Neuroimagenes 1

SMGr up
Neuroimaging in Acute Stroke
Shazia Mirza1* and Sankalp Gokhale1

1
UT Southwestern Medical Center, USA
*Corresponding author: Shazia Mirza, UT Southwestern Medical Center, USA, Email: Shazia.
Mirza@UTSouthwestern.edu
Published Date: July 25, 2016
INTRODUCTION
Every year, about 795000 people experience a new or a recurrent stroke. Cerebrovascular
disease ranks No. 4 among all causes of death and is the leading cause of serious long-term
disability in the United States [1]. Hence the need for rapid diagnosis and management is vital.
The diagnosis of acute stroke is made on the basis of patient history, clinical examination and
neuroimaging.
Temporally, stroke is defined as acute (24 hours), sub-acute (1-5 days) and chronic (weeks)
[2]. The newer category hyper-acute stroke [3] refers to stroke within 6 hours of onset.
NEED FOR IMAGING

Imaging studies in acute stroke have the following aims:
• Differentiate ischemia from hemorrhage which directs further therapy.
• Assess the extent of brain injury (irreversible infarction) and potential complications such as
herniation or midline shift.
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• Identify at-risk,under-perfused tissue which can undergo infarction if perfusion is not restored.
• Identify the possible etiology, type and location of the vascular lesion responsible for the
deficit.
• Rule out stroke–mimics such as tumors or hematomas.
Time is brain! Every minute of an untreated large vessel stroke results in the loss of 1.9 million
neurons, 13.8 billion synapses, and 12 km (7 miles) of axonal fibers [4]. Since recombinant
tissue plasminogen activator (rt-PA) is the only treatment option approved by the Food and
Drug Administration for acute ischemic stroke; within the first 3-4.5 hours of onset [5-7], it is
imperative to rapidly image the patient to exclude hemorrhagic stroke. As treatment modalities
expand such as endovascular thrombectomy [8] neuroimaging continues to expand in its goals
and scope. The American College of Radiology (ACR) continually provides updates to guidelines
for imaging through the ACR Appropriateness Criteria.
COMPUTED TOMOGRAPHY
There are three key CT techniques—unenhanced imaging- NCCT, angiography- CTA, and
perfusion imaging-CTP. A key advantage of this multi-modal CT is rapid imaging (scan time is
under 10 minutes [9]), and risks are related to radiation exposure and the contrast material used
if any.
NON CONTRAST COMPUTED TOMOGRAPHY (NCCT) - BRAIN

NCCT is performed as a first line in neuroimaging as it is usually considered gold standard in
ruling out hemorrhage [10,11] despite MRI being equivalent to CT in this regard [12] due to the
ease of availability [10], rapid results, and safety in both stable and unstable patients [13,14].
Advancements in technology enabling thinner slices (sub millimeter) and enhanced tissue
differentiation [13] allows for a role of NCCT in arterial occlusion and early infarction with a
variable detection rate of about 65% [15] in cases imaged within 6 hours. A description of these
signs is below.
Hyper Dense Artery/MCA Sign

This is a result of a thrombus or embolus (usually in the MCA) resulting in an increased density
of the blocked vessel. The prevalence ranges from about 27% in all types of strokes to 41% with
MCA infarct with a specificity of 100%, but sensitivity of only 30% [16]. This sign disappears with
resolution of the thrombus in a few days. False positives are due to calcification of the walls or a
high hematocrit (Figure 1).
Figure 1: Hyperdense Artery Sign. The “Dense MCA or hyperdense vessel/artery sign” is one of
the early signs of acute middle cerebral artery (MCA) territory infarction. This corresponds to
a hyper-dense cord like MCA seen in the regionof the Sylvian fissure on non-contrast CT which
represents thrombotic material in main stem of the MCA.
Image source: With permission from Dr. Anvekar B., Neuroradiologycases.com , Neuroradiology
unit, S P Institute of Neurosciences, Solapur, India.
Hypo Attenuating Brain Tissue

Ischemia causes cytotoxic edema; an increase in brain water by 1% results in a CT attenuation
decrease of 2.5 HU (Hounsfield Units) [17]. The specificity of ischemic edema on NCCT for brain
infarcts is 85% and sensitivity was 64%, with lack of early CT findings resulting in better 90 day
clinical outcomes and vice versa [18]. Also seen is cortical sulcal effacement (Figure 2).
Figure 2: Left middle cerebral artery (MCA) infarction. Axial nonenhanced computer tomography
shows foci of hypoattenuation in the left parenchyma (arrows) and sulcal effacement in the left
MCA territory, consistent with infarction.
Image source: With permission from Dr. Birenbaum D., Imaging in Acute Stroke, Western
Journal of Emergency Medicine, 2011. 12(1): p. 67-76.
Obscuration of the Lentiform Nucleus

Also called blurred basal ganglia; it is one of the most common and earliest seen sign of
infarction (MCA) due to terminal blood supply pattern. The loss of the grey-white matter interface
and CT hypodensity results in the ‘obscuration’ of the lentiform nucleus [19,20].
Insular Ribbon Sign

Another early and indicative sign of infarction (MCA) refers to hypodensity and swelling of
the insular cortex results in loss of the insular ribbon [19,21] (Figure 3).
Figure 3: Insular ribbon signrefers to loss of the normal grey-white matter differentiation in the
insular cortex. It is one of the earliest imaging signs of middle cerebral artery territory infarction.
The yellow arrow shows a normal insular cortex (ribbon visble). However upon infarction leading
to cytotoxic edema, this ribbon is lost (red arrow).
Image source: Adapted with permission from Dr. Anvekar B., Neuroradiologycases.com ,
Neuroradiology unit, S P Institute of Neurosciences, Solapur, India.
Hemorrhagic Infarct
There is usually a sharp contrast between blood (high attenuating- seen as brighter white
areas) and CSF (low attenuating-dark areas) (Figure 4 A & B).
Figure 4A: Axial nonenhanced CTshows “bright” or hyper attenuating dense subarachnoid
hemorrhage throughout the perimesencephalic cistern (arrow), along the tentorium (double
arrows), and from there to the 4th (double arrowheads) and 3rd (arrowhead) ventricles.
Figure 4B: Nonenhanced axial CT demonstrates a large right basal ganglionic hypertensive bleed
(*) complicated by mass effect, midline shift (subfalcine herniation)to the left (arrows). The blood
is seen as hyper-attenuating or bright.
By altering standard viewing parameters, the sensitivity and specificity of stroke detection can
be increased.
QUANTIFICATION OF ISCHEMIC INVOLVEMENT- ASPECTS

METHOD
Alberta Stroke Program Early CT score (ASPECTS) is a 10-point quantitative topographic CT
scan score developed in 2001 offering a reproducible grading system to score early ischemia in
anterior circulation strokes to better direct treatment and reduce the variability of observations
[15]. Using two standard axial CT slices; one at the level of the thalamus and basal ganglia, and
one just rostral to the basal ganglia, the MCA territory is divided into 10 regions,each accounting
for one point in the total score, for each involved area, a point is subtracted. This score correlated
inversely with the NIHSS (National Institutes of Health Stroke Score) with clinicians agreeing it
superior and more systematic compared to the conventional 1/3 MCA rule to exclude thrombolytic
treatment [23]. The ASPECTS method is not without its limitations; such as difficulty in scoring
due to age related periventricular white matter changes or streak artifacts in the base of the skull
or tilt and motion artifacts. (ASPECTS diagram).
Alberta Stroke Program Early Ct Score (ASPECTS). Schematic diagram showing various areas
used for scoring on the ASPECTS. Level of internal capsule & insula: M1 - cortical area anterior
to Sylvian fissure; M2 - cortical area just posterior to Sylvian fissure; M3 - more posterior cortical
area in MCA distribution at same level.
At cut near top of the lateral ventricles: M4 - anterior third of cortex; M5 - middle third of
cortex; M6 - posterior third of cortex.
COMPUTED TOMOGRAPHY ANGIOGRAPHY-CTA

CTA is a minimally invasive study with an optimally timed rapid injection of iodinated
contrast through a peripheral IV (intravenous) line to cause vascular opacification, obtaining
thin section CT images and using software to stitch the images allowing for a 3-dimensional
image of cerebral and neck vasculature (from the aortic arch to the circle of Willis). This allows
for identification of stenosis and occlusions; assisting therapeutic decisions such as IV or intra-
arterial TPA, mechanical clot retrieval or in cases of carotid dissection, against such a therapy.
CTA also identifies vascular abnormalities such as arterio-venous malformations and aneurysms.
CTA demonstrated occlusion does correlate with the NIH Stroke Score and outcome of TPA [24]
(Figure 4C, 5A, B, C, D).
Figure 4C: Coronal two-dimensional reconstruction from a CT angiogram showingsubfalcine
herniation (arrows) to the left due to large right sided intra-parenchymal hemorrhage. This is the
same patient in Figure 4B.
Figure 5A: Sagital reformatted images from CT angiogram identifyan enhancing vascular
malformation (arrow), which was the etiology of the intraventricular hemorrhage (same patient
in Figure 4A).
Figure 5B: Computed tomography angiogram in the axial projection demonstrates a focal basilar
tip artery aneurysm (arrow).
Figure 5C: Cerebal computed tomography angiogram (CTA) in three-dimensional projection with
skull surface overlay demonstrates an anterior communicating artery aneurysm (1). Dedicated
images from CTA of the Circle of Willis isolate the aneurysm (arrow) (2).
Figure 5D: This patient had subarachnoid hemorrhage on non-contrast CT scan. Images D1, D2,
D3 are 3-D reconstructions from CTA (to identify source of hemorrhage) which show aneurysm
like pouching (red arrows) in the PCOM (2) and ACOM (3,4). On conventional angiography (1),
these aneurysms were proved to be the infundibulum of vessels. The diagnosis of aneurysms <3
mm on CTA is often tenuous and requires angiographic confirmation.
Image source: copyright www.neuroangio.org -Used with permission from Dr. M. Shapiro.
CTA Source Images: CTA SI using the images in a CTA, cerebral perfusion can be assessed as
low density/dark areas in contrast to hyper-attenuated contrast areas allowing for an estimation
of tissue perfusion [25] and a better assessment of tissue at risk compared to NCCT [13] potentially
removing the need for a separate CT perfusion study.
COMPUTED TOMOGRAPHY PERFUSION IMAGING -CTP

CTP (like CTA) tracks an IV bolus of iodinated contrast over time with sections of the brain
imaged repeatedly. This allows the measurements of parameters such as cerebral blood volume,
cerebral blood flow, mean transit time (time difference between arterial inflow and venous
outflow), time to peak enhancement (time from the beginning of the contrast injection to the
maximum concentration in a region of interest). These parameters can be extrapolated to
delineate areas of hypo-perfusion and irreversible infarction by creating perfusion maps. CTP
has shown incremental increased sensitivity and specificity in diagnosing acute ischemic stroke
compared to NCCT or CTA [26]. CTP is easily available and can be performed on a standard helical
CT after NCCT. Clinically, in acute stroke CTP provides information on the penumbra (increased
mean transit time, moderately decreased cerebral blood flow and normal to high cerebral blood
volume due to auto regulation or if blood flow is markedly decreased then decreased cerebral
blood volume) and on the infarcted tissue (severe decrease in cerebral blood flow, and blood
volume with increased mean transit time) with defined cut-offs for each criteria. A drawback of
CTP is the need to analyze several brain slices for accurate flow data, requiring a multi detector
CT with higher slice row, (currently at 2 slices, evolving to 64 slices) and high radiation exposure.
Different techniques are employed such as Dynamic Contrast-enhanced CT and Perfused-

blood-volume Mapping [27]. Dynamic contrast enhanced CT consists of monitoring the passage
of iodinated contrast bolus which causes a transient increase in attenuation which is in linear
relation to the amount of contrast in the region used to generate curves for arterial and venous
Regions of Interest which are converted using mathematical models into the perfusion parameters
and color coded perfusion maps.
Perfusion maps can give a quick visual read for color changes indicative for perfusion deficits
or through measurements (usually not required). Perfused-blood-volume Mapping consists
of subtracting the unenhanced CT data from the CTA source image data giving cerebral blood
volume data with the advantage of allowing evaluation of the whole brain. However, since it does
not allow determination of the mean transit time, blood flow and hence the ischemic penumbra,
it clinically has a lesser use (Figure 6A,B).
Figure 6A: (1) Regional cerebral blood flow map from computed tomography perfusion in a case
of left middle cerebral artery infarct shows a large perfusion defect in the left frontal and temporal
lobes, evidenced by a lack of color display. (2) Regional cerebral blood volume map demonstrates
a penumbra of decreased perfusion (indicated with arrows around blue areas) surrounding the
defect (purple), indicating potentially reversible ischemia around the perfusion defect.
Figure 6B: This perfusion map gives a quick visual estimate of the anterior cerebral artery (ACA)
and middle cerbral artery (MCA) collaterals on the convexity in a case of M1 artery occlusoin. This
patient underwent CT perfusion study in setting of acute aphasia and hemiparesis. A prominent
mismatch is present on CT perfusion with delay in time to peak (TTP) but relatively preserved
rCBV, (cerebral blood volume) indicating adequate collateral supply with the exception of basal
ganglia (M1 thrombus will nearly always take out the lenticulostriate vessels which are effectively
end-arteries without signficant collaterals).
Image source: copyright www.neuroangio.org- used with permission from Dr. M. Shapiro.
MAGNETIC RESONANCE IMAGING

MRI is more sensitive than CT in detecting ischemic changes, similar to CT with respect to
diagnosing hemorrhage, and it remains the gold standard for imaging in acute focal neurological
deficits [12]. Multimodal MRI (different imaging sequences) provides detailed visualization of
brain and vessel anatomy, including perfusion data with a higher sensitivity and specificity than
CT to detect stroke mimics [28]. The complete MR imaging protocol requires approximately 15
to 20 minutes to perform, and an additional 10 minutes for patient positioning and transfer, as
well as calculation of the apparent diffusion coefficient and mean transit time maps [29]. MRI
comes with an advantage of decreased exposure to radiation with higher costs, lesser availability,
claustrophobia experienced by patients as a drawback, along with absolute contraindications
such as metallic implants or pacemakers.
CONVENTIONAL MRI
MR sequences usually used in acute strokes are: T1-weighted spin echo, T2-weighted fast
spin-echo, fluid-attenuated inversion recovery-FLAIR, DWI for acute ischemia, MRA and PWI
for penumbra. T2-weighted gradient-echo- GRE- for hemorrhage and gadolinium-enhanced T1-
weighted spin-echo sequences. Typical findings in acute ischemia include: hyper-intense signal in
white matter on T2-weighted images and fluid-attenuated inversion recovery images, and similar
to CT findings; grey-white matter distinction loss, sulcal effacement and intravascular signal
intensity changes due to occlusion. Hemorrhage is seen as abnormal blooming and while MRI is
effective at detecting bleeds, thrombolytic guidelines utilize CT based evidence alone. With the
onset of Diffusion weighted imaging, the conventional MR sequences play a minor role in acute
stroke evaluation (Figure 7A,B,C).
Figure 7A: Fast spin echo T2-weighted fat suppressed image demonstrates increased signal
intensity and effacement of the right temporal lobe, consistent with sub-acute infarct of the right
middle cerebral artery.
Figure 7B: These are T1 weighted MRI images of a patient with bilateral cortical border zone
infarcts (secondary to hypotension). T1 bright staining is seen along cortical grey matter
suggestive of Cortical Laminar Necrosis.
Figure 7C: MRI axial FLAIR images of brain show an infarct involving left frontal lobe anterior to
the Sylvian fissure,an area which corresponds to the superior division of the left middle cerebral
artery.
MR ANGIOGRAPHY
High resolution imaging of the cranial vasculature can be obtained using a non-contrast 3D
time-of-flight (TOF) MR angiography (MRA). The basis of this technique is that protons in tissue
are saturated by repeated radiofrequency excitation and have low signal intensity but protons
coming in through the vessels are unsaturated and have a high signal intensity producing flow
dependent imaging. TOF can be 2D or 3D and does not expose the patient to radiation, or contrast.
It is limited by both patient motion and flow artifact often resulting in over-estimation of the
stenosis or occlusion. Since it obtains imaging over a short time period, it provides no data on
the speed or direction of blood flow (important to study collateral supply). To overcome this, 4-D
MRA (and CTA) have been developed. This involves reimaging the field of interest at several time
points after the radiofrequency pulse (or contrast injection in CTA) with results similar to those
of catheter angiography [30]. Several studies show that TOF is not as accurate as other modalities
such as DSA or CTA with a sensitivity of 84.2% and specificity of 84.6% [31]. Contrast enhanced
MRA (with gadolinium) is the technique used for extra-cranial vasculature imaging allowing
improved anatomical details with an advantage of better diagnosis of arterial dissections to be
balanced with side-effects of contrast in renally compromised patients and nephrogenic systemic
fibrosis (Figure 8 A,B & C).
Figure 8A: 3-D Time Of Flight (TOF) Non contrast MR Angiography of brain shows severe right
MCA proximal main stem (yellow arrow) with sparse cortical branches of right MCA compared to
left (green arrow).
Figure 8B: The same case as above shows faint serpiginous high signal on T2* axial FLAIR (due
to sluggish flow in the sparse cortical branches of the MCA) known as the “ivy sign” in the right
perisylvian area (yellow arrows).
Figure 8C: An MR angiogram of a patient with bilateral internal carotid artery dissection showing
narrowing of lumen. The lumen is black (blood imaging) and a white hematoma can be visualized
in the vessel wall.
DIFFUSION WEIGHTED MR IMAGING- DWI
MR with diffusion is quickly becoming the gold standard in acute stroke imaging, as it can
be obtained within 10 minutes at certain centers [32]. DW MRI uses fast (echo-planar) imaging
technology, and is resistant to patient motion artefacts with an imaging time of a few seconds to
2 minutes [33]. The sensitivities and specificities are 100% and 86%, respectively, for diffusion-
weighted MRI versus 18% and 100% for conventional MRI [34]. Hence, DW MRI plays an essential
role in the diagnosis of acute infarctions and to rule out stroke mimics.
Principle: is based on the random (Brownian) motion of water molecules in tissues. A change
in the water content of cells affects the rate of molecular diffusion in these tissues. Using T2
weighted spin-echo MR imaging sequence with 2 extra gradient pulses (equal magnitude, opposite
directions) results in signal changes: greater loss of signal is seen in tissues with higher rates of
diffusion and vice versa. Hence, in acute stroke (cytotoxic edema with decreased rate of molecular
diffusion in the affected tissue), ischemic tissue appears brighter than normal brain tissue. DW
MRI cannot be used to calculate the diffusion coefficient, which is obtained from orthogonal
diffusion weighted MR images in all 3 planes and is called Apparent Diffusion Coefficient ADC.
ADC maps are used because occasionally areas on diffusion imaging have a high signal due to
vasogenic edema, but will appear dark on ADC map proving it is not an acute infarct.
In humans restricted diffusion is seen as early as 30 minutes decreasing to reach a low at

3-5 days (hyper intense signal with reduced ADC values due to restricted diffusion), and reaches
baseline at 1-4 weeks, explained by the development of vasogenic edema alongside the cytotoxic
edema, replaced by gliosis which carries an increase in extracellular water (high intensity signal
due to increased T2 signal: T2 shine through and variable ADC values for months). Hence DWI
cannot be reliably used to estimate infarct age without the help of ADC maps.
DW imaging has high sensitivity and specificity with studies showing 94% accuracy for afinal
diagnosis of stroke, compared with a yield of 71%-80% when using conventional MRI (T2W/
PDW or FLAIR sequences) [35]. DWI demonstrated infarct volumes also correlate (with statistical
significance) with NIH Stroke Score and other scales [36]. However false negatives with DWI can
occur in small lacunar infarcts of the brainstem or deep nuclei [34]. False positives may be seen in
abscesses, tumors but can be easily ruled out. Diffusion imaging may show no abnormality in the
setting of ischemia, hence normal DWI with altered perfusion images indicate tissue at risk, and
prompt initiation of therapy [33] (Figure 9).
Figure 9:(A and B) Restricted water diffusion in the region of infarct (right middle cerebral
artery) results in an increased signal intensity on diffusion-weighted imaging (A) and decreased
signal on apparent diffusion coefficient imaging (B).
PERFUSION WEIGHTED MR IMAGING - PWI

The main advantage of Perfusion weighted imaging is its ability to image entire brain and
detect the ischemic penumbra. This technique requires a method of achieving contrast for
perfusion either exogenous (IV contrast agent-gadolinium) or endogenous (labeling hydrogen-1
protons in water or arterial spin labeling).
Principles: Passage of contrast in the vessels causes transient loss of signal (T2 effect).
Tracking these signal change results in a time-signal curve which can create perfusion maps of
cerebral blood volume and mean transit time. Using the arterial spin technique encompasses
using radiofrequency to invert the spin polarity of the protons entering the image plane which
measurably affects the image intensity as they perfuse the tissue. Subtracting the flow sensitive
image from the flow insensitive image gives a measure of the protons perfusing that image plane,
in essence a perfusion map.
PWI detects areas of reduced flow contrasted to DWI which depicts areas of injury. The
difference between the DWI defect and the PWI defect is the ischemic penumbra which helps to
guide further stroke therapy. This is the subject of multiple clinical trials for patients with a DWI-
PWI mismatch who will benefit from thrombolysis [37-42]. In certain cases, DWI defect is larger
than PWI defect which is seen in early reperfusion (Figure 10 A, B).
Figure 10A: Patient presents with a stroke involving left middle cerebral artery. MR perfusion
shows areas of increased time to peak (TTP) which correspond to decreased flow and volume.
Visual key:
For TTP, higher scale (red) means longer TTP (compromised), and lower scale (blue) means
shorter TTP (intact).
For CBF (cerebral blood flow), higher scale (red) means faster flow (preserved), and lower
scale (blue) means less flow (compromised).
For CBV (cerebral blood volume), higher scale (red) means more volume (generally preserved),
and lower scale (blue) less volume (generally compromised).
Figure 10B: TTD -time to drain, (similar to TTP), shows decreased flow in entire middle cerebral
artery territory in a case of infarction. CBF is down in the lenticulo-striate area, but relatively
good over the temporal lobe. CBV is increased implying that temporal lobe vascular bed has
dilated effectively, thereby increasing its volume and almost normalizing temporal lobe CBF.
Image source: copyright www.neuroangio.org- used with permission from Dr. M. Shapiro.
GRADIENT RECALLED ECHO - GRE

This is the preferred MRI sequence to rule out acute or chronic hemorrhage including a
hemorrhagic transformation. It is a T2 weighted sequence sensitive to the change in local
magnetic fields due to the iron in blood and degradation products. As the hemoglobin in the
parenchyma becomes deoxygenated, unpaired electrons make it para-magnetic (non-uniform
field) resulting in a signal loss- known as susceptibility effect seen as hypointense (dark) lesions.
This sequence is used to image acute stroke patients in whom ICH is suspected or has to be ruled
out for thrombolytic therapy and is found to be as accurate as CT in the detection of acute ICH and
more accurate in cases of chronic ICH [12, 43] (Figure 11 A, B).
Figure 11 A: Arterial infarct with hemorrhagic transformation show a low signal intensity (yellow
arrow) on T2* GRE (areas of bleed) in the region of infarct.
Figure 11 B: MRI axial FLAIR study shows focal hyperintensity in the region of corpus callosum
(yellow arrow) which corresponds to the low signal intensity on T2* GRE (green arrow). DWI
shows the corresponding focus of ischemia (red arrow).
MRI – TIMING AND THERAPEUTIC WINDOWS
Treatment with thrombolytics is time dependent (within 3-4.5 hours) hence strokes that
occur in sleep or unwitnessed pose a unique therapeutic challenge for which neuroimaging can
provide decision making criteria. MRI sequences have been proposed to identify strokes in the
therapeutic time window.
One imaging combination includes: DWI to detect lesions within minutes of ischemia and
FLAIR which is sensitive for subacute ischemia. Hence a positive DWI with FLAIR negative
mismatch (94% specific) is likely to provide a time window for safe thrombolysis [44].
An imaging combination of DW-PWI mismatch helps identify the tissue at risk, and potential
benefit from interventions even if outside the 3-4.5 hour window.
Several studies have been conducted to determine the “best” imaging modality in acute stroke,
but the reality is that both CT and MRI will co-exist and complement each other for a long time.
The main drawbacks to CT are that an ischemic brain stroke may not appear in a CT scan for
up to 48 hours period, and that CT does not image the vertebra-basilar (up to 15% of strokes).
While the MRI does provide superior quality of images and anatomical details, in an acute setting
its advantages address the above mentioned two drawbacks of CT. Important contraindications
to MRI are patients with magnetic material in their body such as pacemakers, pins, a vital point
to note as neurologically altered or aphasic patients may be unable to provide this information to
their providers.
The sensitivities and specificities were 100% and 86%, respectively, for diffusion-weighted
MR imaging versus 18% and 100% for conventional MR imaging and 45% and 100% for CT [34].
New guidelines from the American Academy of Neurology state that doctors should use a diffusion
MRI scan to diagnose stroke instead of a CT scan which was published in the July 13, 2010, issue
of Neurology®, the medical journal of the American Academy of Neurology.
The imaging modality of choice will depend upon the specific situation: cost, availability,
clinical setting, contraindications etc. and it remains the purview of a well-educated provider to
determine the imaging to effectively guide the therapeutic goals.
Table 1: CT vs MRI
CHARACTERISTIC [1, 2] CT MRI
Easily available in the emergency Not available in all Emergency

Availability
department departments
Time 5 mins 15 mins
Perfusion study: volume assessed 2-4 cm Entire brain visualized
Iodinated contrast has toxic effects

Gadolinium: minimal toxicity on kidneys,
Side effects: Contrast on kidney, cannot be used in renally
risk of nephrogenic and systemic fibrosis
compromised patients, risk of anaphylaxis.
Side effects: Ionizing radiation YES: increases risk of cancer No ionizing radiation
Side effects: Claustrophobia - +++
Drawback: motion artefact + +++
Contraindication: Pacemaker, shrapnel,

- +++
metal plates
PURPOSE
Chronic hemorrhage +/- +++
Acute ischemic stroke - ++
Angiography ++ +++
Vertebro-basilar visualization - ++
Abbreviations: ICH: Intracerebral hemorrhage, SAH: Sub arachnoid hemorrhage, EDH:

Extradural hemorrhage, SDH: Subdural hemorrhage. AVM: Arterio-venous malformation, TCD:
transcranial Doppler, CDUS: Carotid duplex ultrasound, DSA: Digital subtraction Angiography.
1. Srinivasan, A., et al., State-of-the-Art Imaging of Acute Stroke. RadioGraphics, 2006.

26(suppl_1): p. S75-S95.
2. Zimmerman, R.D., Stroke Wars: Episode IV CT Strikes Back. American Journal of Neuroradiology,
2004. 25(8): p. 1304-1309.
ULTRASOUND METHODS
Carotid Duplex ultrasound (CDUS) and transcranial Doppler (TCD) ultrasound are noninvasive,
adjunct methods for evaluation of the intra and extra cranial vasculature, used to assess patients
with transient ischemic attacks (TIA) and ischemic strokes (large artery –carotid/vertebral
origin). Their role in acute strokes is noted for their use in patients who are unstable, who have
contraindications to standard CT MRI imaging [45]. They are best utilized for their visualization
of the vessels at the base of the brain: middle cerebral artery, anterior cerebral artery, carotid
siphon, vertebral and basilar artery and ophthalmic artery. A major drawback is that in 30% of
patients, impedance from the temporal bone limits meaningful imaging [46].
TCD Ultrasound uses low frequency (2 MHz) pulsed sound to penetrate skull bone and visualize
the intracranial vessels. It is widely accepted as a noninvasive means of assessing the patency
of the intracranial vessels.In patients with acute stroke, TCD can detect occlusion, stenosis,
collateral pathways, embolisms, reperfusion post thrombolysis and vasospasms especially
after subarachnoid hemorrhage [47]. A major drawback similar to CDUS is the temporal bone
impedance, examiner dependence and examiner dependence and low sensitivity in the vertebro-
basilar system [46].
The combination of duplex and TCD in some studies has been shown to have 100% sensitivity
and specificity as compared to digital subtraction angiography has a high in identifying arterial
lesions amenable to treatment about 2 hours after stroke or TIA when done by skilled sonographers
[48]. This method is limited mainly by the lack of easily available skilled personnel (Figure 12 A,
B, C).
Figure 12A: A normal transcranial Doppler imaging of the left middle cerebral artery which
demonstrates normal flow and waveforms, with a peak velocity of 1.28 m/s.
Figure 12B: Longitudinal color Doppler image through the internal carotid artery demonstrates a
“string” sign, with very minimal flow through the ICA in a case of Acute high-grade internal carotid
artery (ICA) occlusion.
Figure12C: Longitudinal sonogram of the left internal carotid artery demonstrates complete flow
void, with no perceptible waveforms in a case of acute complete internal carotid artery occlusion.
ANGIOGRAPHY
Catheter based cerebral angiography or digital subtraction angiography (DSA) is the gold
standard against which all other methods to imaging vasculature are compared. It provides
information onthe degree of arterial stenosis, the presence of dissection, vasculitis vascular
malformations, collateral pathways and perfusion status [13]. Despite this, DSA is rarely
performed in a clinical setting due to the widespread availability of noninvasive techniques, such
as CTA and MRA, CDUS and TCD (discussed above), and side effects which include a small risk of
stroke associated with the procedure (0.5%) and TIA (0.4%) [49] with an overall incidence of
neurological deficits being 1% of which 0.5% are persistent [50]. Clinically silent embolisms post
the angiography procedure have been detected by DWI in a study (51) with frequency directly
related to vascular risk profiles. Hence DSA is usually confined to suspected occlusions of large
vessels, as not only does it offer unparalleled sensitivity but the opportunity for in-situ therapy for
which it is often combined with interventional modalities such as thrombolysis and angioplasty
(Figure 13 A,B,C,D,E).
Figure 13 A: Initial lateral image from cerebral angiogram demonstrates a paucity of vessels in
the middle cerebral artery-MCA distribution.
Figure 13 B: Repeat lateral angiogram after intra-arterial lysis demonstrates recanalization of

flow and normalized perfusion.
Figure 13 C: DSA showing sluggish distal filling of the internal carotid artery in a case of internal
carotid artery ICA stenosis (yellow arrow).
Figure 13 D: DSA showing complete cut off of ICA at its origin (yellow arrow), without any distal
filling implies to occlusion rather than stenosis.
Figure 13E: DSA showing dissecting pseudo-aneurysm of the ICA (white arrow).
CONCLUSION
A thorough understanding of imaging modalities is required for the optimal management of
acute stroke events in patients. Neuroimaging should be sought in all patients having an acute
stroke event. It is essential to select the therapeutic strategy in the acute stroke patient and as
outlined in the goals; to determine the extent, sequelae and etiology which may lend itself to
intervention. Protocols followed in an acute stroke event are available freely online, and may be
modified to fit institutional needs.
Head CT remains the preferred initial imaging choice as it fulfills the critical parameters for
thrombolytic therapy (rule out hemorrhage and meet inclusion criteria) and is widely available.
Although the advantages of MRI - early detection of ischemia with DWI and greater anatomical
visualization are essential, it is limited by cost, contraindications and lack of availability. Since
there is no data yet to prove that selection of patients for thrombolysis using MRI is superior to
CT for selection, MRI should be used only if it does not unduly delay treatment. Advanced CT
techniques; (CTA source images and perfusion imaging) are expanding the mandate of CT in acute
stroke evaluation protocols. However despite the ACR (American College of Radiology) and AAN
(American Academy of Neurology) endorsing MR as first line imaging, lack of access remains a
major hurdle.
Noninvasive methods of vascular imaging (MRA, CTA, and Ultrasound) are generally
preferred over conventional DSA unless therapeutic intervention is planned or previous studies
remained inconclusive; and should never delay the decision of thrombolysis. Use of CTA after
rapid (creatinine) testing to exclude compromised renal function can be performed after the 3
hour window to identify potential occlusion/stenosis which may be amenable to intra-arterial or
mechanical thrombolysis. CT or MR perfusion imaging is used to identify the salvageable tissue-
the ischemic penumbra and is performed if findings may allow extending the time window for the
various interventions in demonstrated “tissue at risk”.
(Refer to Table 2 Summary of Imaging Modalities, summary of stroke protocols, and imaging
stroke protocols)
Table 2: Summary of imaging modalities.

IMAGING MODALITY USE
Diagnose or exclude ICH
Diagnose SAH/EDH/SDH
CT: Non contrast
May show early signs of ischemic infarction
May rule out stroke mimics like tumor
Detect stenosis, occlusion in the intra and extra cranial arterial circulation in ischemic strokes
CT: Angiography
Detect vascular abnormalities such as aneurysms, AVM
CT: Perfusion Quantification of the cerebral blood flow, volume and transit time for blood flow in the brain.
MRI: Diffusion weighted Imaging Can detect ischemia within minutes of onset
Diagnose ischemic stroke 3-8 hours after onset

MRI: FLAIR
Identify older ischemic strokes and small vessel disease
Identification of vasculature without contrast

MRI: Angiography Identify occlusion or stenosis and other vascular abnormalities.
Identifies areas of brain tissue with reduced blood flow

MRI: Perfusion weighted imaging
DWI-PWI mismatch estimates at risk tissue
MRI: GRE Diagnose acute and chronic ICH
Noninvasive imaging for intra- and extracranial vasculature

Ultrasound: CDUS, TCD
Detects occlusion, stenosis, collaterals, reperfusion, vasospasms
Gold standard for vascular imaging

Detects the degree of arterial stenosis, dissection, vasculitis vascular malformations, collateral
Angiography -DSA
pathways and perfusion status
Canbe combined with in-situ ( thrombolysis and angioplasty)
Abbreviations: ICH: intracerebral hemorrhage, SAH: sub arachnoid hemorrhage, EDH: extradural
hemorrhage, SDH: subdural hemorrhage. AVM: arterio-venous malformation, TCD: transcranial
Doppler, CDUS: Carotid duplex ultrasound, DSA: digital subtraction Angiography
1. Srinivasan, A., et al., State-of-the-Art Imaging of Acute Stroke. RadioGraphics, 2006. 26(suppl_1):
p. S75-S95.
2. Zimmerman, R.D., Stroke Wars: Episode IV CT Strikes Back. American Journal of Neuroradiology,
2004. 25(8): p. 1304-1309.
FUTURE DIRECTIONS
Advances in neuroimaging techniques and availability may change the IV Alteplase criteria
from a fixed time cut off criteria to more fluid imaging parameters which may not only lower the
rate of complications by identifying patients with higher risk of hemorrhagic conversions but
also broaden the population which is eligible for thrombolysis with enhanced clinical outcomes
[38,52].
A new technique; MR permeability imaging allows the quantitative determination of blood

brain barrier disruption (increased permeability) which allows identification of patients more
likely to have a hemorrhagic conversion after thrombolytic therapy and as an extension, identify
those outside the time window with an intact blood brain barrier, who may still benefit from
thrombolysis. This may help reduce the morbidity and mortality associated with IV TPA and may
be a useful addition to an acute stroke evaluation protocol [53,54].
With fast paced technological advances, the mandate of imaging will soon encompass
functional recovery and prognostication. Neuroimaging continues to rapidly evolve to provide
more comprehensive imaging, bettering its achievements continuously; not only in visual quality,
ease and availability, speed, accuracy, time of detection of ischemia, detection of potential and
occurred complications, prognosis and recovery all with the goal of improved neurological
outcomes.
Stroke Imaging Protocol: Adapted with permission from Neuroradiologycases.com by Dr.
Anvekar B., (Neuroradiology unit, S P Institute of Neurosciences, Solapur, India).
CASE STUDIES OF STROKE IMAGING PROTOCOLS
Case 1
Non contrast CT scan rules out hypertensive hemorrhage in a patient presenting with left sided
weakness. Insular ribbon sign is positive.
MRI FLAIR: mild effacement of sulci.
MRI diffusion: Left middle cerebral artery (MCA) territory infarct.
MR angiography shows Right MCA- ICA (internal carotid artery) occlusion.
Case 2
Non contrast CT study of Brain shows faint hypodensity involving right basal ganglia and adjacent
insular cortex which is subtle and easily missed.
This was immediately followed by MRI –Diffusion imaging which shows an acute infarct with
restricted diffusion involving right basal ganglia, adjacent insular cortex and right peri-sylvian
cerebral cortex. Area of involvement corresponds to right MCA proximal main stem territory.
MR Angiography (non-contrast 3-D Time of Flight (TOF) does not visualize right ICA - MCA
(yellow arrow points to left branch) thus implying occlusion. Right ACA filled from contra lateral
anterior circulation via Acom.
ACKNOWLEDGEMENT
We thank all the authors who gave us permission for the use their images.
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Neuroimaging in Acute Stroke

Shazia Mirza1* and Sankalp Gokhale1

Published Date: July 25, 2016

NEED FOR IMAGING

• Differentiate ischemia from hemorrhage which directs further therapy.

• Rule out stroke–mimics such as tumors or hematomas.

NON CONTRAST COMPUTED TOMOGRAPHY (NCCT) - BRAIN

Hyper Dense Artery/MCA Sign

Hypo Attenuating Brain Tissue

Obscuration of the Lentiform Nucleus

Insular Ribbon Sign

QUANTIFICATION OF ISCHEMIC INVOLVEMENT- ASPECTS

COMPUTED TOMOGRAPHY ANGIOGRAPHY-CTA

COMPUTED TOMOGRAPHY PERFUSION IMAGING -CTP

Different techniques are employed such as Dynamic Contrast-enhanced CT and Perfused-

MAGNETIC RESONANCE IMAGING

In humans restricted diffusion is seen as early as 30 minutes decreasing to reach a low at

PERFUSION WEIGHTED MR IMAGING - PWI

Image source: copyright www.neuroangio.org- used with permission from Dr. M. Shapiro.

GRADIENT RECALLED ECHO - GRE

Easily available in the emergency Not available in all Emergency

Time 5 mins 15 mins

Perfusion study: volume assessed 2-4 cm Entire brain visualized

Iodinated contrast has toxic effects

Side effects: Claustrophobia - +++

Drawback: motion artefact + +++

Contraindication: Pacemaker, shrapnel,

Acute ischemic stroke - ++

Abbreviations: ICH: Intracerebral hemorrhage, SAH: Sub arachnoid hemorrhage, EDH:

1. Srinivasan, A., et al., State-of-the-Art Imaging of Acute Stroke. RadioGraphics, 2006.

Figure 13 B: Repeat lateral angiogram after intra-arterial lysis demonstrates recanalization of

Table 2: Summary of imaging modalities.

Diagnose ischemic stroke 3-8 hours after onset

Identification of vasculature without contrast

Identifies areas of brain tissue with reduced blood flow

MRI: GRE Diagnose acute and chronic ICH

Noninvasive imaging for intra- and extra- cranial vasculature

Gold standard for vascular imaging

A new technique; MR permeability imaging allows the quantitative determination of blood

MRI FLAIR: mild effacement of sulci.

MR angiography shows Right MCA- ICA (internal carotid artery) occlusion.

2. Schwartz, DT Emergency radiology: case studies. 2008

4. Saver JL. Time is brain--quantified. Stroke. 2006; 37: 263-266.

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