemorrhage can be
distinguished (table 1) based on the MR appearance on T1- and
Recently it has been shown that both parenchymal hematomas and
subarachnoid hemorrhage can be diagnosed immediately by MRI. On
T2-weighted MR images, hyperacute hematomas are surrounded by a low
This is due to the formation of short T2 paramagnetic
deoxyhemoglobin at the interface between the hematoma and the
normally metabolizing brain. Hyperacute subarachnoid hemorrhage
can be diagnosed immediately using FLAIR.
Because the nulling of CSF
is based on its long T1, and because its T1 decreases immediately
due to the protein content of the serum, subarachnoid hemorrhage
(SAH) can be diagnosed within seconds using this technique. Thus,
MRI can be used instead of CT for the detection of hemorrhage in
the acute stroke patient.
In patients presenting with acute stroke, it is likely that
there will only be time to perform one diagnostic imaging study in
order to attempt to reverse ischemic injury. Current protocols for
intravenous tissue plasminogen activator (t-PA) require that the
patient be treated within three hours of observed onset of
symptoms. As CT generally is only used to diagnose hemorrhage, it
is quite likely that it will be replaced by MRI, which can
accurately diagnose both hemorrhage and ischemia. In addition, MRI
diffusion and perfusion sequences are likely to guide not only
thrombolytic therapy but also the newer neuroprotective agents as
they are introduced over the next few years.
In addition to giving a clear picture of the physiology of acute
ischemia in the brain, MRI can noninvasively depict patency of the
carotid arteries and intracranial circulation within a few minutes.
In fact, the entire MRI stroke protocol takes 20 minutes or less.
Clearly, there will be an increasing tendency for newer,
EPI-capable MRI units to be sited near emergency departments to
assist in the management of stroke.