C a u s e s o f A c u t e S t ro k e

A Patterned Approach
Ashley Knight-Greenfield, MD, Joel Jose Quitlong Nario, BS, Ajay Gupta, MD, MS*

KEYWORDS
 Stroke  Infarct  Ischemic  Hemorrhagic  Imaging  Cause

KEY POINTS
 Emergent imaging is performed on a high proportion of patients presenting with acute stroke symp-
toms; as such, imaging plays an important role in early diagnosis and management.
 Determining the cause of an acute stroke is critical for clinicians to initiate appropriate therapy.
 Imaging patterns of acute stroke can suggest the cause, and therefore aid in appropriate
management.
 Once large vessel atherosclerosis, small vessel disease, and cardioembolic sources have been
excluded, unusual causes should be considered.

INTRODUCTION ISCHEMIC STROKE

Acute stroke is a leading cause of morbidity and Ischemic strokes, which account for most infarcts,
mortality in the United States and worldwide, with can be subdivided based on cause. The Trial of
more than 750,000 cases and 140,000 deaths in Org 10172 in Acute Stroke Treatment (TOAST) is
the United States each year.1,2 In the United a system developed to categorize subtypes of
States, patients who arrive at a hospital emer- ischemic strokes and therefore guide proper man-
gency department with acute stroke symptoms agement3 (Box 1).
often undergo immediate computed tomography
(CT) scanning, often before detailed clinical eval- Large Artery Atherosclerosis
uation. Therefore, imaging has a critical role in
early diagnosis of stroke. In addition to aiding in Infarctions larger than 15 to 20 mm, involving the
diagnosis of acute stroke, patterns of infarction cortex, cerebellum, brainstem, and subcortical re-
on imaging can suggest a cause, which not gions, are usually caused by large vessel disease
only influences immediate management strate- arising from atherosclerosis of cervical or proximal
gies, but also informs optimal secondary preven- intracranial vessels,3–5 comprising a major cause
tion therapies to prevent stroke recurrence. It is of acute stroke, ranging from 30% to 43%.5 Eval-
important to recognize these patterns to better uation of the cervical and intracranial vasculature
guide image evaluation, recommend appropriate is critical when large vessel atherosclerosis is sus-
additional imaging as necessary, and ultimately pected as the cause of acute infarction. The mech-
arrive at the underlying cause. This article re- anism of infarction secondary to atherosclerosis of
views imaging patterns and secondary findings the extracranial vasculature is a combination of
that can assist in determining the cause of acute low-flow states and artery-to-artery emboli, with
stroke. the latter thought to be the greater contributing
factor.6
radiologic.theclinics.com

Disclosure: The authors have nothing to disclose.

Department of Radiology, Weill Cornell Medicine, 525 East 68th Street, New York, NY 10065, USA
* Corresponding author.
E-mail address: ajg9004@med.cornell.edu

Radiol Clin N Am 57 (2019) 1093–1108

https://doi.org/10.1016/j.rcl.2019.07.007
0033-8389/19/Ó 2019 Elsevier Inc. All rights reserved.
1094 Knight-Greenfield et al

Box 1 Anterior circulation infarcts from carotid

Trial of Org 10172 in acute stroke treatment atherosclerosis most commonly involve the mid-
classification dle cerebral artery (MCA),5 resulting in a territo-
rial infarction that involves the deep gray matter
 Large artery atherosclerosis (embolus or and cortex. Such infarcts typically involve the
thrombosis) central portion of the brain, including the anterior
 Cardioembolic parietal lobe, the posterior frontal lobe, and the
 Small vessel occlusion (lacune) superior temporal lobe (Fig. 1). The anterior
cerebral artery (ACA) territory is frequently
 Stroke of other determined cause, or unusual
spared, because of an intact circle of Willis.7
cause
Proximal intracranial vascular disease is also un-
 Stroke of undetermined cause der the purview of large artery atherosclerosis.
 Two or more causes identified Multiple mechanisms are postulated regarding
 Negative evaluation the pathogenesis of stroke in these cases,
including artery-to-artery emboli, in situ throm-
 Incomplete evaluation boembolism, and hemodynamic impairment6
The TOAST classification was developed to cate- (Fig. 2).
gorize causes of acute ischemic stroke. It is a Large vessel atherosclerosis affecting the verte-
useful way to categorize stroke in order to brobasilar system may also produce a specific set
guide management decisions. of imaging patterns. For example, in the setting of
proximal or middle basilar artery occlusion, large

Fig. 1. A 54-year-old man presenting with altered mental status. (A) Axial CT images show an acute left MCA ter-
ritory infarction involving the left insular cortex, basal ganglia, posterior frontal, and anterior parietal lobes. (B)
Axial images from CT angiography (computed tomography) of the head and neck show moderate to severe ste-
nosis of the proximal left ICA (red arrow) and left MCA thrombus involving the distal M1 and proximal M2 seg-
ments (yellow arrow).
 Causes of Acute Stroke 1095

Fig. 2. Anterior circulation infarctions. (A) A 96-year-old woman with history of aortic valve repair on Coumadin
presenting with acute-onset left hemiparesis. Axial diffusion-weighted magnetic resonance (MR) shows infarc-
tions involving both deep gray matter and cortex, typical of an MCA territory infarction. (B) Axial MR angiog-
raphy (magnetic resonance) time of flight (TOF) shows stenosis of the right intracranial ICA (red arrow). (C)
Three-dimensional (3D) maximum intensity projection (MIP) image shows occlusion of the M1 segment of the
right MCA (yellow arrow), with infarction probably secondary to a combination of hemodynamic impairment
and artery-to-artery emboli. (D) A 73-year-old woman with hypertension and hyperlipidemia presenting with
acute right MCA syndrome. Axial diffusion-weighted image shows infarct involving the right frontal lobe and
basal ganglia in an MCA distribution. (E) 3D MIP from MRA head shows luminal narrowing of the right M1/
M2 junction of the MCA (white arrow).

infarctions are usually seen in the pons as well as hemodynamic compromise, because the lenticu-
the cerebellum, bilateral inferomedial temporal lostriate vessels supplying these regions have
lobes, occipital lobes, and posterior thalami the lowest perfusion pressure (Fig. 4).12 Poste-
(Fig. 3). Distal basilar occlusions usually involve rior circulation border-zone infarcts are less
the midbrain and thalami, and this is one of the common and, when unilateral, are more often
few instances in which bilateral infarctions are caused by an embolic source from the anterior
seen in the setting of large vessel atherosclerosis.8 circulation in the setting of a fetal-type
Infarction of the lateral medulla should prompt ra- PCA11,13 (Fig. 5).
diologists to evaluate the distal vertebral artery, When any of the imaging patterns discussed
because this is often caused by occlusion of the earlier are encountered, it is critical to evaluate
posterior inferior cerebellar artery, clinically result- the vasculature for large vessel atherosclerosis
ing in a lateral medullary syndrome.9 as the cause of acute stroke. Such evaluation
External border-zone infarcts are cortical in- may be performed with CT angiography (CTA),
farcts that occur at the zones between the ante- magnetic resonance (MR) angiography (MRA), or
rior, middle, and posterior cerebral artery (PCA) digital subtraction angiography (DSA). In addition,
territories. Although the cause of these infarcts using MR imaging sequences beyond diffusion-
is not well understood, the prevailing theory is weighted imaging may shed further light on infarct
that they result from a combination of embolic cause. For example, T2 fluid-attenuated inversion
phenomena and hypoperfusion.10,11 Hypoperfu- recovery (FLAIR) hyperintensity within intracranial
sion may be secondary to actual hemodynamic vasculature may suggest slow flow caused by
compromise from stenosis, or caused by more proximal vascular disease (Fig. 6A). A
these areas being less well perfused at baseline. serpiginous hypointense structure seen on
This condition, in turn, can lead to impaired susceptibility-weighted images may indicate
washout in the setting of an embolic event.10 In thromboembolus in a distal vessel (Fig. 6B). A
contrast, internal border-zone infarcts are more hyperdense MCA may be seen on initial noncon-
often caused by proximal stenoses or trast CT (Fig. 6C).
1096 Knight-Greenfield et al

Fig. 3. Basilar occlusion. (A) Axial diffusion-weighted images show bilateral cerebellar, right and left pontine, and
right thalamic infarcts. (B) 3D MIP image from MRA shows severe stenosis of the V1/V2 segment of the right verte-
bral artery (red arrow). (C) Sagittal MIP image from CTA head shows near-complete occlusion of the distal basilar
artery (yellow arrow), which extended into the proximal PCAs.

Fig. 4. A 72-year-old man with history of transient ischemic attacks, hypertension, and diabetes, presenting with
right arm numbness. (A) Axial diffusion-weighted image shows acute infarction in an internal border zone dis-
tribution in the left frontoparietal lobes. (B) 3D MIP from MRA of the neck shows severe stenosis of the proximal
cervical ICA.
 Causes of Acute Stroke 1097

Fig. 5. A 75-year-old man with history of type 2 diabetes mellitus, hypercholesterolemia, hypertension, present-
ing with word-finding difficulty and right facial droop. (A) Axial diffusion-weighted images show acute infarc-
tions involving MCA/PCA border-zone territories. (B) 3D MIP from MRA head shows complete lack of flow in
the left V4 vertebral artery, as well as multifocal stenoses of the left PCA, both of which likely contributed to
the border zone infarction.

Cardioembolic with left ventricular thrombus, and infective or in-

flammatory endocarditis. In addition, emboli may
Cardioembolic sources account for 20% to 31%
originate from aortic arch disorder, which can be
of acute ischemic infarctions.5,14 Such infarcts
missed on routine transthoracic echo; such cases
most often present on MR imaging as multiple
can lead to bilateral infarctions as well.16
foci of restricted diffusion involving multiple
When isolated ACA infarctions are seen, a cardi-
vascular territories, which are often bilateral15
oembolic source should be considered, although
(Fig. 7). When this pattern is identified, it is critical
there is debate as to the most common cause
to consider further evaluation of the heart,
(Fig. 8A). Some studies have shown that the cause
including additional diagnostic imaging. There
is more often cardioembolic,17,18 whereas others
are several causes of cardioembolic disease,
have shown it is more often secondary to large
including atrial fibrillation, myocardial infarction
vessel atherosclerosis of the ACA itself, the latter

Fig. 6. (A) A 33-year-old woman presenting with confusion and aphasia, found to have a left MCA territory
infarction and nonocclusive left M2 thrombus. Axial T2 FLAIR shows increased signal within multiple left MCA
branches (yellow arrows) secondary to slow flow from the proximal partial occlusion. (B) A 94-year-old woman
presenting with speech difficulties and left facial droop, found to have right MCA territory infarction.
Susceptibility-weighted sequences show a tubular area of blooming in the anterior sylvian fissure, consistent
with thromboembolus (white arrow). (C) A 90-year-old woman with history of congestive heart failure, hyperten-
sion, hyperlipidemia, presenting with left hemiparesis and dysarthria. Initial axial noncontrast head CT shows a
dense right MCA (red arrow).
1098 Knight-Greenfield et al

Fig. 7. Multiple bilateral infarctions from cardioembolic source. (A) Axial diffusion-weighted MR images in a 36-
year-old woman with systemic lupus erythematous and Libman-Sacks endocarditis. (B) Axial T2 FLAIR images in a
38-year-old male intravenous drug abuser with bacterial endocarditis. (C) Axial diffusion-weighted MR images in
a 79-year-old man with atrial fibrillation.

being more common in Asian populations.19,20 Small Artery Occlusion (Lacunar Infarction)
Isolated ACA infarctions are less common than
Small artery occlusions can be surmised as the
MCA infarctions.5,7,17 When infarctions involve
cause of infarcts less than 20 mm, without evi-
both the ACA and MCA territories, the cause is
dence of other disorders, such as vascular dis-
also often cardioembolic. For example, an acute
ease, vasospasm, or a cardioembolic source.4
myocardial infarction in a patient with atrial fibrilla-
These occlusions account for 10% to 23% of
tion may lead to distal emboli and decreased car-
acute strokes.5 Risk factors include diabetes and
diac output7 (Fig. 8B).

Fig. 8. (A) A 77-year-old woman with history of hypertension and advanced congestive heart failure with new-
onset right hemiparesis. Axial diffusion-weighted MR image shows acute left ACA territory infarction likely sec-
ondary to cardioembolic source from advanced heart failure, because no vascular abnormality of the ACA was
seen. (B) An 80-year-old man with history of prior stroke, atrial fibrillation, coronary artery disease, and hyper-
tension presenting with new-onset left-sided weakness after collapse. Axial diffusion-weighted MR images reveal
acute infarction in the right frontal cortex and right caudate head in a combined ACA/MCA distribution, likely
cardioembolic in cause from known atrial fibrillation.
 Causes of Acute Stroke 1099

Fig. 9. Infarctions measuring less than 20 mm in the typical locations for small vessel infarctions, consistent with
lacunar infarcts. (A) Axial diffusion-weighted MR shows acute infarct in the left thalamus in a hyperlipidemic
smoker. (B) Axial diffusion-weighted MR shows acute infarct in the right internal capsule in a patient with mul-
tiple vascular risk factors. (C) Axial diffusion-weighted MR shows acute infarct in the right pons in a patient with
hyperlipidemia and hypertension.

hypertension. Lacunar infarcts are seen most often is important to consider atypical causes once
in the basal ganglia, internal capsule, corona radi- common causes have been excluded, because
ata, and brainstem (Fig. 9). PCA infarcts are more this has important implications for management.
often lacunar in cause, and often present with Vasculopathies represent a large portion of un-
typical clinical syndromes.21 Exclusion of proximal usual causes of stroke, in addition to other causes,
vascular disease is critical to the diagnosis. Sec- such as hypercoagulable states, hematologic dis-
ondary findings on imaging that may suggest small orders, right-to-left vascular shunts, and arterial
vessel disease as the cause of infarction include dissections. Although many of these disease pro-
presence of chronic lacunar infarcts, cerebral cesses look similar, certain patterns of vascular
microbleeds, white matter ischemic disease, involvement and secondary findings on imaging
prominent perivascular spaces, and cerebral may help elucidate the underlying cause.
atrophy.22
Vasculopathies
Vasculopathies involving proximal vessels often
Unusual Causes
result in territorial infarcts of perforating vessels
Approximately 2% to 11% of ischemic strokes supplying deep white matter and the basal ganglia.
have unusual causes.5,23 Although uncommon, it A component of subarachnoid hemorrhage may

Fig. 10. A 49-year-old man with no known past medical history presented with acute-onset right-sided hemipa-
resis and confusion. (A) Axial noncontrast CT of the head shows a large left thalamic hematoma (arrow) with
intraventricular extension. (B) Axial and MIP images from follow-up CTA show stenosis of the left cavernous
ICA (arrow) as well as multiple collateral vessels, consistent with moyamoya.
1100 Knight-Greenfield et al

also be seen.24 Extensive collaterals are present in Vasculopathies involving second-order and
the setting of moyamoya and sickle cell disease. third-order arteries often result in cortical infarc-
Moyamoya disease can present in both children tions in distal vascular territories, typically
and adults, usually as recurrent large territorial without deep tissue involvement. These infarcts
infarctions. In children, infarctions are often are also likely to be hemorrhagic. Contrast-
ischemic, whereas in adults they are more often enhanced MR angiography may show vessel
hemorrhagic. Vascular imaging is critical and wall enhancement. Causes include primary angii-
shows stenosis or occlusion of the distal internal tis of the CNS (PACNS), granulomatosis with pol-
carotid artery (ICA) and its proximal branches, yangiitis, polyarteritis nodosa, and sarcoid.24
with sparing of the posterior circulation.7,25,26 The Infectious causes, such as syphilis and herpes
most salient imaging feature is the extensive collat- zoster, may also affect second-order and third-
eral vascularity, best seen on vascular imaging order vessels. Herpes zoster occurs with reacti-
(Fig. 10). vation of the latent virus, and is often indistin-
Basilar meningitis, as in the case of tuberculosis, guishable from PACNS on imaging. It often
can lead to arterial spasm and vasoconstriction of presents with multiple infarcts, often involving
proximal vessels, resulting in infarction. Additional the basal ganglia and subcortical white matter.
findings that may suggest this cause include Angiography may reveal segmental stenosis,
involvement of the posterior circulation, unlike thrombosis, and beading of the proximal MCA
moyamoya, and involvement of perforating ves- and ACA.26 Subarachnoid hemorrhage may be
sels, leading to basal ganglia and thalamic in- seen30,31 (Fig. 13).
farcts.27 Secondary findings of communicating Small vessel vasculopathies, such as Sjӧgren,
hydrocephalus, ventriculitis, and vasospasm collagen vascular disease, human immunodefi-
further support this as a cause (Fig. 11). Acute ciency virus encephalitis, and radiation vascul-
septic meningitis from Streptococcus pneumo- opathy typically appear normal on angiography.
niae, Neisseria meningitidis, Haemophilus influen- Infarctions may be seen in deep gray structures,
zae, and Staphylococcus aureus have been white matter, and subcortical regions. In contrast
reported to cause infarction as well28 (Fig. 12). with multiple sclerosis, the white matter lesions
Vasospasm may be seen on vascular imaging.29 seen with small vessel vasculopathy often

Fig. 11. A 55-year-old man with naso-

pharyngeal carcinoma presenting
with altered mental status and fever,
found to have Streptococcus interme-
dius meningitis. (A) Axial diffusion-
weighted MR images show left basal
ganglia and internal capsule infarction
(star). On further inspection, the pa-
tient is noted to have mild ventriculo-
megaly and layering foci of restricted
diffusion in the atria of the lateral ven-
tricles, consistent with ventriculitis (yel-
low arrows). Restricted diffusion is also
present in the basilar cisterns, consis-
tent with basilar meningitis (red ar-
rows). (B) Axial TOF image from MRA
head at initial presentation and CTA
head 8 days later. At 8-day follow-up,
there is increased narrowing in the
supraclinoid ICA (yellow arrows) and
basilar artery (red arrows) secondary
to vasospasm from basilar meningitis.
 Causes of Acute Stroke 1101

Fig. 12. A 27-year-old woman presenting with fever and acute visual loss after abscess drainage for lower extrem-
ity necrotizing fasciitis. (A) Axial diffusion-weighted MR image shows a small infarct in the right middle cerebellar
peduncle (circle). (B) Secondary findings of sulcal restricted diffusion (red arrow) and leptomeningeal enhance-
ment on axial T1 postcontrast MR (yellow arrows) suggest meningitis as the cause of infarction.

Fig. 13. Herpes zoster vasculitis. A 65-year-old woman initially presented with sudden-onset left hand weakness
and facial droop. (A) Axial diffusion-weighted MR shows a right parietal infarct (star). (B) The patient was also
noted to have failure of suppression of sulcal cerebrospinal fluid on T2 FLAIR, which corresponded to right con-
vexity subarachnoid hemorrhage on noncontrast CT (yellow arrows). Vascular imaging was normal on initial pre-
sentation. (C) The patient returned 8 months later with right hand clumsiness and was found to have a new left
insular infarct on axial diffusion-weighted MR (red arrow). (D) Axial T1-weighted image shows intrinsic T1 hyper-
intensity, consistent with hemorrhage (circle). (E) 3D MIP from MRA at that time reveals focal high-grade stenosis
of an M2 branch of the left MCA (yellow arrow). Lumbar puncture revealed herpes zoster infection.
1102 Knight-Greenfield et al

parallel the ventricles. These lesions often patients may present with acute infarct. Vessel
present at an earlier age and show rapid occlusion may be seen on angiography. Lym-
progression.24 phoma is usually the cause, with the most com-
Systemic lupus erythematous (SLE) is a mon cause being non-Hodgkin. For example,
collagen vascular disease that can result in diffuse large B-cell lymphoma (DLBCL) may pre-
small vessel vasculopathy (Fig. 14). Infarction sent with acute infarcts and infarctlike lesions,
pattern in lupus is nonspecific. More which are diffusion restricting on MR imaging
often than not, infarction is caused by secondary and show signal abnormality on T2-weighted se-
causes of the disease rather than vasculitis, quences. Infarcts may involve the corpus cal-
such as cardiac valvular disease (Libman-Sacks losum and periventricular white matter, and
endocarditis), hypercoagulability, atheroscle- may be in a watershed distribution. In the case
rosis from hypertension and steroid treatment, of DLBCL, small vessels are often involved, so
and venous thrombosis. Secondary findings angiography may be normal. Secondary findings
to look for include intracranial hemorrhage, include meningeal enhancement and central
and cerebral atrophy, with normal vascular pontine hyperintensity, which may be secondary
imaging.32 to venous congestion in the setting of vascular
Neoplastic vasculopathy is a result of vascular occlusion by tumor cells33,34 (Fig. 15). Less com-
invasion secondary to neoplasm; affected mon causes of neoplastic vasculopathy include

Fig. 14. SLE. A 36-year-old woman with history of SLE presents with change in mental status and palate numb-
ness. (A) Axial diffusion-weighted MR image shows punctate acute right frontal cortical infarct (red arrow). (B)
Secondary findings of chronic right frontal subcortical infarct (yellow arrow) and white matter lesions paralleling
the ventricles (oval) on axial T2 FLAIR images are characteristic of lupus. (C) Additional chronic infarcts were seen
in this young patient, including a chronic right cerebellar infarct on axial T2-weighted MR image (red arrow) and
left caudate infarct on axial T2 FLAIR-weighted MR image (yellow arrow). (D) There is a normal appearance of the
vessels on 3D MIP image from MRA, which is typical of SLE.
 Causes of Acute Stroke 1103

Fig. 15. Intravascular DLBCL. A 54-year-old man presenting with 3 weeks of ascending numbness and malaise,
initially treated for Guillain-Barré syndrome. (A) Patient returned for ongoing symptoms, and axial diffusion-
weighted MR image revealed multiple bilateral areas of acute infarction in a watershed distribution (red arrows).
(B) After 2 months, axial diffusion-weighted and T2 FLAIR images show multiple additional infarcts and infarct-
like lesions, with diffusion restriction and corresponding T2 hyperintensity (ovals). (C) Axial T1 postcontrast im-
ages revealed leptomeningeal enhancement (yellow arrows). (D) Axial T2 FLAIR shows central pontine T2
hyperintensity (white arrow).

Fig. 16. CADASIL. A 38-year-old woman with known CADASIL presented with altered mental status. (A) Axial
diffusion-weighted MR image shows a focus of diffusion restriction in the left temporal subcortical white matter
consistent with acute infarct (star). (B) Axial T2 FLAIR images show confluent periventricular white matter hyper-
intensity involving the anterior temporal and frontal white matter, as well as the external capsule, in a pattern
consistent with CADASIL (red arrows). (C) Axial susceptibility-weighted image shows nonspecific microhemorrh-
ages (yellow arrows).
1104 Knight-Greenfield et al

multiple myeloma, T-cell leukemia, and hairy cell Stroke of Undetermined Cause
leukemia.
This category is invoked when multiple causes or
There are also hereditary causes of acute
no causes of stroke are identified. Causes that
infarction. Cerebral autosomal dominant arterio-
may be missed on conventional cardiac imaging,
pathy with subcortical infarcts and leuko-
cardiac work-up, or vascular imaging should be
encephalopathy (CADASIL) causes focal and
considered as potential causes of cryptogenic
confluent subcortical white matter infarcts pre-
stroke. Such entities include patent foramen
dominantly involving the superior frontal lobes,
ovale (Fig. 18), aortic arch atherosclerosis,
external capsule, and anterior temporal lobes.
paroxysmal atrial fibrillation,3 or nonstenosing
Lacunar infarcts and microbleeds may also be
atherosclerosis of the carotid arteries.38,39
seen35 (Fig. 16).

HEMORRHAGIC STROKE
Dissection
Another unusual cause of acute stroke is Hemorrhagic strokes comprise approximately 5%
arterial dissection. This condition often occurs to 21% of acute strokes.14 One of the most com-
in young patients presenting with focal deficit mon causes of hemorrhagic strokes is hyperten-
and headache or neck pain, with a possible sion.40 Hypertensive strokes occur in typical
inciting event, often trauma. Infarction usually locations, including the basal ganglia, thalamus,
has an embolic cause rather than hypoperfu- pons, and cerebellum (Fig. 19).
sion.36,37 Vascular imaging is critical to evaluate Vascular malformations are another cause of
for a dissection flap and stenosis or occlusion hemorrhagic strokes. Arteriovenous malforma-
secondary to dissection. However, in the tions (AVMs) should be considered in younger
absence of vascular imaging, a distal cervical patients who present with acute hemorrhagic
ICA dissection may be seen on routine brain strokes, because hemorrhage is the most com-
MR imaging, so it is important to evaluate the ca- mon presentation.41 AVMs are characterized
rotid arteries at the skull base for any signs of by abnormal arteriovenous connections with a
dissection (Fig. 17). vascular nidus, and absence of an intervening

Fig. 17. Cervical carotid dissection. A

40-year-old man with no past medical
history presented with acute left facial
droop and right jaw pain. (A) Axial
diffusion-weighted image shows
right-sided parietal and caudate head
infarcts. (B) Axial T1-weighted
sequence shows hyperintensity sur-
rounding the right petrous ICA consis-
tent with blood in the dissection flap
(yellow arrow). (C) MRA neck per-
formed for confirmation shows hyper-
intensity surrounding the proximal
cervical ICA on T1 fat-saturated
sequence (red arrow). (D) 3D MRA
MIP image shows resultant long
segment smooth stenosis extending
from just distal to the bifurcation to
the petrous ICA (yellow arrows).
 Causes of Acute Stroke 1105

Fig. 18. A 61-year-old-woman with

breast cancer and left upper extremity
deep venous thrombosis. Axial
diffusion-weighted images show multi-
ple bilateral infarctions involving mul-
tiple vascular territories. Cause was
presumed as secondary to undetected
patent foramen ovale, because no
large vessel or cardioembolic sources
were identified.

Fig. 19. Three different patients with systemic hypertension, presenting with hemorrhagic infarctions in charac-
teristic locations. In all of these cases, vascular imaging revealed no abnormality. (A) Axial CT with hemorrhagic
infarct in the pons. (B) Axial CT with hemorrhagic infarct in the right basal ganglia. (C) Axial T1-weighted MR im-
age with hemorrhagic infarct in the left thalamus.

Fig. 20. A 16-year-old boy with no significant past medical history presenting with acute-onset left-sided weak-
ness, headache, and subsequent coma. (A) Axial noncontrast head CT revealed right basal ganglia and intraven-
tricular hemorrhage causing a leftward midline shift. (B) Subsequent CT angiography of the head revealed an
arteriovenous malformation with its nidus at the junction between the thalamus and posterior limb of the right
internal capsule, supplied by a PCA branch with deep venous drainage.
1106 Knight-Greenfield et al

Fig. 21. A 53-year-old woman with history of breast cancer presented after being found down unresponsive. (A)
Noncontrast head CT at time of presentation shows hemorrhagic infarctions of the bilateral basal ganglia and
thalami. (B) Tubular hyperdensity is seen in the bilateral internal cerebral veins (red arrows), vein of Galen (yellow
arrows), and straight sinus (white arrow), consistent with venous sinus thrombosis and venous infarction.

capillary bed. Vascular imaging with CTA, MRA, or is often hemorrhagic. Secondary findings to
DSA is critical in making the diagnosis (Fig. 20). search for include presence of a hyperdense
Venous infarction should be considered when venous sinus or cortical vein on noncontrast CT,
the location of the infarct does not correspond or absence of flow-related signal void in venous
with an arterial vascular distribution, or spans structures on MR imaging. Further evaluation
more than 1 arterial distribution (Fig. 21). These with MR venography or CT venography is
patients may initially present with vasogenic often performed for confirmation. Hypercoagula-
edema on T2 FLAIR sequences, which, if not ble states are the most important contributing
addressed, usually progresses to infarction, which factor in adults.41,42

Fig. 22. Cerebral amyloid angiopathy.

A 65-year-old woman with recurrent
transient neurologic symptoms of un-
clear cause and migraine with aura,
presenting with acute-onset right face
and right arm numbness and weak-
ness. (A) Axial noncontrast head CT
and axial T1-weighted MR image
show a left high parietal intra-
parenchymal hemorrhage. (B) Axial
susceptibility-weighted images reveal
multifocal subarachnoid and subcor-
tical microhemorrhages. Brain biopsy
was positive for b-amyloid plaques.
 Causes of Acute Stroke 1107

Cerebral amyloid angiopathy is another cause 6. Derdeyn CP. Mechanisms of ischemic stroke sec-
of hemorrhagic infarction to be considered ondary to large artery atherosclerotic disease. Neu-
in older patients who present with multiple, roimaging Clin N Am 2007;17(3):303–11, vii–viii.
recurrent cortical and subcortical hemorrhagic 7. Zimmerman RD. Vascular diseases of the brain. In:
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ACKNOWLEDGMENTS
cance of acute multiple infarcts in multiple cerebral
Dr. Ajay Gupta’s effort is in part supported by circulations on initial diffusion weighted imaging in
NIH grants R01HL14454 and R21HL145427. stroke patients. J Neurol Sci 2014;337(1–2):151–5.
16. Capmany RP, Ibañez MO, Pesquer XJ. Complex
atheromatosis of the aortic arch in cerebral infarc-
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