Imaging in acute ischaemic stroke: Essential for modern stroke care

Abstract

Stroke is the second most common cause of death worldwide and the third most common in the UK. 'Time is brain' in ischaemic stroke; early reperfusion has been shown to lead to improved clinical outcomes, yet the majority of patients with acute stroke do not attend in time for thrombolysis as it is currently licensed, hence the interest in trials extending the therapeutic window. Defining the ischaemic penumbra is of crucial importance in choosing the appropriate patients for thrombolytic therapy who attend outside the optimal therapeutic window. Integrated stroke imaging, including demonstration of potentially salvageable tissue with either MR perfusion/diffusion studies or CT perfusion, is increasingly likely to play a central role in future management strategies and widening of the potential therapeutic window. This review highlights the basic imaging findings of acute stroke and discusses the role of advanced CT and MR techniques as well as options for vascular imaging.

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doi: 10.1136/pgmj.2010.097931
2010 86: 409-418Postgrad Med J
Daniel J Warren, Rachel Musson, Daniel J A Connolly, et al.
modern stroke care
Imaging in acute ischaemic stroke: essential for
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Imaging in acute ischaemic stroke: essential for
modern stroke care
Daniel J Warren,
1
Rachel Musson,
1
Daniel J A Connolly,
1
Paul D Griffiths,
2
Nigel Hoggard
2
ABSTRACT
Stroke is the second most common cause of death
worldwide and the third most common in the UK. ‘Time
is brain’ in ischaemic stroke; early reperfusion has been
shown to lead to improved clinical outcomes, yet the
majority of patients with acute stroke do not attend in
time for thrombolysis as it is currently licensed, hence
the interest in trials extending the therapeutic window.
Defining the ischaemic penumbra is of crucial importance
in choosing the appropriate patients for thrombolytic
therapy who attend outside the optimal therapeutic
window. Integrated stroke imaging, including
demonstration of potentially salvageable tissue with
either MR perfusion/diffusion studies or CT perfusion, is
increasingly likely to play a central role in future
management strategies and widening of the potential
therapeutic window. This review highlights the basic
imaging findings of acute stroke and discusses the role
of advanced CT and MR techniques as well as options
for vascular imaging.
INTRODUCTION
Stroke is defined as ‘a clinical syndrome consisting
of rapidly developing clinical signs of focal (or
global in the case of coma) disturbance of cerebral
function lasting more than 24 h or leading to death
with no apparent cause other than a vascular
origin’.
1 2
Stroke is the second most common cause
of death worldwide and the third most common in
the UK after heart disease and cancer. It is the
leading cause of severe adult disability in the UK,
affecting over 100 000 people in England each year,
with significant emotional, physical and mental
sequelae.
3
The financial burden on the health
system is immense, costing the NHS alone £2.8
billion per annum.
1
The goal of early brain imaging is to exclude
intracranial haemorrhage, identify ischaemic
change, and exclude stroke mimics. Imaging also
allows assessment of the intracranial and extracra-
nial vasculature and facilitates delineation of the
status of cerebral perfusion, demonstrating the
infarct core and also the penumbra (potentially
salvageable parenchyma), the identification of
which may aid future management strategies.
Stroke can be subclassified into two major cate-
gories: ischaemic (accounting for w80% of all acute
stroke events) and haemorrhagic (20%). This
review will focus on imaging of ischaemic stroke;
haemorrhagic stroke (such as secondary to
subarachnoid haemorrhage, subdural or extradural
haemorrhage) is not further addressed in this
review.
Ischaemic stroke encompasses multiple aetiol-
ogies including thrombosis, embolism, venous
thrombosis and systemic hypoperfusion. Throm-
bolytic therapy with recombinant tissue plasmin-
ogen activator (rt-PA) is the treatment of choice for
ischaemic stroke presenting within 3 h of clinical
onset, provided that there is no contraindication to
this treatment, including exclusion of intracranial
haemorrhage by CT. Using a 3 h time period cut-off
for thrombolysis, the NINDS trial
4
showed efficacy,
with the number needed to treat to benefit
one patient being eight; however, there was
a 6.4% treatment-related incidence of intracranial
haemorrhage. A narrow time window for patient
presentation, assessment and start of therapy
results in only a small proportion of eligible
patients receiving thrombolysis. Consequentially,
fewer than 10% of patients with acute stroke
actually receive rt-PA; in the NINDS trial, only 4%
of patients met criteria for alteplase rt-PA. The
European Medicines Agency granted approval of
alteplase in 2002.
5
‘Time is brain’is a frequently used idiom; the
sooner a diagnosis of acute ischaemic stroke is made
and thrombolysis treatment instigated (where
indicated), the better is the patient outcome.
1
Much of the literature addresses licensed use of
alteplase rt-PA within 0e3 h of symptom onset;
recently published data from the third European
Cooperative Acute Stroke Study (ECASS III) lends
support to the efficacy of rt-PA alteplase, and shows
that extension of the treatment window to 4.5 h is
efficacious in a large subgroup of patients.
56
There
is an argument that the therapeutic window should
be widened, with decisions to treat being guided by
improved and integrated imaging strategies.
7
Optimisation of management of patients with
acute stroke relies on prompt clinical assessment
and stroke diagnosis followed by urgent brain
imaging. In the UK in 2008, the National Institute
for Health and Clinical Excellence (NICE) produced
guidelines for diagnosis and initial management of
acute stroke and transient ischaemic attack.
1
These
guidelines recommend that patients with acute
stroke with indications for thrombolysis or early
anticoagulation treatment, receiving anticoagulant
treatment, who have a known bleeding diathesis,
depressed level of consciousness, unexplained
progressive or fluctuating symptoms, neck stiff-
ness, fever or papilloedema, or severe headache at
onset of stroke symptoms should undergo imme-
diate (next scan slot and definitely within 1 h)
brain imaging.
1
All other patients with stroke
should receive brain imaging within 24 h of
symptom onset.
1
Radiology Department, Royal
Hallamshire Hospital, Sheffield
NHS Teaching Hospitals Trust,
Sheffield, UK
2
Academic Unit of Radiology,
University of Sheffield, Sheffield,
UK
Correspondence to
Dr Daniel J Warren, C Floor,
Department of Radiology, Royal
Hallamshire Hospital, Glossop
Road, Sheffield S10 2JF, UK;
daniel.warren@sth.nhs.uk
Received 26 January 2010
Accepted 25 April 2010
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In this review, we will outline the characteristic imaging
features of acute ischaemic stroke on both non-contrast CT and
MRI. The role of advanced CT/MRI techniques including angi-
ography and perfusion will be discussed, as well as options for
vascular assessment, with consideration of both the intracranial
and extracranial vasculature.
NON-CONTRAST CT IMAGING
CT is the imaging technique of choice in many institutions for
the initial assessment of suspected stroke. It is readily available
and permits rapid assessment of patients with acute stroke.
Multidetector technology permits image acquisition within
seconds and at sub-millimetre image resolution.
7
Non-contrast
CT allows detection of intracranial haemorrhage with a high
degree of sensitivity, identification of stroke mimics, and also
identification of early parenchymal ischaemic change.
Major current guidelines on the use of thrombolysis include
non-contrast CT as an acceptable investigation from which to
make a decision about the benefits of thrombolysis. The ECASS
III major inclusion criteria were acute ischaemic stroke, age
18e80 years, stroke symptoms present for at least 30 min with
no significant improvement before the start of lysis. The major
exclusion criteria included intracranial haemorrhage and severe
stroke as assessed clinically (a National Institutes of Health
Stroke Scale score >25 (range 0e42, with the higher score
indicating more severe cerebral infarct and neurological impair-
ment)) and severe stroke as assessed by imaging (defined as
a stroke involving more than one-third of the middle cerebral
artery (MCA) territory).
5
Approximately three-quarters of all ischaemic cerebral infarcts
occur within the territory supplied by the MCA. Detection of
early ischaemic change on non-contrast CT can be difficult, with
many of the early radiological features being subtle. A system-
atic review by Wardlaw and Mielke,
8
which included assessment
of observer reliability in detecting these early radiological signs,
identified a mean sensitivity of 66% (range 20e87%) and spec-
ificity of 87% (range 56e100%) for detection of early infarction
signs with CT; observer experience improved detection. Early
radiological signs relate to parenchymal infarction and the
cellular sequelae and also pathological vessel occlusion.
8
Acute
cerebral infarction results in cerebral hypoperfusion and cyto-
toxic oedema; an abrupt alteration and reduction in cellular
oxygen and glucose supply leads to rapid failure of the sodium/
potassium pump, with a resultant shift of water from the
extracellular to intracellular space and subsequent cytotoxic
oedema.
The CT manifestation of this compartmental water shift is
afocal mass effect with local cortical/gyral swelling and sulcal
effacement (figure 1); furthermore, loss of the grey/white
interface evolves. The most common areas of cerebral hypo-
attenuation identified are in the MCA territory, within the
lentiform nucleus (figure 2),
9
insular ribbon (figure 3),
10
cerebral
cortex and basal ganglia (figure 4). Delineation of early ischaemic
change can be accentuated by use of variable window width and
centre level settings to maximise the parenchymal contrast
(figure 4A,B).
11
A common finding on the non-contrast scan in
the hyperacute phase is a normal study, and, as such, the earlier
these ischaemic parenchymal changes are evident, the more
severe is the degree of ischaemia.
7
Figure 1 Non-contrast CT showing a large acute right middle cerebral
artery infarct with diffuse right hemispheric swelling manifest by sulcal
effacement and obliteration of the right sylvian fissure (black arrow).
Figure 2 Subtle low attenuation
within the right lentiform nucleus on
non-contrast CT performed 3 h after
sudden-onset left-sided weakness
consistent with an acute right middle
cerebral artery territory infarct (A);
follow-up scan at 24 h (B) shows clear
hypoattenuation within the right
lentiform nucleus and within the
posterior right frontal lobe.
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ECASS I highlighted that early evidence of cortical hypo-
attenuation affecting over one-third of the MCA territory was
a predictor of poor outcome after intravenous thrombolysis
within 6 h of stroke onset, with increased risk of symptomatic
intracranial haemorrhage.
12
The Alberta Stroke Program Early
CT (ASPECT) score allows a more reliable assessment tool for
estimation of infarct extent within the MCA territory, within
3 h of symptom onset, and also serves as a prognostic
indicator.
13e17
The ASPECT score is a validated semiquantitative
scoring system whereby the MCA territory is divided into 10
regions of interest. The overall score is formulated by point
deduction depending on the number of areas displaying early
ischaemic change; thus a normal brain scan would score 10
points, and a score of zero indicates evidence of extensive
ischaemic change throughout the MCA territory.
14 17
An
ASPECTscore of >7 is associated wit h improved post-thromb olysis
outcome.
15
A further important sign that can be identified on the non-
contrast CT study is vessel occlusion, seen as hyperdensity
within the lumen of the vesseld‘hyperdense MCA sign’. This is
most often identified as linear hyperdensity within the proximal
M1 segment of the MCA (figure 5A) or as a hyperdense ‘dot’
within the sylvian fissure (figure 5B).
7 18
Hyperdensity can be
detected within any occluded vessel, and another example
encountered quite commonly is thrombosis of the basilar artery
(figure 6), although identification of this sign can be difficult
secondary to vessel wall calcification and lack of a paired vessel
for comparison. Hyperdensity may reflect flow stasis distal to
a thrombus or the thrombus per se.
MRI
MRI can be used as an alternative or an adjunct to non-contrast
CT, as much of the information is complementary to the non-
contrast CT study. CT has the benefit of being readily available,
inexpensive and fast; however, increasingly there is provision of
out-of-hours MRI, continued sequence refinement leading to
reduced MRI acquisition time, and improved sensitivity in
detection of acute ischaemic change over non-contrast CT,
especially in detection of early ischaemic change and identifica-
tion of small infarcts and those within the posterior fossa. MRI
provides improved anatomical detail and does not use ionising
radiation; in comparison, the mean effective dose from a non-
contrast CT brain scan is similar to that of a year ’s natural
background radiation.
Perhaps the single most significant MRI sequence in the
imaging of acute stroke is diffusion-weighted imaging (DWI).
19 20
Fiebach et al
21
have previously demonstrated the improved
sensitivity of DWI over CT. Barber et al
22
compared detection of
early signs of cerebral ischaemia on CTand DWI in patients with
acute disabling stroke within 6 h of symptom onset, using the
ASPECT score. They concluded that CT and DWI were ‘compa-
rable for detecting and quantifying signs of cerebral ischaemia’,
although ASPECT scores were lower when assessed with DWI,
Figure 3 Hypoattenuation with the left insular ribbon in an acute left
middle cerebral artery infarct (white arrow).
Figure 4 (A) Right basal ganglia infarct at 3 h using standard window width (W) 90 Houndsfield units (Hu) and centre length (L) 40 Hu. (B) Use of
variable/narrow window levels accentuates the grey/white interface and makes the acute infarct more conspicuous, W 34 Hu, L 36 Hu. (C) Maturation
of the right basal ganglia infarct at 18 h.
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implying DWI to be more sensitive. In a prospective blinded study,
Chalela et al
23
showed MR sensitivity of 83% vs 26% for CT in the
diagnosis of any acute stroke; the MRI, however, encompassed
both DWI and susceptibility-weighted images.
DWI uses the measurement of Brownian motion of molecules.
As mentioned above, the cellular process during a cerebral infarct
is rapid disruption of the sodium/potassium pump and influx of
water molecules into the intracellular compartmentdcytotoxic
oedema. There is a resultant reduction in hydrogen ion diffusion
(‘restricted diffusion’) and hence a low apparent diffusion coef-
ficient (ADC), which manifests as a black area on the ADC map
and as hyperintensity on DWI, (figure 7).
24 25
Acquisition time
for this sequence is under 1 min on most 1.5 T MR systems, and
detection of acute/hyperacute infarction is possible within
minutes of the event.
17
Diffusion restriction is not exclusive to
acute cerebral infarcts; it can be seen in a variety of other
conditions including cerebral abscess formation and encephalitis,
highly cellular tumours such as lymphoma, haemorrhage, active
demyelination (rarely) and following seizure activity. A review
of clinical history and conformation (or lack of) to a vascular
territory may aid differentiation.
Other MR sequences offer complementary information in
the evaluation of patients with acute stroke. Multiplanar spin-
echo scans (T2-weighted and proton density imaging) identify
the same early signs as those depicted on the non-contrast CT
study but with increased sensitivity and specificity.
26
Increased T2-weighted signal secondary to cytotoxic oedema
resultsinlossofgrey/whitedifferentiation.Localsulcal
effacement can be readily identified, and loss of normal arterial
flow voids, depicting flow stasis distal to a thrombus, can be
detected (figure 8).
26
Many of these signs are not seen within
the initial hours after infarction; as is the case on the non-
contrast CT study, T2 hyperintensity may take several hours
to develop.
Gradient-recalled echo imaging is highly susceptible to the
paramagnetic effect of the blood product deoxyhaemoglobin,
and hence this sequence is highly specific for identifying areas of
microscopic and macroscopic haemorrhage (figure 9).
27
Fluid-attenuated inversion recovery (FLAIR) MR, a heavily
T2-weighted sequence, suppresses cerebral spinal fluid signal and
shows other fluid with high conspicuity; hence intracranial
haemorrhage is readily depicted.
27 28
The development of signal
Figure 5 Hyperdensity within the
lumen of the vesseld‘hyperdense
middle cerebral artery (MCA) sign’dis
detected as (A) linear hyperdensity
within the proximal M1 segment of the
MCA (black arrow) or (B) as
a hyperdense ‘dot’ within the sylvian
fissure (black arrow head).
Figure 6 A patient with a history of anabolic steroid use and acute presentation with reduced level of consciousness. Presentation non-contrast CT
(A) shows hyperdensity within the basilar artery consistent with thrombosis (black arrow); there is evidence of early right posterior cerebral artery
territory infarction (B) with loss of grey/white differentiation. Follow-up imaging at 24 h shows extensive infarction within the brain stem extending into
the middle cerebellar peduncles (C). The resultant white matter oedema results in partial fourth ventricular effacement and evolving hydrocephalus
(note the temporal horn dilatation (white arrow)).
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change within infarcted cortical or central grey matter is
consistently seen earlier on FLAIR imaging (within 3 h) than it is
depicted with conventional spin-echo imaging.
29 30
MRI does offer improved anatomical detail and increased
sensitivity for acute infarct detection over CT. However, it is less
readily available than CTand its usage in the acute stroke setting
can be hampered by contraindications (such as cardiac pros-
theses) or confused patient status. In one study comparing CT
and MRI in acute stroke, 45% of 112 patients had ‘contraindi-
cations’toMRI; reasons includedmedical instability, uncooperative
patient or MR-specific exclusions.
22
Advanced CT and MRI techniques
CT angiography (CTA) allows rapid non-invasive assessment of
the intracranial and extracranial circulation at high resolution
with multislice technology. By using a contrast bolus tracking
technique, a chosen volume (eg, circle of Willis or from the aortic
arch to vertex) can be obtained within seconds. CTA permits
assessment of arterial stenosis, occlusion (figure 10), craniocer-
vical arterial dissection, and identification of stroke mimics such
as arteriovenous malformations.
Magnetic resonance angiography (MRA) also allows non-
invasive assessment of both the intracranial and extracranial
vessels. Various techniques exist including both two-dimen-
sional and three-dimensional time-of-flight (TOF), multiple
overlapping thin slab acquisition (MOTSA) and contrast-
enhanced MRA.
7
Assessment of the intracranial vasculature
with TOF-MRA in the setting of acute stroke allows depiction
of large-vessel occlusion. Guidance from the American Heart
Association recommends that, in the acute setting, this should
only be performed if it does not delay intravenous thrombolysis
within 0e3 h of ictus or if intra-arterial thrombolysis or
mechanical thrombectomy is being considered and this facility is
available.
731
TOF-MRA is limited by its spatial resolution, and,
as such, it’s depiction of more distal vessel occlusion is inferior to
conventional catheter digital subtraction angiography.
Where craniocervical arterial dissection is considered as the
underlying aetiology, MRA assessment of the carotid and
vertebral arteries is advised from the level of the aortic arch to
the circle of Willis, and this can be easily added on to the initial
brain MRI assessment.
32
Spontaneous craniocervical arterial
dissections account for only 2% of all ischaemic strokes,
33
yet are
responsible for up to 20% of such strokes in patients under
45 years of age.
32
Routinely utilised sequences include axial T1
and T2 and MRA, either with or without contrast enhance-
ment, and findings include detection of an intimal flap, loss of
normal flow void, intraluminal high signal on T1 consistent
with stasis, and classical tapering of the vessel lumen on MRA
(figure 11).
34
Some authors advocate use of axial T1 fat
suppression to detect intraluminal haematoma; this sign,
however, may not occur within the initial hours after ictus and
may therefore be more relevant in the sub-acute setting.
7
Conventional catheter digital subtraction angiography was
previously the reference standard technique for evaluation of
craniocervical dissection. However, the evolution of sensitive
non-invasive techniques has superseded this technique in the
routine setting; both MRA and CTA have been shown to be
highly sensitive in the evaluation of this condition.
33 35 36
Figure 7 Non-contrast CT (A) shows
diffuse left hemispheric swelling and
early subtle loss of grey/white
differentiation within the middle cerebral
artery (MCA) territory; note the
hyperdense vessel in the left sylvian
fissure (black arrow). Diffusion-
weighted imaging MR (B) defines the
acute MCA infarct with increased
conspicuity, with hyperintensity
throughout the left MCA territory
consistent with diffusion restriction and
a large acute infarct.
Figure 8 Axial T2-weighted MRI delineates loss of flow void within the
left internal carotid artery (black arrow). Note the normal flow void
within the right internal carotid artery.
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DELINEATION OF THE ISCHAEMIC PENUMBRA
Increasingly, multimodal imaging is being used to tailor optimal
management strategies in the acute stroke setting.
37e42
Advanced imaging allows assessment of the intracranial and
extracranial vasculature and facilitates delineation of the status
of cerebral perfusion, revealing the infarct core and the
penumbra.
The ischaemic penumbra can be defined as ‘ischemic tissue
potentially destined for infarction but not yet irreversibly
injured and the target of acute therapies’.
43
The ischaemic
Figure 9 (A) Non-contrast CT
performed 24 h after presentation with
an acute left middle cerebral artery
territory infarct shows low attenuation
within the left head of the caudate
nucleus and lentiform nucleus; high
attenuation within the centre of the left
lentiform infarct was thought to
represent probable micro-haemorrhage
into the infarct. (B) A coronal gradient-
recalled echo MRI study performed the
same day clearly shows the presence of
blood products at this site.
Figure 10 Patient with acute left arm weakness and neck pain. The presentation non-contrast CT (A) shows low attenuation within the right head of
the caudate and lentiform nuclei. Axial CT angiography (CTA) source data (B) show the proximal right internal carotid artery occlusion (white arrow),
and the dissection flap is confirmed on three-dimensional volume-rendered CTA imaging (C,D) and also on Doppler ultrasound (E).
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penumbra is therefore hypoperfused parenchyma in which
neuronal electrical activity is disrupted but remains salvageable
with restoration of blood flow; imaging evaluation of cerebral
perfusion is hence critical in determination and calculation of
the penumbra. The infarct core displays low cerebral blood flow
(CBF), which is probably irreversible.
In July 2009, the Stroke Therapy Academic Industry Round-
table (STAIR) consortium recommended that ‘future extended
Figure 11 High-resolution T2 imaging of the posterior fossa (A) reveals an acute infarct within the left posterior inferior cerebellar artery territory in
a young patient presenting with left-sided neck pain and unsteadiness of gait. Diffusion imaging shows increased diffusion (B) and low apparent
diffusion coefficient (C) consistent with diffusion restriction and acute infarction. Axial T1 imaging of the neck (D) confirms high T1 intraluminal signal
within the left vertebral artery (black arrow), and (E) axial MR angiography (MRA) acquisition confirms this loss of left vertebral artery flow void.
Maximum intensity projection reconstruction of three-dimensional time-of-flight MRA (F) clearly shows lack of flow in the left vertebral artery depicted
as vessel absence, implying thrombus, although an underlying dissection cannot be excluded.
Figure 12 Non-contrast CT (A) shows
a large right middle cerebral artery
infarct; the CT perfusion cerebral blood
volume (B) highlights the extent of the
infarct ‘core’.
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time window trials initially should focus on selected patient
groups most likely to respond to investigational therapies and that
penumbral imaging is one tool that may identify such patients’.
44
Several imaging techniques have been used to define the ischaemic
penumbra including positron emission tomography, CTand MRI.
Access and availability of positron emission tomography are
limited, and hence most work with regard to mapping of the
penumbra is focused on CT and MRI acquisition.
43
CT perfusion (CTP) imaging uses a contrast bolus tracking
technique (although this technique can also be performed with
xenon inhalation). In contrast with MR perfusion, CTP offers
both qualitative and quantitative measurements of CBF, cerebral
blood volume (CBV) and mean transit time (MTT).
45
A series of
images is acquired at a given level, usually a level that encompasses
portions of the anterior, middle and posterior cerebral arter-
iesdthat is, at the level of the basal ganglia (figure 12). CBF/CBV
mismatch with prolonged MTT is akin to the MR perfusion/
diffusion mismatch. When CTP is used, if the complete study
includes a preliminary non-contrast CT brain scan, CTA (arch to
vertex) and CTP, then the overall radiation dose is considerable.
One recent study from Canada reviewed 95 case images on a 64-
slice CT scanner and showed a mean effective dose from baseline
non-enhanced CT brain scan to be 2.7 mSv, while additional CTA
and CTP took the mean effective dose to 13 mSvdnearly five
times the dose of the non-contrast study in isolation.
46
MR perfusion imaging is most often performed using a bolus
injection of gadolinium and T2* susceptibility-weighted
sequence.
26 47
Images are acquired every 1e2 s; as the contrast
passes through the intracranial vasculature, there is a resultant
signal drop-off, the degree of which is proportional to the CBF.
This transient signal drop-off can be plotted on a timeeintensity
curve, from which various variables can be gleaned, including
relative CBV (this is the area under the curve and would reduce
in areas of hypoperfusion), relative CBF, MTT and time to
peak.
47
MR perfusion is a qualitative study, and selected regions
of interest are compared with the contralateral hemisphere.
DWI depicts what is deemed to be the infarct core, and hence
the ‘diffusion/perfusion’mismatch potentially represents
salvageable parenchyma (figure 13).
NECK VESSEL ASSESSMENT
Assessment of the extracranial vasculature is important when
craniocervical dissection is considered as the underlying aeti-
ology of stroke and also for assessment of vascular (predomi-
nantly carotid) stenosis. The NICE guidelines recommend that
‘all people with suspected non-disabling stroke or transient
ischaemic attack who, after specialist assessment, are consid-
ered as candidates for carotid endarterectomy should have
carotid imaging within 1 week of onset of symptoms’.
1
Doppler
ultrasound is the most widely available, cheapest and minimally
invasive test for this purpose, but CTA and MRA, as mentioned
above, can also be used. In the acute stroke setting, the principal
role of neck vessel imaging is to identify an underlying mech-
anism, such as arterial occlusion (secondary to either thrombus
Figure 13 MRI of an acute right middle cerebral artery (MCA) infarct at 4 h. Axial T2-weighted image (A) shows subtle increased T2 signal within the
right lentiform nucleus, diffusion-weighted imaging (B) shows the infarct core with improved conspicuity, while perfusion imaging (C) shows partial
reperfusion of the infarct core but with profoundly reduced perfusion throughout the right MCA territorydthe diffusion/perfusion mismatch
representing potentially salvageable parenchyma.
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7
Non-invasive imaging techniques for neck
vessel assessment, including Doppler ultrasound, CTA and
MRA, offer similar levels of accuracy, the choice of which is
often therefore determined by local availability and preference.
CONCLUSIONS
Optimisation of acute stroke management pathways is ongoing.
‘Time is brain’, and hence early patient presentation and expe-
ditious clinical and imaging assessment are paramount. Multi-
modal imaging techniques often offer complementary
information, but, increasingly, protocols to extend the time to
therapeutic intervention will be driven by the delineation of the
ischaemic penumbra. Non-contrast CTas the initial imaging test
remains the reference standard.
MULTIPLE-CHOICE QUESTIONS (TRUE (T)/FALSE (F); ANSWERS
AFTER THE REFERENCES)
1. Regarding diffusion imaging on MR:
A. Diffusion restriction is specific to acute ischaemia
B. Diffusion restriction can be seen in cerebral abscess formation
C. Restricted diffusion does not occur within the first hour of
acute infarction
D. An area of acute infarction is high signal on the
ADC map
E. An area of acute infarction is low signal on diffusion
2. Regarding MRI in acute stroke:
A. Gradient-recalled echo MRI is insensitive to the detection of
acute subarachnoid haemorrhage
B. Signal change is seen earlier on conventional dual echo
imaging than FLAIR imaging
C. MRI is less sensitive in the detection of acute stroke than CT
D. DWI can be acquired in <1 min on most 1.5 T MR scanners
E. CT affords the same anatomical detail as MRI
3. Spontaneous craniocervical arterial dissections:
A. Account for only 2% of all ischaemic strokes
B. Are responsible for 40% of ischaemic strokes in patients
under 45 years of age
C. Assessment with CTA is unreliable
D. Should not routinely be sought in young patients presenting
with acute ischaemic stroke
E. Confirmation of flow void on axial MRI assessment is
diagnostic
4. The Alberta Stroke Program Early CT (ASPECT) score:
A. Is less reliable than the one-third MCA rule at predicting
MCA infarct extent and prognosis
B. Is a qualitative scoring system
C. An ASPECT score of >7 is associated with improved post
thrombolysis outcome
D. Overall score is formulated by point summation depending
on the number of areas displaying early ischaemic change
E. A normal CT brain scan with no evidence of ischaemic
change would score zero points
5. Regarding CT in the assessment of acute stroke:
A. Multidetector technology permits image acquisition within
minutes
B. Major current guidelines pertaining to thrombolysis accept
non-contrast CT as sufficient basis for formulating decision
to proceed to thrombolysis
C. The cumulative radiation dose of non-contrast CT, CTA and
CT perfusion is negligible
D. Acute cerebral infarction results in vasogenic oedema
E. In the clinical setting, CT perfusion is most commonly
performed with inhalation of xenon
Competing interests None.
Provenance and peer review Commissioned; externally peer reviewed.
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<‘Time is brain’. Rapid clinical and imaging assessment of
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<How can identification of areas of programmed apoptosis be
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<By what criteria and with which imaging modalities can the
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ANSWERS
1. (A) F; (B) T; (C) F; (D) F; (E) F
2. (A) F; (B) F; (C) F; (D) T; (E) F
3. (A) T; (B) F; (C) F; (D) F; (E) F
4. (A) F; (B) F; (C) T; (D) F; (E) F
5. (A) F; (B) T; (C) F; (D) F; (E) F
418 Postgrad Med J 2010;86:409e418. doi:10.1136/pgmj.2010.097931
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