Clinical Imaging 95 (2023) 10–23

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Clinical Imaging
journal homepage: www.elsevier.com/locate/clinimag

Neuroradiology

Etiologies of spontaneous acute intracerebral hemorrhage: A

pictorial review
Julien Rossi a, Marc Hermier a, Omer Faruk Eker a, Yves Berthezene a, b, Alexandre Bani-Sadr a, b, *
a
Department of Neuroradiology, East Group Hospital, Hospices Civils de Lyon, 59 Bd Pinel, 69500 Bron, France
b
CREATIS Laboratory, CNRS UMR 5220, INSERM U 5220, Claude Bernard Lyon I University, 7 avenue Jean Capelle O, 69100 Villeurbanne, France

A R T I C L E I N F O A B S T R A C T

Keywords: Spontaneous acute intracerebral hemorrhage (SAIH) is a common and life-threatening condition that affects
Hemorrhagic stroke more than three million patients each year. Of these, one in three patients die within one month of onset and the
Computed-tomography remaining two in three patients have varying degrees of disability and neurological impairment. The role of
Magnetic resonance imaging
radiology is paramount in optimizing patient outcomes by diagnosing SAIH, its potential complications, and the
Digital subtraction arteriography
most likely etiology. While the positive diagnosis of SAIH is straightforward, the etiologic diagnosis is broad,
covering primary SAIH (hypertension, cerebral amyloid angiopathy) and secondary SAIH (vascular malforma­
tions, nonatheromatous vasculopathies, neoplasia, coagulation disorders, toxicants). This pictorial review il­
lustrates the imaging of spontaneous SAIH with an emphasis on etiologic workup.

1. Introduction patient outcomes.

Spontaneous acute intracerebral hemorrhage (SAIH) is the second
most common subtype of stroke after ischemic stroke, accounting for
nearly 10% to 20% of all strokes.1 It refers to the occurrence of a he­
matoma within the brain parenchyma that may extend into the ven­
tricular system, subarachnoid and subdural spaces without a traumatic
context. Each year, it is estimated that 3.4 million people will suffer from
SAIH worldwide.2
Depending on the underlying cause, SAIHs are classified as primary
or secondary.3 Primary SAIHs predominates in elderly patients and
represent nearly 90% of cases.3 They result from the rupture of small
vessels damaged by chronic hypertension or cerebral amyloid angiop­
athy (CAA).3 Secondary SAIHs are the manifestation of underlying pa­
thology including vascular malformations, non-atheromatous
angiopathies, vasospasm, tumors and coagulopathy. Few urgent treat­
ments are available for primary SAIHs, but their diagnosis is important
because they may warrant preventive antihypertensive therapy.
Conversely, secondary SAIHs may require urgent treatments to prevent
recurrence. Therefore, determination of etiology is essential to optimize
In clinical practice, the cornerstone of the positive and etiologic
workup is imaging. Because the imaging modality (i.e., computed to­
mography angiography (CTA), MRI, and/or digital subtraction angiog­
raphy (DSA)) and treatment depend on the presumed underlying cause
of SAIH, knowledge and rapid identification of primary and secondary
SAIH are mandatory for any radiologist.
This pictorial review aims to illustrate the imaging of primary and
secondary SAIHs.
2. Primary SAIH
Primary SAIH accounts for nearly 90% of all SAIH and predominates
in patients over 50 years.4
2.1. Hypertension
Chronic and uncontrolled hypertension is by far the most common
cause of SAIH. A meta-analysis reported that hypertensive patients had
an almost 3.5 fold higher risk of SAIH than normotensive patients.5

Abbreviations: AA, arterial aneurysm; AVM, arteriovenous malformation; CVT, cerebral venous thrombosis; DAVF, dural arteriovenous fistula; CAA, cerebral
amyloid angiopathy; CMB, cerebral microbleeds; CNS, cerebral nervous system; CTA, computed-tomography angiography; DSA, digital subtraction angiography;
MMD, moyamoya disease; PRES, posterior reversible encephalopathy syndrome; RCVS, reversible cerebral vascular syndrome; SAIH, spontaneous acute intracerebral
hemorrhage; SAH, subarachnoid hemorrhage; SWI, susceptibility-weighted imaging; T2*-weighted images, T2*-WI; TOF-MRA, Time-Of-Flight MR Angiography.
* Corresponding author at: Department of Neuroradiology, East Group Hospital, Hospices Civils de Lyon, 59 Bd Pinel, 69500 Bron, France.
E-mail address: alexandre.bani-sadr@chu-lyon.fr (A. Bani-Sadr).

https://doi.org/10.1016/j.clinimag.2022.12.007
Received 3 October 2022; Received in revised form 26 November 2022; Accepted 13 December 2022
Available online 21 December 2022
0899-7071/© 2022 Elsevier Inc. All rights reserved.
J. Rossi et al. Clinical Imaging 95 (2023) 10–23

Fig. 1. Hypertensive spontaneous acute

intracerebral hemorrhage.
In this sudden coma patient,
susceptibility-weighted imaging (A, B,
and C) revealed spontaneous deep acute
intracerebral hemorrhage (white
chevron), left lenticular hematoma
sequelae (white arrowhead), and mul­
tiple central cerebral microbleeds (black
arrows). On the 3DT1-weighted post­
contrast image (D), note multiples foci
of spot signs (white arrows) indicating
active bleeding.

As illustrated in Fig. 1, the typical location of hypertensive SAIH is in clinical outcome.14

the basal ganglia, thalami, cerebellum and pons.6,7 Signs of small vessel has an interesting prognostic value since it predicts expansion of the
disease including age-related white matter changes, lacunar and cortical hematoma.
infarcts can be seen on CT and MRI.8,9 When MRI is performed, T2*-
weighted images (T2*-WI) or susceptibility–weighted (SWI) imaging
2.2. Cerebral amyloid angiopathy
are warranted because the presence of cerebral microbleeds (CMB) in
the brainstem and basal ganglia is a hallmark of chronic hypertension.10
CAA is the second cause of primary SAIH accounting for 5–10% of
The age of the patient (i.e., >50 years old), the history of hypertension,
SAIH and its incidence increases with age.4 Definitive diagnosis of CAA
the typical deep location of SAIH and associated signs of small vessel
requires postmortem examination. In clinical practice, the modified
disease on imaging may be sufficient to determine the etiology.11
Boston criteria (Table 1) are used to stratify the likelihood of CAA.15
The spot sign (Fig. 1) refers to foci of enhancement within the he­
As illustrated in Fig. 2, CAA-related hematomas are lobar and typi­
matoma that can be found on CTA or MRI.12,13 This sign is assumed to
cally present subcortical finger-like projections.16 Associated abnor­
reflect continued bleeding from a ruptured vessel.12 It is not specific to
malities to look for are extensive age-related white matter changes,
an etiology is associated with early hematoma expansion and poor
sequelae of lobar hematomas, evidence of deep lacunar infarcts, and

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Table 1 direct connections between cerebral arteries and veins.19

Modified Boston Criteria for cerebral amyloid angiopathy.15
Definite CAA
Full postmortem examination demonstrating
- Lobar, cortical, or cortical-subcortical hemorrhage
- Severe CAA with vasculopathy
- Absence of other diagnostic lesion
Probable CAA with supporting pathology
Clinical data and pathological tissue (evacuated hematoma or cortical biopsy)
demonstrating:
- Lobar, cortical, or cortical-subcortical hemorrhage (including ICH, CMB, or cSS)
- Some degree of CAA in specimen
- Absence of other diagnostic lesion
Probable CAA with supporting pathology
Clinical data and MRI or CT demonstrating:
- Multiple hemorrhages (ICH, CMB) restricted to lobar, cortical or cortico-
subcortical regions (cerebellar hemorrhage allowed), or single lobar cortical or
cortical – subcortical hemorrhage and cSS (focal or disseminated)
- Age ≥ 55y
- Absence of other cause of hemorrhagea
Possible CAA
Clinical data and MRI or CT demonstrating:
- Single lobar, cortical, cortical-subcortical ICH, CMB, cSS (focal or disseminated)
- Age ≥ 55y
- Absence of other cause of hemorrhagea
Abbreviations: CAA: Cerebral Amyloid Angiopathy; CMB: Cerebral Microbleeds;
cSS: cortical superficial siderosis; ICH: Intracerebral Hemorrhage.
a nals and foramen spinosum.21 On venous phase, enlarged cortical veins
Other causes of hemorrhage (differential diagnosis of lobar hemorrhages):
antecedent head trauma, hemorrhagic transformation of an ischemic stroke,
arteriovenous malformation, hemorrhagic tumor, warfarin therapy with inter­
national normalization ratio > 3, and vasculitis.
brain atrophy.17 MRI and specifically T2*-WI may reveal superficial
cortical hemosiderosis and multiple peripheral CMBs in contrast to
central hypertensive CMBs.17
3. Secondary SAIH
Secondary SAIH is more common in young patients and results from
vascular malformations in up to 50% of patients under 40 years old.18
3.1. Vascular malformations
Vascular malformations that can cause SAIH include arterio-venous
malformation (AVM), dural arterio-venous fistulas (DAVF), arterial an­
eurysms (AA) and cavernous malformation.
3.1.1. Arteriovenous malformations
AVMs are congenital anomalies of anomalies of the blood vessels that
derived from maldevelopment of the capillary network, resulting in
SAIH typically presents as a lobar hematoma with irregular margins
due to high-pressure hemorrhage dilacerating the brain parenchyma. On
imaging, AVMs typically consists of a conglomeration of vessels with
signal flow voids on T2*-WI. Three distinct components can be seen,
including enlarged feeder arteries, a nidus of very tight vascular chan­
nels, and dilated draining vein. Angioarchitectural characteristics
including the location of the nidus and its size, the presence of associated
arterial aneurysms or venous varices, and the quality of venous drainage
must be carefully analyzed. The Spetzler-Martin angiographic grading
system (Table 2) is widely used in clinical practice to stratify the risk of
morbidity and mortality of surgery and includes three criteria: size of
nidus, eloquence of adjacent brain and venous drainage.20 An example
of ruptured AVM can be found in Fig. 3.
3.1.2. Dural arteriovenous fistulae (DAVF)
DAVF are arteriovenous shunt in which the arterial afference are
related to meningeal supply.21 As opposed to AVM, the presence of a
nidus is rare.21
DAVF-related SAIH are usually peripheral in location and may be
associated with subdural hematoma and/or SAH. CTA may demonstrate
enlarged afferent arteries, most commonly meningeal arteries from the
external carotid artery, which may lead to an enlargement of bony ca­
may be observed, and chronic vein or dural sinus thrombosis should be
sought. When MRI is performed, it is important to include a Time-Of-
Flight MR angiography (TOF-MRA) covering the entire brain to objec­
tify abnormal arterialization of cortical veins and dural sinuses. An
example can be found in Fig. 4.
Cognard et al. proposed a widely used classification (Table 3) that
stratifies the risk of hemorrhage.22
3.1.3. Cavernous malformation
Cerebral cavernous malformation are vascular malformations con­
sisting of clustered, abnormally dilated and leaky capillary caverns that
Table 2
Spetzler-Martin arteriovenous malformation grading system.20
Size of nidus
- Small (<3 cm) = 1
- Medium (3-6 cm) = 2
- Large (>6 cm) = 3
Eloquence of adjacent brain
- Non-eloquent = 0
- Eloquent = 1
Venous drainage
- Superficial veins only = 0
- Deep veins = 1

Fig. 2. Cerebral amyloid angiopathy.

In this 70-year-old patient, non-contrast CT scan (A, B) revealed a left frontal lobar hematoma with finger-like projections and a convex subarachnoid hemorrhage
(white arrowhead). Susceptibility-weighted images (C, D) demonstrated convex hemosiderin deposits (white arrowheads) and multiple peripheral cerebral micro­
bleeds (black arrows). T2 Fluid-attenuated inversion recovery images (E) indicated moderate age-related white matter changes.

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Fig. 3. Ruptured arteriovenous malformation.
In this patient with sudden neurological deterioration, non-contrast CT (A) revealed an acute spontaneous intracerebral hemorrhage (white star). CT angiography (B,
C and, D) revealed an arteriovenous malformation fed by left anterior cerebral artery (white chevron) with a compact nidus (arrowhead) and drained by left internal
cerebral artery (white arrow). Selective brain digital subtraction angiography (E) confirmed these findings.
circulate at low-flow. They may cause SAIH at any age.23,24
The most common clinical presentation is SAIH occurring in 35.6%
of patients.25 On CT, intraparenchymal hematomas related to cavernous
malformation typically present as well-limited and round or ovoid he­
matoma.26,27 Associated hemorrhages, including intraventricular hem­
orrhage or subdural hemorrhage, are extremely rare. As shown in Fig. 5,
cavernous malformations may have multiple locules of different signal
surrounded by a peripheral hemosiderosis cap. On T2*-WI, cavernous
malformations may have a “popcorn” or “blackberry” appearance. The
association of a developmental venous anomaly in the vicinity is highly
suggestive of the diagnosis. Peripheral enhancement of these lesions is
rare and an alternative diagnosis, such as neoplasia, should then be
considered. Finally, cavernous malformations are angiographically
occult on DSA.
3.1.4. Arterial aneurysms
Cerebral arterial aneurysms are focal dilatations of intracranial ar­
teries where the arterial wall is fragile and at risk of rupture. They are
considered giant if their greatest diameter is >25 mm. Although typical
saccular aneurysms mainly induce SAH, those affecting the middle ce­
rebral artery, internal carotid artery terminus, pericallosal and distal
posteroinferior cerebellar artery may cause SAIH.28 On CT, the location
of the hematoma predominates in the basal cisterns and posterior fossa
near the causative cerebral aneurysm. SAH is often associated and its
severity is assessed using the modified Fisher scale (Table 4), which
allows for risk stratification of vasospam.29 Although CTA has a sensi­
tivity of almost 100%, brain DSA should be performed subsequently in
patients with massive SAH, even if CTA did not reveal an aneurysm.30
An example of ruptured aneurysm can be found in Fig. 6.
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Clinical Imaging 95 (2023) 10–23
3.2. Other vasculopathies
Other vasculopathies including cerebral venous thrombosis (CVT),
infectious arterial aneurysms, non-atheromatous vasculopathies,
vasculitides, and vasoconstrictive syndromes may also manifest as SAIH.
3.2.1. Cerebral vein thrombosis
CVT refers to clots in the dural sinuses and cortical veins and usually
affects patients under 50 years old.31 CVT may occur in deep or super­
ficial venous system and subsequently results in focal neurological
manifestations.32
As shown in Fig. 7, the hematomas are usually subcortical close to
the occluded sinus.33 Associated convex SAH is classic finding in supe­
rior longitudinal sinus thrombosis. One in two patients may have a
venous stroke consisting of edematous and hemorrhagic lesions that do
not respect arterial territories.34 On unenhanced CT, acute clots usually
appear hyperdense. CTA and post-contrast T1-weighted images show an
unopacified vein or segment with the “empty delta sign”. Certain con­
ditions may simulate CVT, such as aplastic, hypoplastic or functional
transverse sinus stenosis. Aplasia or hypoplasia of the jugular foramen
can affirm aplastic or hypoplastic transverse sinus, whereas functional
stenosis may be associated with signs of idiopathic intracranial
hypertension.
3.2.2. Infectious intracranial aneurysms
Infectious intracranial aneurysms result from the degradation of
arterial wall by an infectious process.
They occur as a complication of infective endocarditis and the most
common causative agent is Staphylococcus Aureus.35 The rupture rate of
infectious intracranial aneurysms is high, and carries a mortality rate of
J. Rossi et al. Clinical Imaging 95 (2023) 10–23

Fig. 4. Ruptured dural arteriovenous

fistula.
In this 30-year-old patient with sudden
left visual deficit, T2*-weighted images
(A) showed an acute left occipital
subcortical intraparenchymal hema­
toma (black arrow). Time-Of-Flight MR
angiography (B and C) showed
enlargement of the left middle menin­
geal artery (white arrow) and arteriali­
zation of the left temporo-occipital
veins (white arrowhead). Postcontrast
3DT1-weighted images (D) revealed
engorgement of the temporo-occipital
cortical veins (black arrowhead). Selec­
tive digital subtraction arteriography of
the left external carotid artery revealed
a left occipital dural arteriovenous fis­
tula (white chevron) fed by the left
middle meningeal artery with cortical
venous reflux, and early opacification of
the left transverse sinus (black
chevron).

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J. Rossi et al. Clinical Imaging 95 (2023) 10–23

Table 3 Table 4
Cognard classification for dural arteriovenous fistulas.22 Fischer scale.29
Type I Grade 0
- Confined to sinus - No SAH
- Antegrade flow - No IVH
- No cortical venous drainage/reflux - Risk of symptomatic vasospasm: 0%
Type II Grade 1
IIa - Focal or diffuse, thin SAH
- Confined to sinus - No IVH
- Retrograde flow (reflux) into sinus - Risk of symptomatic vasospasm: 24%
- No cortical venous drainage/reflux Grade 2
IIb - Thin focal or diffuse SAH
- Drains into sinus with reflux into cortical veins - IVH present
- Antegrade flow - Risk of symptomatic vasospasm: 33%
IIa + b Grade 3
- Drains into sinus with reflux into cortical veins - Thick SAH
- Retrograde flow - No IVH
Type III Grade 4
- Drains directly into cortical veins (not into sinus) drainage - Thick SAH
- 40% hemorrhage - IVH present
Type IV - Risk of symptomatic vasospasm: 40%
- Drains directly into cortical veins (not into sinus) drainage with venous ectasia
- 65% hemorrhage Abbreviations: SAH: Subarachnoid Hemorrhage; IVH: Intra-Ventricular
Type V Hemorrhage.
- Spinal perimedullary venous drainage, associated with progressive myelopathy

infarcts. CTA and MR angiography may reveal steno-occlusive changes

35,36 in the basal portions of middle cerebral artery, anterior cerebral artery
13–32%. As shown in Fig. 8, hematomas are usually cortical-
and collateral vessels in the basal ganglia.40 On T2 FLAIR images, linear
subcortical and associated with SAH. CTA and TOF-MRA may demon­
or serpentine hyperintensities along the cortical sulci, termed “Ivy Sign”,
strate distal aneurysms of cortico-subcortical topography that may be
are seen in 50% of patients and result from reduced arterial flow in the
either fusiform, saccular or sacculofusiform.37 On T2*-WI, multiple pe­
pial circulation.40 As shown in Fig. 9, brain DSA remains the gold
ripheral hypointense punctiforms images may be observed. TOF-RMA
standard and may show “smog-like” vessels in the basal ganglia.40
and post-contrast T1-weighted images help characterize these findings
to objectify arterial flow, unlike CMBs. In patients with suspected IIA on
3.2.4. Posterior reversible encephalopathy syndrome (PRES) and reversible
MRI or CT, further DSA is required.37
cerebral vasoconstriction syndrome (RCVS)
PRES and RCVS are frequently associated neurotoxic conditions that
3.2.3. Non-atheromatous angiopathy
share common and numerous etiologies.
Moyamoya disease/syndromes (MMD) is characterized by progres­
As illustrated in Fig. 10, PRES imaging consists of vasogenic edema
sive occlusion of the supraclinoid intracranial carotid artery and its
that largely predominates in posterior brain areas, particularly in oc­
branches in the circle of Willis, uni- or bilaterally.38 The clinical features
cipital areas. In most patients, these abnormalities are reversible but
of MMD differ according to the age of the patients. Children present
permanent damage may occur.41 Involvement of the brainstem, basal
primarily ischemic events, including transient ischemic attack and ce­
ganglion, cerebellum or spinal cord is possible in atypical forms.42 PRES-
rebral infarcts.38 In adults, nearly one in two patients presents with
related hemorrhages occur in 15% of patients and include peripheral
intracranial hemorrhage and the rest ischemic events.38
SAIH, SAH, and CMBs, alone or in combination.43 On post-contrast T1-
At CT, hematomas may be localized in cortical watershed zones,
weighted images, superficial leptomeningeal enhancement may be
basal ganglia, deep white matter or periventricular regions.39 They may
found.41
be associated with SAH, intraventricular hemorrhages, and cerebral

Fig. 5. Hemorrhagic cavernoma.

In this 47-year-old patient with a left hemicorporeal deficit, T1-weighted MRI (A) showed a round, well-limited intraparenchymal hematoma with regular margins
(white arrow) surrounded by a cap of hemosiderosis (white chevrons) on susceptibility-weighted images (B). The lesion showed heterogeneous intralesional signal
suggesting hemorrhagic remodeling of different ages (black arrowhead). Postcontrast 3DT1-weighted images (C) did not show peripheral enhancement.

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J. Rossi et al.
Fig. 6. Ruptured intracranial arterial aneurysm.
In this patient presenting with a sudden coma, non-contrast CT scan (A, B) demonstrated an acute left frontal hematoma (black star) with intraventricular hem­
orrhage (white arrow) and a subarachnoid hemorrhage (white arrowhead) predominating in the basal cisterns. The CT angiography (C) indicated the presence of a
saccular aneurysm of the anterior communicating artery (white arrow), confirmed (black arrow) on brain digital subtraction arteriography.
Because 10% of patients with PRES also have RCVS, arterial assess­
ment with TOF-MRA images is required, preferably with 3 T MRI.41 As
shown in Fig. 11, SAIH is often associated with posterior location and
associated with sparse SAH of the convex sulci. No SAH is found within
the basal cisterns. TOF-MRA typically shows multifocal spasm of the
small arteries resulting in a string of pearls pattern.
Brain DSA is mandatory to confirm diffuse arterial irregularities that
are also encountered in cerebral nervous system (CNS) vasculitides.
3.2.5. CNS vasculitides
CNS vasculitides can be primary and secondary to systemic vascu­
litides. The clinical presentation of CNS vasculitis includes headache,
psychiatric symptoms and cerebral infarction in young patients.44 CT
and MRI may demonstrate the association of SAIH, SAH, CMB and ce­
rebral infarction especially in cortical watershed zones.45 As illustrated
in Fig. 12, RCVS, CTA and MRA may demonstrate diffuse arterial ir­
regularities. Post-contrast T1 Black Blood-weighted images can help by
directly visualizing the inflammation of arterial wall.46
3.3. Other etiologies
Other etiologies of SAIH include neoplasia, coagulation disorders,
toxic and hemorrhagic transformation of acute ischemic stroke.
3.3.1. Neoplasia
Intracranial hemorrhage is a common complication of cancer ac­
counting for nearly half of cerebrovascular events in these patients.47
As shown in Fig. 13, SAIH may be peripherally located at gray-white
matter junction and associated with SAH. Excessive surrounding edema
and peripheral enhancement is highly suggestive of an underlying solid
tumor.48 On MRI, the identification of multiple lesions revealed by
multifocal hemorrhages and enhancing foci may facilitate the diag­
nosis.49 A peripheral enhancement does not necessarily imply the
presence of an underlying tumor, as this may be encountered in subacute
hematomas due to a breakdown of blood-brain barrier. Late resolution
of the hematoma and persistence of edema on follow-up imaging are
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Clinical Imaging 95 (2023) 10–23
also arguments to suggest neoplasia.49 Finally, the use of dual-energy CT
has been proposed with promising results because it may allow better
delineation of the enhanced tumor portions.50
3.3.2. Coagulation disorders
Coagulation disorders are a rare cause of SAIH and usually occur in
conditions such as iatrogenic coagulopathies, hemophilia, acute leuke­
mia or severe liver failure.51
As shown in Fig. 14, SAIH are often lobar and may have fluid-blood
levels.52 Fluid-blood levels may be found in 50% of patients and are
highly specific. They are thought to reflect the inability to produce or
maintain a clot matrix.52 Associated hemorrhages may consist of sub­
dural hematomas.52
3.3.3. Drug abuse
Drug abuse, particularly cocaine and amphetamines, is a recognized
cause of SAIH especially among young adults.
The typical radiological presentation of drug-related SAIH is poorly
defined. Some authors have reported that SAIH may localize preferen­
tially in the basal ganglia, whereas others have found an association
with subcortical localization.53,54
3.3.4. Hemorrhagic transformation
Hemorrhagic transformation is a frequent complication of ischemic
stroke.55 European Cooperative Acute Stroke Study classification is
commonly used in clinical practice.56 Although hemorrhagic trans­
formation is rarely revelatory of ischemic stroke, the presence of an
infarcted area and the systematization of abnormalities to an arterial
territory contribute to the diagnosis. An illustration is shown in Fig. 15.
4. Conclusion
SAIH is a frequently encountered and potentially life-threatening
emergency in which imaging is essential.
J. Rossi et al. Clinical Imaging 95 (2023) 10–23

Fig. 7. Cerebral venous thrombosis.

In this patient, the non-contrast CT scan (A) showed a subcortical parietal hematoma and spontaneously hyperdense material within the cortical veins (white arrows).
Venous angioscan (B) demonstrated a filling defect of the superior longitudinal sinus and a cortical vein (white arrowheads). On MRI, T2 FLAIR images (C) confirmed
a venous infarction and post-contrast 3DT1-weighted images (D) revealed an extensive thrombosis of the superior longitudinal sinus (white chevrons).

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J. Rossi et al. Clinical Imaging 95 (2023) 10–23

Fig. 8. Ruptured infectious intracranial arterial aneurysm.

In this patient with infective endocarditis, MRI revealed a subcortical intracerebral hematoma (white arrow), contiguous subarachnoid hemorrhage (white
arrowhead) on susceptibility-weighted images (A) and, perilesional edema (black star) on T2 fluid-attenuated inversion recovery images (B). Time-Of-Flight MR
angiography (C) and post-contrast T1-weighted images demonstrated infectious arterial aneurysm (white chevrons). Digital subtraction arteriography of the brain
(D) confirmed an arterial aneurysm (black arrow) of the opercular segment of a right middle cerebral artery branch.

Fig. 9. Moya-moya disease.

In this 6-year-old child, MRI revealed a left deep intracerebral hematoma (black arrow) with intraventricular hemorrhage on T2*-weighted images (A) and bilateral
internal carotid artery stenosis on Time-Of-Flight MR angiography (B). Brain digital substruction arteriography (C: frontal view, D: profile view) confirmed a tight
stenosis of the intracranial left internal carotid artery and “smog-like” lenticulostriate vessels (black arrowhead) indicating Moya-Moya disease.

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J. Rossi et al. Clinical Imaging 95 (2023) 10–23

Fig. 10. Hemorrhagic posterior reversible encephalopathy syndrome.

In this 56-year-old woman, a heart transplant recipient on cyclosporine, MRI showed bilateral occipital intraparenchymal hematomas (black arrows) on T2*-
weighted images (A, B, and C). T2 fluid-attenuated inversion recovery (T2 FLAIR) images (D, E and F) revealed extensive vasogenic edema of the posterior cere­
bral regions (white arrows).

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Fig. 11. Reversible cerebral vasoconstriction syndrome.

In this patient with headache for one-week, non-contrast CT scan (A and B) revealed an acute right frontal intracerebral hematoma (black star) and a scattered
subarachnoid hemorrhage of the right frontal convexity (white chevrons). CT angiography (C) revealed short stenoses followed by dilatation (white arrows) of the
middle cerebral artery on CT angiography realizing a string of pearls pattern. Cerebral arteriography by digital subtraction confirmed the presence of multiple short
stenoses (white arrows) indicating a reversible cerebral vasoconstriction syndrome.

Fig. 12. Central nervous system vasculitis.

In this 75-year-old patient with abrupt dysarthria, MRI revealed an acute intracerebral hematoma and a right fronto-insular subarachnoid hemorrhage (black arrow)
on T2*-weighted images, vasogenic edema (white arrow) on T2 fluid-attenuated inversion recovery images and, caliber irregularities of the right middle cerebral
artery (white arrowhead) on Time-of-Flight MR angiography (C). Cerebral digital subtraction arteriography (D) confirmed these arterial irregularities (white
chevrons) suggesting cerebral vasculitis. The leptomeningeal biopsy and the rest of the explorations supported the diagnosis of primary cerebral vasculitis.

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J. Rossi et al. Clinical Imaging 95 (2023) 10–23

Fig. 13. Neoplasia.

In this 10-year-old child with rapid neurological deterioration, non-contrast CT scan (A) and T2*-weighted images (B) revealed an acute deep hematoma (white
arrows) and intraventricular hemorrhage (white arrowheads). Pre- (D) and post-contrast T1-weighted images (E) indicated peripheral enhancement (white chevron)
suggesting neoplasia that was confirmed after biopsy.

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J. Rossi et al. Clinical Imaging 95 (2023) 10–23

Fig. 14. Coagulation disorder.

In this patient with chronic hepatic failure, non-contrast CT (A) scan revealed right frontal hematoma (white arrow) with fluid-blood levels (white arrowhead). There
was not enhancement on post-contrast T1-weighted images (B).

Fig. 15. Hemorrhagic transformation.

In this patient with 24-hour left facial palsy, MRI revealed a right superficial sylvian ischemic lesion (white arrows) on diffusion-weighted images (A) and Apparent-
Diffusion-Coefficient map (B) with intracerebral hematoma (black arrow) on the T2*-weighted images; indicating hemorrhagic transformation.

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