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Stroke is a leading cause of mortality and morbidity in the developed world. The goals of an
imaging evaluation for acute stroke are to establish a diagnosis as early as possible and to
obtain accurate information about the intracranial vasculature and brain perfusion for
guidance in selecting the appropriate therapy. A comprehensive evaluation may be
performed with a combination of computed tomography (CT) or magnetic resonance (MR)
imaging techniques. Unenhanced CT can be performed quickly, can help identify early signs
of stroke, and can help rule out hemorrhage. CT angiography and CT perfusion imaging,
respectively,can depict intravascular thrombi and salvageable tissue indicated by a
penumbra. These examinations are easy to perform on most helical CT scanners and are
increasingly used in stroke imaging protocols to decide whether intervention is necessary.
While acute infarcts may be seen early on conventional MR images, diffusion-weighted MR
imaging is more sensitive for detection of hyperacute ischemia. Gradient-echo MR sequences
can be helpful for detecting a hemorrhage.
The status of neck and intracranial vessels can be evaluated with MR angiography, and a
mismatch between findings on diffusion and perfusion MR images may be used to predict the
presence of a penumbra. The information obtained by combining various imaging techniques
may help differentiate patients who do not need intravenous or intraarterial therapy from
those who do, and may alter clinical outcomes.
• acute cerebral ischemia may result in a central
irreversibly infarcted tissue core surrounded
by a peripheral region of stunned cells that is
called a penumbra .Evoked potentials in the
peripheral region are abnormal, and the cells
have ceased to function, but this region is
potentially salvageable with early
recanalization .
• A penumbra can be evaluated both on CT images (on which it is
evidenced by a discrepancy in perfusion parameters) and on MR
images (on which it is indicated by a mismatch between diffusion
and perfusion parameters). The presence of a penumbra has
important implications for selection of the appropriate therapy and
prediction of the clinical outcome. Intravenous thrombolytic
treatment is not typically administered to patients with acute stroke
beyond the conventional 3-hour period after the onset of
symptoms, because such treatment results in an increased risk of
hemorrhage . However, the results of recent studies have
demonstrated that intravenous thrombolytic therapy may benefit
patients who are carefully selected according to findings of a
diffusion or perfusion mismatch or a penumbra at imaging
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•Posterior Inferior
Cerebellar Artery (PICA in blue)
The PICA territory is on the inferior occipital surface of the cerebellum and
is in equilibrium with the territory of the AICA in purple, which is on the
lateral side (1).
The larger the PICA territory, the smaller the AICA and viceversa.
•Superior Cerebellar Artery (SCA in grey)
The SCA territory is in the superior and tentorial surface of the cerebellum.
•Branches from vertebral and basilar artery
These branches supply the medulla oblongata (in blue) and the pons (in
green).
•Anterior Choroideal artery (AchA in blue))
The territory of the AChA is part of the hippocampus, the posterior limb of
the internal capsule and extends upwards to an area lateral to the posterior
part of the cella media.
•Lenticulo-striate arteries
The lateral LSA' s (in orange) are deep penetrating arteries of the middle
cerebral artery (MCA).
Their territory includes most of the basal ganglia.
The medial LSA' s (indicated in dark red) arise from the anterior cerebral
artery (usually the A1-segment).
Heubner's artery is the largest of the medial lenticulostriate arteries and
supplies the anteromedial part of the head of the caudate and
anteroinferior internal capsule.
•Anterior cerebral artery (ACA in red)
The ACA supplies the medial part of the frontal and the parietal lobe and
the anterior portion of the corpus callosum, basal ganglia and internal
capsule.
•Middle cerebral artery (MCA in yellow)
The cortical branches of the MCA supply the lateral surface of the
hemisphere, except for the medial part of the frontal and the parietal lobe
(anterior cerebral artery), and the inferior part of the temporal lobe
(posterior cerebral artery).
The deep penetrating LSA-branches are discussed above.
•Posterior cerebral artery (PCA in green)
P1 extends from origin of the PCA to the posterior communicating artery,
contributing to the circle of Willis.
Posterior thalamoperforating arteries branch off the P1 segment and
supply blood to the midbrain and thalamus.
Cortical branches of the PCA supply the inferomedial part of the temporal
lobe, occipital pole, visual cortex, and splenium of the corpus callosum.
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Watershed infarcts occur at the border zones
between major cerebral arterial territories as
a result of hypoperfusion.
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There are two patterns of border zone
infarcts:
1.Cortical border zone infarctions
Infarctions of the cortex and adjacent
subcortical white matter located at the
border zone of ACA/MCA and MCA/PCA
2.Internal border zone infarctions
Infarctions of the deep white matter of the
centrum semiovale and corona radiata at the
border zone between lenticulostriate
perforators and the deep penetrating
cortical branches of the MCA or at the border
zone of deep white matter branches of the
MCA and the ACA.
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• On the left three
consecutive CT-images of a
patient with an occlusion of
the right internal carotid
artery.
• The hypoperfusion in the
right hemisphere resulted in
multiple internal border
zone infarctions.
• This pattern of deep
watershed infarction is
quite common and should
urge you to examine the
carotids.
• On the left images of a patient
who has small infarctions in
the right hemisphere in the
deep borderzone (blue
arrowheads) and also in the
cortical borderzone between
the MCA- and PCA-territory
(yellow arrows).
• There is abnormal signal in
the right carotid (red arrow) as
a result of occlusion.
• In patients with abnormalities
that may indicate borderzone
infarcts, always study the
images of the carotid artery to
look for abnormal signal
• On the left the CT nicely demonstrates the
dense thrombosed transverse sinus (yellow
arrow). The FLAIR image demonstrates the
venous infarction in the temporal lobe.
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The clinical presentation of thrombosis of the deep cerebral venous system are severe dysfunction of the diencephalon,
reflected by coma and disturbances of eye movements and pupillary reflexes. Usually this results in a poor outcome.
However, partial syndromes without a decrease in the level of consciousness or brainstem signs exist, which may lead to
initial misdiagnoses.
Deep cerebral venous system thrombosis is an underdiagnosed condition when symptoms are mild and should be
suspected if the patient is a young woman, if the lesions are within the basal ganglia or thalamus and especially if they are
bilateral.
On the left images of a patient with deep cerebral vein thrombosis. Notice the bilateral infarctions in the basal ganglia.
• CT has the advantage of being
available 24 hours a day and is
the gold standard for
hemorrhage.
• Hemorrhage on MR images can
be quite confusing.
• On CT 60% of infarcts are seen
within 3-6 hrs and virtually all are
seen in 24 hours.
• The overall sensitivity of CT to
diagnose stroke is 64% and the
specificity is 85%.
• In the table on the left the early
CT-signs of cerebral infarction are
listed.
• Hypoattenuation on CT is highly specific for irreversible
ischemic brain damage if it is detected within first 6
hours (1).
• Patients who present with symptoms of stroke and
who demonstrate hypodensity on CT within first six
hours were proven to have larger infarct volumes,
more severe symptoms, less favorable clinical courses
and they even have a higher risk of hemorrhage.
• Therefore whenever you see hypodensity in a patient
with stroke this means bad news.
• No hypodensity on CT is a good sign.
• Obscuration of the lentiform
nucleus
• Obscuration of the lentiform
nucleus, also called blurred
basal ganglia, is an important
sign of infarction.
• It is seen in middle cerebral
artery infarction and is one of
the earliest and most
frequently seen signs (2).
• The basal ganglia are almost
always involved in MCAinfarction.
• Insular Ribbon sign
• This refers to hypodensity and swelling of the insular
cortex.
• It is a very indicative and subtle early CT-sign of
infarction in the territory of the middle cerebral artery.
• This region is very sensitive to ischemia because it is
the furthest removed from collateral flow.
• It has to be differentiated from herpes encephalitis.
• Dense MCA sign
• This is a result of thrombus or embolus in the
MCA.
• On the left a patient with a dense MCA sign.
• On CT-angiography occlusion of the MCA is
visible.
• Hemorrhagic infarcts
• 15% of MCA infarcts are initially hemorrhagic
• Hemorrhage is most easily detected with CT,
but it can also be visualized with gradient echo
MR-sequences.
• First look at the images on the
left and try to detect the
abnormality.
• The findings in this case are
very subtle.
• There is some hypodensity in
the insular cortex on the right,
which is the area we always
look at first.
• In this case it is suggestive for
infarction, but sometimes in
older patients with
leukencephalopathy it can be
very difficult.
• A CTA was performed
• CT Perfusion (CTP)
• With CT and MR-diffusion we can get a good
impression of the area that is infarcted, but we cannot
preclude a large ischemic penumbra (tissue at risk).
• With perfusion studies we monitor the first pass of an
iodinated contrast agent bolus through the cerebral
vasculature.
• Perfusion will tell us which area is at risk.
• Approximately 26% of patients will require a perfusion
study to come to the proper diagnosis. The limitation
of CT-perfusion is the limited coverage.
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Studies were performed to compare CT with
MRI to see how much time it took to perform
all the CT studies that were necessary to
come to a diagnosis.
It was demonstrated that Plain CT, CTP and
CTA can provide comprehensive diagnostic
information in less than 15 minutes,
provided that you have a good team.
In the case on the left first a non-enhanced
CT was performed.
If there is hemorrhage, then no further
studies are necessary.
In this case the CT was normal and a CTP
was performed, which demonstrated a
perfusion defect.
A CTA was subsequently performed and a
dissection of the left internal carotid was
demonstrated.
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On PD/T2WI and FLAIR infarction is seen as
high SI.
These sequences detect 80% of infarctions
before 24 hours.
They may be negative up to 2-4 hours postictus!
On the left T2WI and FLAIR demonstrating
hyperintensity in the territory of the middle
cerebral artery.
Notice the involvement of the lentiform
nucleus and insular cortex.
High signal on conventional MR-sequences
is comparable to hypodensity on CT.
It is the result of irreversible injury with cell
death.
So hyperintensity means BAD news: dead
brain.
• Diffusion Weighted Imaging (DWI)
• DWI is the most sensitive sequence for stroke imaging.
• DWI is sensitive to restriction of Brownian motion of
extracellular water due to imbalance caused by
cytotoxic edema.
• Normally water protons have the ability to diffuse
extracellularly and loose signal.
• High intensity on DWI indicates restriction of the
ability of water protons to diffuse extracellularly.
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First look at the images on the left and try to
detect the abnormality.
Then continue reading.
The findings in this case are very subtle.
There is some hypodensity and swelling in
the left frontal region with effacement of
sulci compared with the contralateral side.
You probably only notice these findings
because this is an article about stroke and
you would normally read this as 'no
infarction'.
Now continue with the DWI images of this
patient.
When we look at the DWI-images it is very
easy and you don't have to be an expert
radiologist to notice the infarction.
This is why DWI is called 'the stroke
sequence'
• Pseudo-normalization of DWI
• This occurs between 10-15
days.
• The case on the left shows a
normal DWI.
• On T2WI there is may be
some subtle hyperintensity in
the right occipital lobe in the
vascular territory of the
posterior cerebral artery.
• The T1WI after the
administration of Gadolinium
shows gyral enhancement
indicating infarction.
• First it was thought that
everything that is bright on DWI
is dead tissue.
• However now there are some
papers suggesting that probably
some of it may be potentially
reversible damage.
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If you compare the DWI images
in the acute phase with the T2WI
in the chronic phase, you will
notice that the affected brain
volume in DWI is larger compared
to the final infarcted area
(respectively 62cc and 17cc).
• Perfusion MR Imaging
• Perfusion with MR is
comparable to perfusion CT.
• A compact bolus of Gd-DTPA
is delivered through a power
injector.
• Multiple echo-planar images
are made with a high temporal
resolution.
• T2* gradient sequences are
used to maximize the
susceptibility signal changes.
• The area with abnormal
perfusion can be dead
tissue or tissue at risk.
• Combining the
diffusion and perfusion
images helps us to
define the tissue at risk,
i.e. the penumbra.
• On the DWI there is a large
area with restricted
diffusion in the territory of
the right middle cerebral
artery.
• Notice also the
involvement of the basal
ganglia.
• There is a perfect match
with the perfusion images,
so this patient should not
undergo any form of
thrombolytic therapy.
• Vasculitis of the CNS is characterized by the size of the
affected vessel, as illustrated in Fig. Determining size
and location of the predominantly affected vessels is
useful to obtain an optimal tissue biopsy and establish
appropriate treatment . Large artery vasculitis usually
responds well to steroids alone,while small and
medium-sized vessel vasculitis respond better to a
combination of cytotoxic agents and steroids.
Therefore, a clear understanding of the size of the
vessels involved and the pathophysiologic mechanisms
are useful for the treatment decision.
• Digital subtraction catheter angiography and
brain biopsy are the diagnostic foundations in
establishing the diagnosis. However, angiography
has a false-negative rate of 20–30%, as small
arteries with a diameter of less than 100–200 μm
are beyond the limit of resolution of digital
subtraction angiography . Good-quality MR
angiography can demonstrate stenosis or
occlusion of large to middle-sized arteries,but the
resolution is not sufficient to detect
abnormalities of small arteries.
• MR imaging, on other hand, is sensitive to detect gray and
white matter lesions in CNS vasculitis, but the appearance
of these lesions is usually not specific .
• Whether the lesions on MR imaging are reversible or
irreversible depends on the severity of ischemia and seems
to be related to size and location of the vessels involved.
Occlusion or stenosis involving large, medium or small
arteries mainly results in infarction,whereas lesions
involving arterioles, capillaries,venules or veins
predominantly cause vasogenic edema or gliosis.
• DW imaging can be useful to differentiate an acute or
subacute infarction from vasogenic edema or gliosis,which
is important both for choice of treatment and to predict the
long-term prognosis.
• Multifocal and multiphasic ischemia are some of the
characteristic sequelae of CNS vasculitis.DW imaging
can differentiate the phases of cerebral infarction as
hyperacute, acute, subacute or chronic.
• The hyperacute phase of an infarction usually has a
decreased apparent diffusion coefficient (ADC) and a
normal or subtle increase in signal intensity on T2weighted or fluid-attenuated inversion-recovery
(FLAIR) images. The acute phase has a decreased ADC
with hyperintensity on T2-weighted images. In the
subacute phase, ADC values are normalized; in the
chronic phase, DW imaging shows hypointensity with
increased ADC.
CNS VASCULITIS
NONINFECTIOUS
Necrotizing Vasculitides
PACNS (primary angiitis of the central nervoussystem)
Polyarteritis nodosa
Giant cell arteritis
Takayasu's arteritis
Wegener's granulomatosis
Lymphomatoid granulomatosis
Neurosarcoidosis
Vasculitis Associated with Collagen Vascular Diseases
Systemic lupus erythematosus
Scleroderma
Rheumatoid arthritis
Sjogren's syndrome
Drug-Related Vasculitis
Others
Susac's syndrome (retinocochleocerebral
vasculopathy)
Behcet's syndrome
Sneddon syndrome
Eales disease
Degos disease (malignant atrophic papillosis)
INFECTIOUS
Haemophilus influenzae
Syphilis
Tuberculosis
Herpes Zoster
HIV
Other
• Primary angiitis of the central nervous system (PACNS), also
known as noninfectious granulomatous angiitis of the
central nervous system or granulomatous angiitis of the
nervous system, affects parenchymal and leptomeningeal
vessels of the central nervous system with a predilection
for small arteries and arterioles (200 to 500 mm in
diameter). It strikes middle-aged persons with complaints
of headache and signs of focal or global neurologic
dysfunction. This can be a rapidly progressive disease and is
frequently fatal. The sedimentation rate is elevated in more
than two thirds of patients, and cerebrospinal fluid (CSF)
demonstrates elevated protein and pleocytosis in more
than 80% of cases.
• Primary angitis of the central nervous system tends to affect small
to medium sized vessels of the brain parenchyma and meninges,but
can affect vessels of any size. Angiography typically shows a “stringof-beads” appearance, but it has a false-negative rate of 20–30% .
Brain and meningeal biopsies are diagnostic in only 50–72% of
patients with primary angitis of the central nervous system
• The vasculitis process results in multiple regions of deep white
matter infarction, hemorrhage, or tumor like masses that may be
easily imaged on MR. Lesions are usually multiple and
supratentorial, involving both hemispheres.
• Lesions detected on MR have a positive angiographic correlation;
however, not all lesions seen angiographically have positive MR
findings. Angiography is more sensitive than MR at detecting vessel
involvement.
• Magnetic resonance imaging findings in primary angitis of the
central nervous system are highly variable,ranging from multiphasic
cerebral infarction,vasogenic edema and gliosis, to hemorrhage and
leptomeningeal enhancement . The lesions caused by occlusion of
large or medium-sized arteries affect the cortical or deep gray
matter. If the vessels involved are small, MR imaging may show
discrete or diffuse lesions in the deep or subcortical white matter.
On follow-up MR imaging, the lesions may change with regard to
number and size, and they may even disappear. DW imaging is
useful in differentiating an acute or subacute infarction from
reversible vasogenic edema and can demonstrate multiphasic
infarctions.Prompt diagnosis is important, as primary angitis of the
central nervous system is often fatal if not treated with aggressive
immunosuppression
• The criteria of the American College of
Rheumatology for the diagnosis of giant cell
arteritis include at least three of the following:
(1) age at disease onset >50 years, (2) new onset
of headache, (3)claudication of jaw or tongue, (4)
tenderness of the temporal artery on palpation
or decreased pulsation, (5) erythrocyte
sedimentation ratio >50 mm/h and(6) temporal
artery biopsy showing vasculitis with
multinucleated giant cells.
• Giant cell arteritis is probably a T cell-mediated
vasculitis and it can affect medium to large arteries.
• The superficial temporal, vertebral and ophthalmic
arteries are more commonly involved than the internal
carotid arteries,while the intracranial arteries are rarely
involved .Abrupt and irreversible visual loss is the most
dramatic complication of giant cell arteritis,while a TIA
and stroke are rare (7%),but when present most often
involve the vertebrobasilar territory. Steroids are
effective, and giant cell arteritis is usually self-limited
and rarely fatal.
• Takayasu’s arteritis is a primary arteritis of unknown cause
but probably also related to T cell mediated inflammation.
Takayasu’s arteritis commonly affects large vessels including
the aorta and its major branches to the arms and the head.
It is more commonly seen in Asia and usually affects young
women. Pulseless upper extremities and hypertension are
the common clues to suggest the diagnosis.
• Most patients are treated with steroids alone to reduce the
inflammation. The prognosis is relatively good and 90% of
patients are still alive after 10 years.
• TIA or stroke is rare but can occasionally occur in severe
cases with significant stenosis of arteries supplying the CNS.
• Polyarteritis nodosa is a multisystem disease characterized by
necrotizing inflammation of the small and medium size arteries
with CNS involvement occurring late in the disease in more than
45% of cases. The CNS manifestations include encephalopathy,
seizures, and focal deficits. It is an immune-mediated disease with
about 30% of patients having hepatitis B surface antigen. The
diagnosis is confirmed by nerve, muscle, or kidney biopsy, which
demonstrates multiple small aneurysms or arteritis. Polyarteritis is
closely related to allergic angiitis and granulomatosis (ChurgStrauss) disease and a polyangiitis overlap syndrome (combination
of Churg-Strauss and polyarteritis nodosa).
• Imaging findings include cortical or subcortical infarction as well as
nonspecific high intensity T2WI lesions in the white matter.
Intracranial hemorrhage (SAH,intraparenchymal) and vascular
dissection have been reported.Aneurysms, which are common in
the renal and splanchnic vessels, are unusual in the CNS.
• Wegener Granulomatosis
• This granulomatous necrotizing systemic vasculitis
affects the kidneys, upper and lower respiratory tracts,
but can affect the brain producing stroke, visual loss,
and other cranial nerve problems. The peak incidence
is in the fourth to fifth decade with a slight male
predominance.
• The vasculitis affects small and medium-size arteries
and veins while sparing larger vessels. High intensity
abnormalities on T2WI occur in about 28% of cases.
History plus positive c-ANCA tests help make
thediagnosis.
• Behçet’s disease is a multisystem vasculitis of unknown
origin. It is especially common in Middle Eastern and
Mediterranean countries. CNS involvement has been
described in 4–49% of cases [6]. The parenchymal
distribution of lesions, especially at the mesodiencephalic
junction (46%) supports small vessel vasculitis involving
both the arterial and venous systems; mainly venules. The
lesions are occasionally reversible on MRI, which mainly
represents vasogenic edema,which is why DW imaging is
useful in distinguishing them from infarction . The
treatment is usually a combination of cytotoxic agents and
steroids. In other types of collagen diseases,such as
scleroderma or rheumatoid arthritis,involvement of the
CNS is very rare.
• Vasculopathy is caused by a wide variety of
underlying conditions such as degenerative,
metabolic, inflammatory,embolic, coagulative
and functional disorders . This presentation
focuses on vasculopathies that mimic
vasculitis, but have no inflammation in the
wall of the blood vessel
• Involvement of the CNS occurs in 14–75% of
patients with systemic lupus erythematosus
(SLE). Pathologically,microinfarcts and small
vessel vasculopathy are the most
common.Vasculopathy affects predominantly
the arterioles and capillaries, resulting in
vessel tortuosity, vascular hyalinization,
endothelial proliferation and perivascular
inflammation or gliosis.
• True vasculitis is very rare (0–7%). This vasculopathy may be related to
both acute inflammation and ischemia [28]. In recent reports, the
mechanism of vasculopathy in CNS involvement of SLE has been attributed
to intravascular activation of a complement,which leads to adhesion
between neutrophils and/or platelets and endothelium, resulting in
leukothrombosis in the microvasculature (Shwartzman phenomenon)
• In this vasculopathy, despite widespread microvascular occlusions,
parenchymal damage is minimal and potentially reversible. Sibbit et al.
reported that up to 38% of CNS lesions in SLE were potentially reversible
on MR imaging [30]. MR angiography and conventional angiography may
provide additional information concerning vascular abnormalities.
• DW imaging shows primarily two patterns of parenchymal lesions with
acute or subacute CNS symptoms: one is an acute or subacute
infarction,and the other is vasogenic edema with or without microinfarcts
.CNS involvement in SLE is also due to associated uremia, hypertension,
infection, Libman–Sacks endocarditis, and corticosteroid or
immunosuppressive therapy.
• On T2WI, high signal is recognized in the white matter,sometimes in
a vascular distribution but also involving cortical and subcortical
areas, particularly in the occipital region. Such high-intensity
regions have been reported in a symmetric distribution in young
female patients with diffuse C S lupus. Periventricular white matter
appears to be relatively spared even in patients with diffuse C S
lupus, which may differentiate it from multiple sclerosis, where
there is a predilection for periventricular lesions. Atrophy is
commonly found in these patients,related either to the
encephalopathy itself or to the effect of steroid treatment. Data
suggest that some lesions may evolve within a 7- to 10-day course
in patients with rapidly changing neurologic symptoms and that
certain lesions may be responsive to steroid therapy.Subarachnoid
hemorrhage and intraparenchymal hemorrhage have also been
reported in C S lupus. The presence of saccular and fusiform
aneurysms has also been observed.