Clinical Neurology and Neurosurgery 221 (2022) 107368

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Clinical Neurology and Neurosurgery

journal homepage: www.elsevier.com/locate/clineuro

Review article

Application of susceptibility weighted imaging (SWI) in diagnostic imaging

of brain pathologies – a practical approach
Aleksandra Rubin a, *, Łukasz Waszczuk a, Grzegorz Trybek b, Stylianos Kapetanakis c,
Joanna Bladowska a
a
Department of General and Interventional Radiology and Neuroradiology, Wroclaw Medical University, Wroclaw, Poland
b
Department of Oral Surgery, Pomeranian Medical University in Szczecin, Szczecin, Poland
c
Spine Department and Deformities, Interbalkan European Medical Center, Thessaloniki, Greece

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

Keywords: Susceptibility weighted imaging (SWI) has been broadly incorporated to MR protocols as it provides unique
Susceptibility weighted imaging additional diagnostic information in a wide variety of neurological conditions. SWI exploits local field in­
Acute stroke and penumbra homogeneities created by various paramagnetics (deoxyhaemoglobin, blood breakdown products), diamagnetics
Neurodegenerative diseases and multiple
(calcium) or oxygenated blood, hereby provides contrast based on magnetic susceptibility. In this review we
sclerosis
Traumatic brain injury and cerebral
present various examples from everyday clinical practice including, among others, acute stroke, neurodegen­
microbleeds and hemorrhages erative disorders, haemorrhagic lesions, vascular malformations, mycotic intracranial aneurysm, primary central
Brain tumors and metastasis nervous system vasculitis, neoplasms in which SWI was essential for diagnosis. The strongest indications for SWI
applications are the neurodegenerative and neuro-vascular diseases, therefore this review is aimed at a wide
range of clinicians, mainly neurologists, neurosurgeons and radiologists.

1. Introduction
Susceptibility weighted imaging (SWI) was first introduced to diag­
nostic imaging in 1997 and was primarily known as blood oxygenation
level dependent (BOLD) venographic imaging [1]. It is now known that
this three-dimensional, fully flow compensated and high spatial reso­
lution gradient echo imaging technique, provides much more informa­
tion than venography [2]. SWI uses magnitude and filtered-phase
information, both separately and in combination with each other, to
create new sources of endogenic contrast enhancement [1].
SWI offers information about any tissue that has a different magnetic
susceptibility from its surroundings, such as iron or calcium depositions,
deoxygenated blood, haemosiderin and ferritin. SWI can detect minute
haemorrhage, old microbleeds, thrombosed veins or sinuses [3] and
enables more accurate imaging of brain pathologies, such as stroke,
traumatic brain injury (TBI), cerebral microbleeds (CMBs), degenerative
disorders, demyelination, vascular malformations, primary central ner­
vous system vasculitis and brain tumours [2].
From its first application SWI is increasingly being included into a
wide range of MRI protocols, supporting the differential diagnosis
mainly of central nervous system (CNS) disorders [2]. The purpose of
this review is to show the clinical applications of SWI in the diagnostic
process.
MR vendors offer sequences sensitive to the change of magnetic
susceptibility: SWI (Siemens), SWAN (GE), SWI-phase (Philips), Blood
Sensitive Image (Hitachi) and Flow Sensitive Black Blood (Canon). The
findings which the authors showed in this article are applicable to SWAN
(GE Signa HDxt 1.5 T MR unit) or SWI-P (Philips Ingenia 3 T MR unit).
2. Acute stroke
Restoration of blood flow (via endovascular thrombectomy or/and
intravenous thrombolysis) is the only treatment for ischemic stroke [4].
It implies existence of penumbra - considerably amount of tissues at risk
of stroke progression to irreversibly damaged, which could be salvaged
if the rapid reperfusion is taken within a suitable time frame [4,5].
Perfusion-weighted imaging/diffusion-weighted imaging (PWI/
DWI) mismatch model has been proposed to identify acute stroke in
patients who benefit from reperfusion treatment [6]. However, there
were difficulties and trial failures regarding effectiveness of this

* Corresponding author.
E-mail addresses: aleksandra.rubin@student.umw.edu.pl (A. Rubin), lukasz.waszczuk@umw.edu.pl (Ł. Waszczuk), grzegorz.trybek@pum.edu.pl (G. Trybek),
spineklinik@gmail.com (S. Kapetanakis), joanna.bladowska@umw.edu.pl (J. Bladowska).

https://doi.org/10.1016/j.clineuro.2022.107368
Received 21 March 2022; Received in revised form 3 July 2022; Accepted 12 July 2022
Available online 14 July 2022
0303-8467/© 2022 The Authors. Published by Elsevier B.V. This is an open access article under the CC BY license (http://creativecommons.org/licenses/by/4.0/).
A. Rubin et al. Clinical Neurology and Neurosurgery 221 (2022) 107368

Fig. 1. Ischaemic stroke. Patient presented to the emergency room with symptoms of wake-up stroke. Emergency MR examination in stroke protocol without
contrast administration was performed. SWI (A) revealed signal void in left Sylvian fissure representing thrombus in the left middle cerebral artery (MCA) branch.
SWI (B, C) also revealed prominent cortical vessels representing venous stasis. DWI (D) showed only focal area of restricted diffusion in the insular cortex. Subsequent
CT has confirmed left MCA occlusion (not shown). Patient underwent immediate angiography (E) proving an occlusion of dominant branch of the left MCA. Curative
thrombectomy was performed with complete recanalization of left MCA (F). (SWI-P; Philips Ingenia 3 T MR unit).

approach. Beyond the risk of administration of gadolinium-based

contrast agent, there are difficulties in interpretation of PWI data and
concerns about insufficient standardization, and lack of evidence to
classify perfusion imaging in the setting of ischaemic stroke [5,67].
Moreover, the PWI prolongs the imaging and time required to provide
information on infarct core to the treating physician [5]. For these
reasons, alternatives to identify penumbra have been proposed, among
which are DWI, DWI-clinical mismatch, and DWI-SWI mismatch.

2.1. Asymmetric prominent vessel sign and penumbra

In acute stroke compensatory processes (vasodilation, decrease

blood flow, increased oxygen extraction) occur to minimize the effects of
acute ischaemia, resulting in a higher amount of deoxyhemoglobin and
hence, venous prominence [4]. SWI is highly sensitive to a paramagnetic
properties of deoxyhemoglobin and is the most suitable for imaging the
areas covered by the above processes [3]. SWI images show increased
hypointensity, number or caliber of the asymmetric medullary veins in
relation to the opposite side (not affected by the stroke) – which is
known as asymmetric prominent vessel sign (APVS)/ fish signs/brush
signs [8] (Fig. 1) and is highly corresponding to the penumbra of the
affected brain area. Recently reported studies have shown the potential
of SWI in the qualitative assessment of penumbra, proving that pen­
umbra assessment using SWI-DWI can provide an alternative to the
PWI-DWI approach and this can also reduce the overall scan-time [4,5]
[7].
Fig. 2. Wake up stroke. SWI (A) revealed prominent hypointensity of the left
middle cerebral artery (MCA) consistent with MCA occlusion. DWI (B) shows an
area of restricted diffusion corresponding to ischaemic oedema in the left basal
ganglia region. (SWAN; GE Signa HDxt 1.5 T MR unit).
2.2. Thrombus Identification
SWI may detect arterial occlusion as a signal void within large artery,
representing thrombus. (Figs. 1, 2). It has been reported that SWI is more
sensitive and specific than the hyperdense artery sign on CT and
hyperintense vessel sign on FLAIR. SWI may also be used to assess
reperfusion effect after treatment [9].
SWI has been accepted as a method available to evaluate deep
venous flow in acute or chronic ischemia (in case of cerebral artery

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A. Rubin et al.
Fig. 3. Multiple sclerosis and central vein sign (A,B). SWI (A) and T2- weighted image (B) showed fine, tubular signal void (A) corresponding to the hyperintense
focus (B) within the right basal ganglia region consistent with central vein sign in the MS plaque.
stenosis of different etiology) and to demonstrate increased oxygen
extraction fraction (OEF) in focal cerebral ischemia [10,1112].
3. Cerebral hyperperfusion
Cerebral hyperperfusion syndrome (CHS) is a potentially devastating
complication of carotid endarterectomy (CEA) [13] or carotid artery
stenting. CHS may lead to neurological deficits due to cerebral edema or
haemorrhage. While positron emission tomography (PET) and
single-photon emission computed tomography (SPECT) are the gold
standards for the evaluation of cerebral hyperperfusion, both methods
are costly and require the use of radionuclides [13].
Chronic ischemia with severely impaired cerebrovascular reactivity
(CVR) may cause vasoparalysis, making cerebral artery branches unable
to respond quickly enough to the rapid restoration of normal perfusion
pressure after CEA. It was reported that cerebral vascular reserve
gradually improve over time after CEA.
Yamaguchi et al. described a clinical case after right internal carotid
artery (ICA) CEA. Their analysis showed that changes in the resting
cerebral blood flow (rCBF) evaluated in SPECT correlate with the
changes in the signal intensity of cortical arteries, cortical veins, and
perilateral ventricular veins of the right middle cerebral artery (MCA)
territory on SWI [13] before and after CEA.
Starting from the first day after CEA the SWI showed a prominent
hyperintensity of cortical arteries in the right MCA territory. The
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Clinical Neurology and Neurosurgery 221 (2022) 107368
hyperintensity gradually decreased over time and finally became
indistinct. At the same time SWI showed an increased signal intensity of
cortical veins and perilateral ventricular veins during the peak of rCBF,
but later, the signal intensity decreased as rCBF decreased and finally it
returned to normal. These results suggest that changes in the SWI signal
intensity of mentioned vessels in an ipsilateral MCA territory after CEA
may provide valuable information regarding hyperperfusion, where
abnormally increased CBF and decreased oxygen extraction fraction
may not allow for sufficient elevation of deoxyhemoglobin levels [13]
causing adequate susceptibility effects. Susceptibility effect visible on
SWI in the follow-up MR after CEA might be useful in the assessment of
the recovery of cerebral circulation and the risk of CHS. Nevertheless,
further studies concerning the effectiveness of SWI in assessing cerebral
hyperperfusion are necessary.
4. Intracranial artery stenosis and moyamoya disease
Intracranial artery sclerosis is most often caused by atherosclerosis
[14], but it can also be associated with inflammatory diseases (arteritis,
systemic vasculitis, Takayasu’s disease or Horton’s disease), systemic
diseases, traumatic brain injuries, etc. as well as rare pathologies, such
as moyamoya disease (MDM) [15].
MMD is an infrequent disease of cerebral vasculature characterized
by long-standing and progressive occlusion of large intracranial arteries
[15] that leads to the compensatory formation of an abnormal network
A. Rubin et al.
of perforating blood vessels, named moyamoya vessels, that provide
collateral circulation [10].
The clinical presentation is variable - children mainly present with
ischemia-related neurologic episodes whereas MMD in adults can
manifest as either an ischemic event or an intracranial haemorrhage
(ICH) [15]. The gold standard investigation for diagnosis is cerebral
angiography which.
reveals a smoky appearance of arteries (moyamoya vessels) at the
base of the skull [15]. Patients with MMD are in a chronic state of ce­
rebral vasodilation, necessary to maintain cerebral blood flow (CBF). In
MMD patients the value of cerebrovascular reactivity (CVR) is crucial
because the combination of the lower CVR and lower CBF in SPECT is a
reliable index for accurately detecting the existence of increased OEF,
which is known as misery perfusion [10].
Horie et al. found that SWI stage strongly correlates with ischemic
MMD and also correlates with haemodynamics in SPECT, especially
CVR. Increased visibility of deep medullary veins (DMVs) known as
“brush sign” with SWI, although being a non-specific [15], could predict
the severity of MMD [10].
The MMD treatment is mostly surgical revascularization, which
prevent the recurrence of both ischemic and haemorrhagic strokes [15].
5. Multiple sclerosis
Multiple sclerosis (MS) is an autoimmune, neurodegenerative dis­
order, characterized by chronic inflammation, demyelination, axonal
and neuronal loss [16,17]. The diagnosis of MS may be challenging and
the cases that are not correctly diagnosed or the degree of overdiagnosis
remains at a high level [18]. While no single laboratory test is yet
available to prove or exclude MS, MR is a great help in reaching a
definitive diagnosis. MR is sensitive to demyelinating plaques which are
the hallmark of MS and occur as white matter lesions (WMLs). However,
its specificity may not be adequate enough, since WML commonly occur
in other (vascular, degenerative, inflammatory) CNS diseases. The
presence of iron deposits and the central vein sign visible on SWI within
the demyelinating plaques, gives valuable information in assessment of
MS disease activity.
5.1. Central vein sign
MS plaques are formed along the course of cerebral vessels and their
ovoid shape is determined by the location and orientation of veins [19].
SWI demonstrates the central vein sign (CVS) as fine linear hypointen­
sity within the lesion (Fig. 3). The CVS is more common in MS than in
other diseases and therefore it becomes a valuable marker, which can be
useful for confirming MS diagnosis [19,20].
5.2. Iron deposition
Iron deposition occurs in the brain tissue in the process of normal
ageing. However, excessive iron accumulation in the certain brain re­
gions may be indicative of ongoing disease [21,22]. Scientific research
have demonstrated correlations between ring-shaped iron depositions
and clinical progression [23,24], cognitive impairment and brain atro­
phy [25,26] in patients diagnosed with MS.
Haacke et al. showed that SWI is particularly sensitive to iron de­
posits within MS plaques, basal ganglia and pulvinar thalamus. SWI may
detect more iron-laden plaques than T2-weighted images and FLAIR
[26]. The signal hypointensity on SWI consistent with iron deposition
may be seen at the lesion edge in a ringlike fashion or in the centre
indicating nodular iron-laden lesions [27] (Fig. 3).
It is assumed that the morphology of iron-laden lesions changes
throughout the course of the disease. Classic, reactive, slowly expanding
chronical lesions have peripheral iron distribution at the beginning.
Over the time myelin and oligodendrocytes are gradually decreased
from the perilesional regions toward the lesion centre and become
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Clinical Neurology and Neurosurgery 221 (2022) 107368
visible as nodular iron-laden lesion, with a variable degree of iron de­
positions within a different compartments [27].
Multiple sclerosis and iron deposits within the plaque (C,D). SWI (C)
and T2- weighted image (D) show small, diffuse hypointenstity (C)
corresponding to the hyperintense focus (D) in the white matter of the
right frontal lobe, consistent with iron deposits in the MS plaque. (SWI-
P; Philips Ingenia 3 T MR unit).
5.3. Neuromyelitis optica vs multiple sclerosis
Neuromyelitis optica (NMO) and MS are distinct inflammatory CNS
disorders with different pathophysiology [27] and approaches to treat­
ment. The overlap in clinical manifestations and imaging findings hinder
an early differentiate between MS and NMO [27] and makes NMO being
commonly misdiagnosed as MS [28].
Chawla et al. estimated that 66% of MS lesions were traversed by
intralesional central venules visible in SWI, while only 6% NMO lesions
showed this feature. In patients with MS, iron deposits were visible in
SWI in at least one lesion at a different state of the disease, while none of
the NMO-lesions were associated with abnormal iron deposition and all
of the NMO-lesions remained non-iron laden at follow-up MRI exami­
nation. Chawla et al. estimated that the central vein sign is 100% specific
for MS patients, and the presence of at least one iron-laden lesion allows
to differentiate MS from NMO with a sensitivity of 100% [27].
6. Traumatic brain injury
Traumatic brain injury (TBI) is a common emergency with high
incidence, hospitalisation rate and related deaths [29]. While CT is the
preferred first choice imaging modality in the setting of acute TBI,
providing fast and accurate assessment of injury in most cases, the MRI
with SWI is valuable when CT findings are normal and there are
persistent unexplained neurologic symptoms [29]. The SWI is more
sensitive for the detection of haemorrhage including micro­
haemorrhages, subarachnoid haemorrhage (SAH) (Fig. 6) and haemor­
rhagic diffuse axonal injury (DAI) (Fig. 5). The detection of small
amount of blood or blood products on SWI may explain the mechanism
of injury and may be crucial for the diagnosis [30]. The MRI with SWI
may be also helpful at subacute and chronic phase of injury.
6.1. Intracranial haemorrhage
MRI with SWI may be essential for evaluation of ICH during all stages
of evolution of haematoma. The appearance of haemorrhage depends on
the signal of blood elements and their degradation products. According
to the magnetic properties, oxyhaemoglobin is diamagnetic, deoxy­
haemoglobin and methaemoglobin are paramagnetic, and haemosiderin
is superparamagnetic [31].
The early extravasated blood consists of plasma and cellular ele­
ments and presents no paramagnetic effect. The early hyperacute hae­
matoma may appear similar to other brain lesions with iso- or
hypointense signal on T1 weighted images and hyperintense signal on
T2 weighted images. The hypointense rim at the periphery of the hae­
matoma appears within the first hours due to the conversion oxy­
haemoglobin to deoyxyhaemoglobin in the surrounding brain
parenchyma. Paramagnetic effect of deoxyhaemoglobin is better pro­
nounced on SWI compared to T2 weighted imaging [32]. As the hae­
moglobin deoxygenation progresses, the MRI image of the hyperacute
haematoma clarifies with three distinguishable areas. The centre (con­
sisted of oxyhaemoglobin) - isointense to heterogeneous hyperintense
on SWI and T2 weighted images. The periphery (consisted of deoxy­
haemoglobin) - hypointense on SWI and T2 weighted images, especially
more pronounced on SWI because of blooming effect. The vasogenic
oedema surrounding haematoma - hyperintense on T2 weighted images
[33].
After one to three days, the acute haematoma essentially consists of
A. Rubin et al. Clinical Neurology and Neurosurgery 221 (2022) 107368

Fig. 4. Multiple cerebral microbleeds (CMBs) and subacute haemorrhage. SWI (A) showed multiple small, round foci of signal void consistent with multiple CMBs.
Subacute haematoma in the left temporal lobe exhibits hyperintense signal on SWI (A) corresponding to hyperintensity on the T2- and T1- weighted images. The
peripheral hypointense rim is visible due to the presence of haemosiderine at the periphery of the haematoma. This effect is more pronounced on SWI (A) than on T2-
weighted image (B). (SWI-P; Philips Ingenia 3 T MR unit).

Table 1
MRI characteristics and SWI usefulness in intracerebral haematoma assessment depending on its duration.
Haematoma T1 T2 DWI and ADC value SWI
duration

hyperacute heterogenous lesion, clot center iso- or heterogenous lesion, clot center iso- or hyperintense on DWI, heterogenous lesion, center iso-
< 12 h slightly hypointense slightly hyperintense, hypointense rim reduced ADC values or hyperintense, hypointense rim
acute clot mostly iso- or slightly hypointense hypointense, may be sedimentation hypointense on DWI, hypointense
24 – 48 h reduced ADC value
early subacute signal intensity of the lesion increases from hypointense, may be sedimentation, hypointense on DWI, hypointense
2. – 7. day the outside to the lesion core; perifocal perifocal oedema reduced ADC value
oedema
late subacute 7. - high signal intensity of some part of the signal slowly increases, hypointense rim hyperintense on DWI, hyperintense/
14/28. day lesion periphery or of the complete lesion surrounding the lesion reduced ADC values heterogenous
Chronic iso- or slightly hypointense lesion center/ hyperintense lesion center/cavity, center - hypointense on markedly hypointense rim,
> 14 – 28 day cavity, hypointense rim surrounding the hypointense rim surrounding the lesion DWI, increased ADC values blooming artifact
lesion cavity cavity

DWI - diffusion-weighted imaging, ADC - apparent diffusion coefficient, SWI - susceptibility weighted imaging.

deoxyhaemoglobin that results in markedly hypointense signal both on
T2 weighted images and SWI. In the low field scanners the acute hae­
matoma may be isointense to brain parenchyma and SWI would improve
the detection of haematoma in that condition [33].
In the early subacute stage approximately after 2–7 days, oxy­
haemoglobin is oxidized to methaemoglobin at the periphery of the
haematoma. The peripheral hyperintense rim appears on T1 weighted
images and hyperintense signal progresses in the following days from
outside to inside. Both on T2 weighted images and SWI the haematoma
continues to be markedly hypointense.
In the late subacute stage, approximately after 7 days, the signal
changes due to impaired cellular integrity and the presence of

Fig. 5. Extensive axonal injury (DAI) in a 28-year-old patient after a car accident. Very numerous, different in size, scattered, low-signal foci on SWI are visible
within the cerebral hemispheres, bilaterally in the basal ganglia, midbrain (A) (B), and pons and in the fissures of both cerebellar hemispheres (C). The lesions are
located along the vessels within white matter and on the border of white and grey matter. Changes are not visible on other MR sequences. (SWI-P; Philips Ingenia 3 T
MR unit).

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A. Rubin et al. Clinical Neurology and Neurosurgery 221 (2022) 107368

Fig. 6. Subarachnoid haemorrhage (SAH). CT (A) shows hyperdense sulci in left fronto-parietal region corresponding to fine sulcal hypointensities on SWI (B). (SWI-
P; Philips Ingenia 3 T MR unit).

methaemoglobin in extracellular compartment. Haematoma continues
to be hyperintense on T1- and becomes hyperintense on T2 weighted
images. Similarly on SWI haematoma presents with hyperintense signal
(Fig. 4), due to the lack of significant susceptibility effects of extracel­
lular methaemoglobin [31,34].
During the chronic phase, the haemosiderin rim appears hypointense
on T1 and T2 weighted images and this effect is more pronounced on
SWI [32].
Table 1 summarizes signal intensity alterations in MR images within
various stages of intracranial haemorrhage (Table 1).
6.2. Diffuse axonal injury
Diffuse brain injury (DAI) is caused by shearing or strain of axons
typically caused by translational and rotational forces in rapid acceler­
ation and deceleration of the head [30]. Usually DAI manifests with brief
cerebral concussions or more prolonged posttraumatic coma. There are
three histopathological and clinically valid grades of DAI: [1] evidence
of axonal injury in the grey-white matter junction, corpus callosum,
brain stem and cerebellum; [2] addition focal lesion in the corpus cal­
losum; [3] addition focal lesion/lesions in the brainstem. [35,36].
The diagnosis is best made on MRI where it is characterized by
several small regions of susceptibility artifacts seen on SWI (Fig. 5),
which is more sensitive in the detection of haemorrhagic shearing le­
sions as compared to other imaging methods [37]. SWI also provides
detailed information about distribution of injury and adds information
in the prediction of clinical outcome. The presence of microbleeds on
SWI is associated with worse cognitive outcome [38].
6.3. Subarachnoid haemorrhage
The SWI is sensitive to small amount of extravasated blood in sub­
arachnoid space (Fig. 6) and in ventricular system which in some cases
may be not distinguishable on CT [39]. However, subdural haematoma
may be difficult to differentiate from adjacent skull based solely on SWI,
unless it is large enough or has heterogeneous signal.
In the acute phase of subarachnoid haemorrhage (SAH), the lack of
low signal on SWI within the subarachnoid space (due to the relative
lack of breakdown of the red blood cells) does not exclude SAH. How­
ever, SWI can be particularly useful to look for SAH along the inter­
hemispheric fissures, where the haemorrhage can be mistaken for a
normal hyperattenuating dura on CT [30].

Fig. 7. Differentiation diamagnetics and paramagnetics on SWI and phase images. Both diamagnetics and paramagnetics are hypointense on SWI (B). Differentiation
is possible with a phase image (A): calcifications in pineal gland and other diamagnetics are hyperintense (arrow) while veins consisted of deoxygenated blood and
other paramagnetics are hypointense. (SWI-P; Philips Ingenia 3 T MR unit).

6
A. Rubin et al.
Fig. 8. Multiple system atrophy type P (MSA-P) with predominance of parkinsonian signs and symptoms. SWI (A) shows hypointense rim within the putamen. T2-
weighted image (B) shows the corresponding subtle linear rim of high signal (arrows) and the atrophy of the putamen. (SWI-P; Philips Ingenia 3 T MR unit).
7. Calcium vs haemorrhage differentiation
SWI is a sensitive and reliable method for detection and differenti­
ation of chronic microbleeds and calcifications. Haemoglobin and its
degradation products as well as calcifications are well seen on SWI as
hypointensities because of signal attenuation caused by T2 * shortening.
Differentiation between microhaemorrhages and calcifications is
possible on the basis of their opposite magnetic properties using phase
images (Fig. 7). Paramagnetic materials slightly amplify the external
magnetic field resulting in a negative phase shift in the right hand co­
ordinate system (RHS). Conversely, calcium being a diamagnetic, tends
to weaken the external magnetic field resulting in a positive phase shift
in RHS [40,41].
Differentiation between microhaemorrhages and calcifications is
possible using phase-based images, where haemorrhages and other
paramagnetics appear hypointense opposite to calcifications and other
diamagnetics appearing hyperintense in RHS [39]. Conversely, in
left-hand coordinate systems (LHS) the paramagnetics will appear
hyperintense while diamagnetics hypointense. The actual sign of the
phase for a given MRI system depends on several factors including its
geometry and orientation of the object with respect to the main static
field, gradient polarity and other technical details of the hardware. As a
reference may serve areas of known calcifications like pineal gland and
choroid plexus and areas of known paramagnetics like cortical veins.
Previous study has confirmed that detection of calcifications with SWI
may be similar to CT [42].
8. Cerebral microbleeds
Cerebral microbleeds (CMBs) have become a common finding in MRI
after incorporation of SWI into the routine imaging protocols, where
CMBs appear as small, round or ovoid signal voids with blooming
artifact.
Presents of CMBs is related to cerebrovascular disease, dementia, and
normal ageing [43] and is associated with microscopic evidence of small
deposits of perivascular haemosiderin following old subclinical leaks of
blood [44,45] (Fig. 4 A). In the Roterdam population-based studies the
overall incidence of CMB was 15%, with gradual increase depending on
age [46]. CMBs are also seen in a chronic hypertensive encephalopathy,
cerebral amyloid angiopathy, septic or fat emboli, vasculitis, and
CADASIL (cerebral autosomal dominant arteriopathy with subcortical
infarcts and leukoencephalopathy) [47].
When CMBs are associated with hypertensive vasculopathy or
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Clinical Neurology and Neurosurgery 221 (2022) 107368
cerebral amyloid angiopathy (CAA) those two entities can be distin­
guished at imaging based on their characteristic distribution. In the
hypertensive vasculopathy the CMBs typically occur in the basal
ganglia, thalamus, brainstem and cerebellum while the CAA-related
microbleeds are most frequently seen in the occipital and temporal
cortex, followed by the parietal and frontal location. CAA typically in­
volves small vessels of the cerebral cortex and leptomeninges prefer­
entially in the posterior cortical regions. In the advanced stage of CAA,
the CMBs may be present in the cerebellum, whereas basal ganglia,
thalamus, and brainstem are typically spared [46].
It should be noted that an overlap exists in the distribution of CMBs
in hypertensive microangiopathy and CAA. Commonly the hypertension
related CMBs located in basal ganglia are associated with subcortical
lesions. Similarly, in some cases of CAA the CMBs are present in lobar
locations and may also occur in deep white matter nuclei [45]. Never­
theless, it has been recently described that CMBs located deep in the
cerebellum such as near the dentate nuclei are more likely due to hy­
pertension while superficially located CMBs, restricted to cerebellar
cortex and vermis are more likely due to CAA [48].
Additionally convexity subarachnoid haemorrhage (cSAH) and
cortical superficial siderosis (cSS) have been recently identified as a
characteristic neuroimaging findings of CAA [49,50]. cSAH demon­
strates a distinct pattern of subarachnoid bleeding localized to one or
more adjacent cortical sulci at the convexity of the brain. The basal
cisterns, Sylvian fissures, and ventricles are typically spared. cSAH is
visible on SWI images as linear hypointensities in the subarachnoid
space [51]. Cortical superficial siderosis (cSS) is characterized by the
chronic deposition of haemosiderin after cSA in the superficial layers of
the cortex. The cSS is best seen on SWI images as a linear hypointensities
[51].
Both CMBs and cSS were incorporated to Modified Boston Criteria
for diagnosis of CAA. The diagnosis of CAA is possible with specific
findings on SWI without the biopsy. CAA is probable when SWI shows
multiple CMBs in lobar distribution or a single lobar CMB is associated
with cSS in one or more cortical sulci [52,5351].
9. Neurodegenerative disorders
9.1. Multiple system atrophy type P
Multiple system atrophy type P (MSA-P) with predominance of
parkinsonian signs and symptoms is one of an atypical parkinsonian
disorders (APD) and is characterized by autonomic dysfunction and
A. Rubin et al. Clinical Neurology and Neurosurgery 221 (2022) 107368

Fig. 9. Cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy (CADASIL). T2-weighted images (A,B) shows diffuse hyper­
intensities involving subcortical white matter. SWI (C) shows multiple, small, round shaped hypointense foci representing past microhaemorrhages. (SWAN; GE Signa
HDxt 1.5 T MR unit).

variable combinations of parkinsonism - parkinsonian variant MSA-P,
and cerebellar ataxia - cerebellar variant MSA-C [54]. These two can
be distinguished clinically by their predominant motor symptoms. SWI
may reveal hypointensity of the putamen as a sign indicative of MSA-P
[55] (Fig. 8).
9.2. CADASIL
Cerebral autosomal dominant arteriopathy with subcortical infarcts
and leukoencephalopathy (CADASIL) is an inherited nonatherosclerotic,
nonamyloid small vessel disease [56], leading to dementia and disability
in mid-life [57].
Clinical and neuroimaging features resemble those of sporadic small-
artery disease [56]. MRI hallmark of CADASIL are diffuse white matter
signal intensity abnormalities typically located in the temporal lobe and
circumscribed subcortical lesions suggestive of lacunar infarcts [58] as
well as hypointense foci in SWI corresponding to past microbleeds
(Fig. 9).
The CMBs visible on SWI may be an auxiliary tool in the differential
diagnosis. Common locations of CMBs in CADASIL are thalamus, basal
ganglia, subcortical white matter, brainstem, cerebellum, and the grey-
white matter junction [59].
10. Cerebral vascular malformation
10.1. Developmental venous anomalies
Developmental venous anomalies (DVAs) are congenital variants of
venous drainage. They are composed of dilated medullary veins which
drain the normal brain parenchyma and converging to an enlarged
collector vein. Their imaging appearance may resemble caput medusa or
inverse umbrella seen only in the venous phase. DVAs in contrast to
arterio-venous malformations (AVMs), do not express early venous
drainage and do not require treatment. DVA may occur in association
with cerebral cavernous malformation (CCM). SWI allows to depict DVA
without the need of contrast medium administration (Fig. 14).
10.2. Capillary teleangiectasia
Cerebral capillary teleangiectasias (CCTs) are slow-flow vascular
malformations that may occur sporadically or may be associated with
hereditary syndromes. Teleangiectasias may be also acquired as a result
of endothelial injury and were described after therapeutic brain irradi­
ation of intracranial tumours [60]. Typically sporadic teleangiectasias
are asymptomatic. CCTs are most often located in pons and basal ganglia
[61].
CCTs may present as a small focal lesions with T2 hyperintensity and
contrast enhancement on T1 weighted images and pose diagnostic

Fig. 10. Cerebral capillary teleangiectasia (CCT). T2-weighted image (C) shows small hyperintense focus in the pons. Post-contrast T1-weighted image (B) shows
lesion enhancement. SWI (A) demonstrates low signal intensity representing paramagnetic. All features are fairly typical for CCT. (SWAN; GE Signa HDxt 1.5 T
MR unit).

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A. Rubin et al. Clinical Neurology and Neurosurgery 221 (2022) 107368

Fig. 11. Multiple cavernous haemangiomas in the brain. SWI (B,C) shows uncountable, different size cavernous haemangiomas in the cortex and white matter of
both hemispheres, basal ganglia, thalamus, in the corpus callosum and in the cerebellum (not shown). The vast majority of haemangiomas visible on SWI (especially
smaller ones) are not visible on T2-weighted (A) images. (SWI-P; Philips Ingenia 3 T MR unit).

challenge. SWI is essential for a diagnosis and may reveal signal hypo­ multiple haemangiomas, including very small ones, without the need of
intensity representing slow venous flow [62] which may be not visible contrast agent administration.
on other sequences (Fig. 10).

10.4. Arteriovenous malformation

10.3. Cerebral cavernous malformations
Cerebral cavernous malformations (CCMs) or cerebral cavernous
hemangiomas are low flow vascular malformations in the brain and
spinal cord [63]. Most CCMs are asymptomatic and are found inciden­
tally. However, they may become symptomatic and in severe cases
present with seizures or cerebral haemorrhages.
CCMs exhibit varied signal intensity depending on the presence of
haemorrhage and the age of blood products often described as popcorn
or mulberry like. The periphery of the lesion usually demonstrate
hypointense rim representing deposition of haemosiderin. CCM can vary
in size up to several centimetres in diameter. Small CCM may be missed
at conventional spin echo sequences while hey may be well seen on SWI
(Fig. 11) [64].
Multiple CCMs occur in up to a third of sporadic cases and also,
although these are less common, in patients with a rare, genetic Familial
Multiple Cavernous Malformation Syndrome (FCCMS). In FCCMS the
number of cavernomas is higher (typically five or more) and further
changes may appear over time. Follow-up MRI with SWI is particularly
important [65] in managing the treatment of the familial form of the
disease, preventing cerebral hemorrhage and complications.
SWI with blooming artifacts has the greatest sensitivity in detecting
Arteriovenous malformations (AVMs) are relatively uncommon,
high flow brain vascular malformations (BVMs) with high propensity to
bleed. AVMs are one of the least cause of brain haemorrhage, however –
the most common cause of parenchymal brain haemorrhage in young
adults [66] and in these cases accurate differentiation between
high-flow and low-flow BVM is crucial. AVMs can be treated with sur­
gery, endovascular embolization, radiosurgery, or a combination of
these methods [67].
SWI enables simultaneous and distinct evaluation of the arterial and
venous systems of the brain, without the need of contrast administration
[67]. SWI offers unique advantages in the detection of arterio-venous
shunting (AVS), given the intrinsic contrast between rapidly flowing,
oxygenated and hyperintense arterial blood and slowly flowing, deox­
ygenated, hypointense venous blood. This phenomenon is observed
regardless of vessel caliber. Additionally, it has been investigated that in
case of high-flow BVM hyperintensity seen on SWI within the venous
structures draining BVM is an accurate indicator of AVS [67] and venous
hypertension, and is directly associated with an increased risk of ICH in
the surrounding area [67,68].
In contrast, hypointensity on pretreatment SWI might indicate a
relatively low-velocity flow shunt with normal venous flow (NVF) and

Fig. 12. Mycotic aneurysm in a 49-year-old patient with infective endocarditis. The T2 weighted images (A) show a 5 mm lesion surrounded by a small hyperintense
zone of oedema located in the antero-lower region of the right frontal lobe. On SWI (B) the lesion is adjacent to the low-signal dilated vessel, showing a low-signal and
blooming artifact. Another SWI low-signal linear lesion (C) in the right cerebellar hemisphere, not visible on other MR sequences - a possible new mycotic aneurysm
being formed. (SWAN; GE Signa HDxt 1.5 T MR unit).

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A. Rubin et al.
the area surrounding those vessels might have a low risk of ICH because
venous hypertension might not be so severe [68]. It should be remem­
bered that these assessment of NVF using SWI is not applicable to
high-flow BVM after treatment [68].
Previous haemorrhage is also an important predictor of subsequent
haemorrhage [34]. Signs of previous bleeding detected on SWI and seen
as a focal signal void, may influence further clinical management.
Although conventional MRI or MRA can reliably differentiate be­
tween a typical DVA with a pathognomonic medusa-head appearance
and a typical AVM or dural arterio-venous fistulas, it is often difficult to
differentiate between an atypical DVA and a high-flow BVM, especially
in the presence of ICH. Likewise, in some cases it may be difficult to
differentiate small venous structures from small haemorrhages and
thrombosis only with SWI image because of similar signal characteristics
[69]. In these cases invasive evaluation with DSA is often required [67].
11. Infectious intracranial aneurysm (mycotic aneurysm)
Patients with infective endocarditis (IE) may present with a variety
of cerebrovascular complications [70], one of which is infectious
intracranial aneurysm (IIA), called as mycotic aneurysms [71]. Unrup­
tured IIAs present with non-specific clinical features, sometimes leading
to ischemic stroke. In severe cases, the mycotic aneurysm can rupture,
causing ICH or SAH [70].
IIAs arise from either septic micro-emboli to the vasa vasorum or
occur secondary to bacterial escape from a septic embolus that has
occluded a vessel [72]. Bacterial infection stimulates the release of
pro-inflammatory cytokines, which attracts neutrophils. At the same
time the activation of matric metalloproteinases leads to focal break­
down to the vessel wall, resulting in the formation of an pseudoaneur­
ysm [73] through hydrostatic pulsations [72]. All these inflammatory
processes and the local widening of the arterial lumen cause the sus­
ceptibility effect seen on SWI as a non-specific local signal loss.
Digital subtraction angiography (DSA) remains the gold standard
though invasive method for detecting IIAs [70]. S. Cho and Migdady
et al. have retrospectively compared DSA and MRI results in patients
with confirmed IIA. They have showed that MRI characteristics, such as
sulcal SWI lesion (defined as linear or curvilinear hypointense signal
within subarachnoid space or superficial layers of cerebral cortex) with
or without contrast enhancement, are associated with the presence of
IIA [70] (Fig. 12). SWI lesions with contrast enhancement and sulcal
SWI lesions have a high sensitivity and negative predictive value in
detection of IIAs [74]. Furthermore, SWI lesions may be the only
changes visible on MRI, suggesting a formation of the new inflammatory
aneurysm (Fig. 12 C).
In IE patients who present neurological symptoms, MRI with SWI is a
sensitive and non-invasive tool to identify potential underlying IIA. This
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Clinical Neurology and Neurosurgery 221 (2022) 107368
Fig. 13. Primary CNS vasculitis in a patient suspected of
having a brain tumor, admitted for biopsy. At admission
the follow-up MR showed a high-signal area on T2
weighted images (A), covering the basal ganglia, subcor­
tical white matter and the cortex of the island on the right
side. SWI (B) showed numerous, punctate/linear low-signal
foci in the basal ganglia (more on the right sight), corre­
sponding to a small blood vessels, not visible on other MR
sequences – typical SWI findings suggestive of vasculitis.
(SWI-P; Philips Ingenia 3 T MR unit).
is especially important in cases that may require intervention to prevent
life-threatening complications [70].
Thrombosed aneurysm has a unique characteristic on SWI. The pe­
riphery of thrombosed aneurysm is SWI-hypointense, likely due to the
superparamagnetic effects of accumulating hemosiderin and ferritin,
when the centre is SWI-hyperintense, due to the long T2-relaxation of
dissolving haemoglobin [76].
Giant cerebral aneurysms, defined as > 25 mm, are histopathologi­
cally distinct aneurysms, associated with loss of type I collagen and
fibronectin. Scarring of the aneurysm wall results from the formation of
thrombi within the wall, laminar necrosis [75] and recurrent haemor­
rhages in the aneurysmal wall (possible cause of a giant aneurysm’s
slower growth rates compared with smaller aneurysms [76]), resulting
with the same characteristics on SWI as other thrombosed aneurysms.
12. Primary central nervous system vasculitis
Primary central nervous system vasculitis (PCNSV) is a an uncom­
mon, poorly understood, neuroinflammatory disease of the CNS,
affecting the intracranial and spinal cord vasculature [77,78]. Although
PCNSV manifests as a multifocal beaded narrowing of the intracranial
vessels, some patients may not have angiographic abnormalities [78]. In
this setting histopathologic examination remains the gold standard for
definitive diagnosis [78]. However, open brain biopsy is an invasive
method with low sensitivity [79]. Typical PCNSV changes had a hypo­
intense signal on T1 weighted imaging and intermediate to hyperintense
signal on T2 weighted imaging. Marked perilesional high signal of
vasogenic oedema may be seen on T2 weighted images (Fig. 13 A). Most
of the PCNSV cases demonstrate intralesional microhaemorrhages seen
as small linear or punctate patterns on either GRE-T2 * or SWI [78]
(Fig. 13 B,C) and these are typical MR findings highly suggestive of CNS
vasculitis. Localized leptomeningeal and subependymal enhancement
adjacent to the lesions may also be seen.
A rare subset of PCNSV patients present with masslike brain lesions
that can closely mimic brain neoplasm (Fig. 13 A). Differentiating im­
aging features include a cortical/subcortical enhancing masslike lesion
with intralesional punctate/linear microhaemorrhages seen on SWI,
lack of diffusion restriction, and low relative cerebral blood volume
(rCBV) [78].
13. Brain tumours
SWI may identify foci of haemorrhage or calcification as well as may
reveal pathological microvascularity inside the tumour. Differentiation
between blood breakdown products and calcium deposits is possible
based on phase images. SWI may be useful in differentiation cer­
ebellopontine angle Schwannomas from meningiomas. The
A. Rubin et al. Clinical Neurology and Neurosurgery 221 (2022) 107368

Fig. 14. Cerebellopontine angle (CPA) Schwannoma and incidentally found developmental venous anomaly (DVA). Phase image (A) and SWI (B) reveal suscepti­
bility changes within CPA tumour. Dot shaped hypointense signals on phase image (A) and SWI (B) similar to the signal of veins containing deoxygenated blood.
Those foci are identified as microhaemorrhages, features characteristic of CPA Schwannoma. (SWI-P; Philips Ingenia 3 T MR unit).

Fig. 15. Glioblastoma multiforme (GBM) with intra-tumoral susceptibility signals (ITSS). T2-weighted image (B) shows heterogeneous mass in the right frontal lobe,
surrounded by oedema and resulting in extensive mass effect. Post-contrast T1-weighted image (C) shows peripheral and partially central enhancement. SWI (A)
shows multiple, fine linear and dot-shaped hypointensities termed ITSS representing CMBs and pathological vessels. (SWI-P; Philips Ingenia 3T MR unit)..

microhaemorrhages may occur in Schwannomas and are not typical for
meningiomas (Fig. 14). Calcifications are present in about 70–90% of
oligodendrogliomas and may be easily detected with SWI.
SWI differentiates glioblastoma from primary CNS lymphoma
(PCNSL) with high sensitivity and specificity. The basis for the assess­
ment are so termed intratumoural susceptibility signals (ITSS). The ITSS
are defined as fine linear or dot-shaped structures presenting low signal
intensity on SWI. The ITSS may result from tiny blood deposits or
microcalcifiacations. It has been also proposed that ITSS may represent
tumour pathological vessels. The presence of ITSS on SWI indicates neo-
angiogenesis and increased CBV and are typical for glioblastoma
(Fig. 15). Conversely, ITSS are an uncommon feature prior to treatment
in B-cell PCNSL [80].
13.1. Lipoma
Intracranial lipoma is an uncommon neoplasm which can be easily
identified by virtue of its characteristic signals on MRI [81]. Lipomas
show typical appearance on CT and MRI, including susceptibility
blooming artifact on SWI [81]. All the intracranial lipomas show pe­
ripheral, complete or mixed pattern of blooming. Lipomas typically
demonstrate very thin peripheral hypointense rim on SWI, commonly
known as India ink artifact [81,82]. Microscopic mineralization within
the lesion and chemical shift artefact appear to be the major cause of
susceptibility blooming [81] (Fig. 16). Lipoma and haematoma show
similar MRI characteristic - both appear hyperintense on T1 and show
blooming on SWI but yet their differentiation is possible with FLAIR,
where lipoma appear hypointense, whereas haematoma maintains its
hyperintense signal [81].
13.2. Intracranial dermoid
Intracranial dermoid is a benign, slow-growing, congenital, ectopic
tumour. It is characterised as a thick-walled mass, lined by keratinized
squamous epithelium with ectodermal elements like hair, sebaceous,
sweat glands, teeth, nails and contain fat in varying proportions [83,84].
It mostly occurs in the midline suprasellar region, followed by the pos­
terior cranial cavity, fourth ventricle, and cisterna magna [85,8687].
Uncomplicated dermoid cysts typically remains asymptomatic [85].
Rupture of intracranial dermoid may cause serious complications such
as chemical meningitis, vasospasm, infarction, and death [88].
The classical imaging appearance of ruptured intracranial dermoid is
a fat-containing lesion with tiny fat droplets in the subarachnoid space
or ventricular system. The lesion and the fat droplets show blooming
artifact on SWI, similar to lipoma (Fig. 17).

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A. Rubin et al. Clinical Neurology and Neurosurgery 221 (2022) 107368

Fig. 16. Choroid plexus lipoma. SWI (A) reveals peripheral complete signal void due to local field inhomogeneity. T1- and T2- weighted images (B, C) show
hyperintense signal. Post-contrast T1 weighted image shows no enhancement. (SWAN; GE Signa HDxt 1.5 T MR unit).

Fig. 17. Ruptured dermoid cyst (A,B,C). SWI (A) shows multiple round hypointense foci in the suprasellar cistern and Sylvian fissure. SWI (B) shows heterogenous,
hyper- and hypointense mass in the left cerebellopontine angle expanding to the middle cranial fossa. T1 weighted (C) shows multiple, small, round, hyperintense
foci. Those features are consistent with a ruptured dermoid cyst. (SWI-P; Philips Ingenia 3 T MR unit).

13.3. Brain abscess localized cerebritis and evolving into a suppurative collection, circum­
scribed by a well-vascularized fibrotic capsule [89,90]. MR differenti­
Brain abscesses (BAs) are focal infections of the CNS that start as a ating BAs from other intracranial cystic mass lesions with peripheral rim

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A. Rubin et al. Clinical Neurology and Neurosurgery 221 (2022) 107368

Fig. 18. Cerebral abscess (D,E,F), dual rim sign. SWI (D) demonstrates two concentric rims surrounding the pyogenic abscess cavity, outer is hypointense, and the
inner is hyperintense. Post-contrast T1 weighted image (E) shows ring enhancement. DWI (F) reveals an area of the restricted diffusion. All features are consistent
with cerebral abscess. (SWI-P; Philips Ingenia 3 T MR unit).

enhancement may be challenging because of overlap between pyogenic
and non-pyogenic abscesses and necrotic tumours [89].
SWI helps to differentiate pyogenic BA from other ring-enhancing
lesions. On SWI the dual-rim sign consists of two concentric rims sur­
rounding the pyogenic abscess cavity: outer is hypointense, and the
inner relatively more hyperintense (Fig. 18). In pyogenic abscess the
hypointense rim is complete and borders the lesions entirely, whereas
gliomas and abscesses of different than bacterial aetiology have hypo­
intense rim that is incomplete and only partially borders the lesion [90].
Contrast-enhancing rims of brain abscesses on CT and MR imaging
correspond to the abscess capsule on histology [91]. Granulation tissue
lines the inner part of the fibrocollagenous abscess capsule and it is
postulated that together they form the histological basis of the dual rim
sign. The magnetic susceptibility in the abscess capsule is thought to
result from the production of paramagnetic free radicals by macro­
phages, whereas irregular, incomplete hypointense rims found in glio­
blastomas are likely due to random deposition of haemorrhagic products
at the edge of the necrotic cavity [92].
14. Cerebral venous thrombosis
Cerebral venous thrombosis (CVT) is relatively rare, potentially life-
threatening condition. An occlusion can involve dural venous sinuses as
well as deep or superficial cerebral venous system. Clinical presentation
is variable depending on the phase, location and extent of the
thrombotic process. Patient may present with headache, focal neuro­
logic deficits, altered consciousness, signs and symptoms of intracranial
hypertension or encephalopathy. Appropriate and prompt treatment can
reverse the disease process and reduce the risk of serious complications.
The anticoagulation is the mainstay of acute and subacute treatment for
CVT and should be started as soon as the diagnosis is established [93].
Since the clinical presentation is nonspecific, imaging plays a crucial
role in establishing the diagnosis. Imaging may reveal direct sign of
thrombus and focal oedema due to venous hypertension. SWI has
become useful method in diagnosing CVT since it provides relevant in­
formation complementary to other MR sequences.
Direct signs of CVT on unenhanced CT images are not common, and
are seen in only one third of cases as a dense clot and cord sign. A CT
with contrast may reveal empty delta sign [46]. MRI is more sensitive for
the venous occlusion. However, thrombus exhibits variable pattern of
signal intensity depending on its evolution through the stages of oxy­
haemoglobin, deoxyhaemoglobin, methomoglobin, and haemosiderin.
In the acute stage the venous thrombus may be very hypointense on T2
weighted images and may mimic normal venous flow void. In the sub­
acute stage the thrombus becomes more apparent as its signal intensity
is increased both on T1 and T2 weighted images. In the chronic stage of
thrombosis, the thrombus exhibits variable pattern of signal intensity
and can be more difficult to identify.
The SWI improves detection of CVT, particularly in the acute and
chronic stage of thrombosis. The clot can be directly visualized as an

Fig. 19. Cerebral venous thrombosis. SWI (A, B) shows prominent hypointensity in the transverse and superior sagittal sinus representing sinus thrombosis. Small
foci of signal void are consistent with haemorrhagic lesions. Post-contrast T1 weighted images shows thrombus in the right transverse sinus. (SWI-P; Philips Ingenia
3 T MR unit).

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A. Rubin et al.
Table 2
The characteristic SWI features and signs in different pathologies of central
nervous system.
Disease SWI findings useful in differential diagnosis
Acute stroke – Asymmetric prominent vessel sign (APVS)
corresponds to the penumbra of the affected brain
area; a positive DWI/SWI mismatch is an indicator
of ischaemic penumbra
– Thrombus identification: signal void within large
artery represents thrombus
– Haemorrhage and cerebral microbleeds (CMBs):
SWI is sensitive to hyperacute haemorrhage, it may
reveal deposits of haemosiderin consistent with
previous bleeding
Cerebral hyperperfusion – Prominent hyperintensity of cortical arteries in the
after CEA MCA territory. The hyperintensity gradually
decreases over time and finally becomes indistinct.
– An increased signal intensity of cortical veins and
perilateral ventricular veins; the signal intensity
decreases as rCBF decreases and finally it returns to
normal
Myoamoya disease – “Brush sign” - prominent hypointense signals in the
deep medullary draining veins within areas of
impaired perfusion
Multiple sclerosis – Central vein sign (CVS): formation of demyelinating
plaques around small veins seen as fine, linear
hypointensity
– Iron deposits: nodular iron-laden plaque is consis­
tent with chronic lesions without enhancement
– Differential diagnosis MS vs. NMO
Traumatic brain injury – Haemorrhagic DAI: low signal foci and CMBs along
(TBI) the vessels within white matter and on the border of
white and gray matter
– Micro- and macrohaemorrhages
MSA-P – Marked hypointensity of the putamen
CADASIL – CMBs in the thalamus and basal nuclei
Hypertensive – CMBs in thalamus, basal ganglia, brainstem,
microangiopathy cerebellum and subcortical white matter
Cerebral amyloid – CMBs typically in superficial lobar locations: most
angiopathy (CAA) frequently in the occipital and temporal cortex
followed by the parietal and frontal location
Mycotic Aneurysm – Low-signal lesion with blooming artifact adjacent
to the low-signal dilated vessel; contrast
enhancement
Primary CNS Vasculitis – Numerous, small, low-signal foci (micro­
haemorrhages) in the basal ganglia and within the
affected white matter
High grade glioma – Intra-tumoral susceptibility signals (ITSS): fine
linear or dot-shaped hypointensities represent CMB
and/ or pathological vessels
B-cell lymphoma – ITSS are uncommon in B-cell lymphoma prior
treatment
Lipoma – Peripheral, complete or mixed pattern
hypointensity with blooming
– Should be differentiated with haematoma
Dermoid – Unruptured – heterogeneously hypointense mass
with blooming artefacts
– Ruptured – multiple hypointense droplets within
subarachnoid space
Abscess – Dual-rim sign: complete and smooth, consists of
two concentric rims surrounding the pyogenic
abscess cavity, the outer is hypointense, the inner
relatively more hyperintense
Cerebral venous – Prominent hypointensity in dural venous sinuses
thrombosis (CVT) represents thrombus
– Engorgement and prominent hypointensity in
affected regions suggests venous congestion
DWI - diffusion-weighted imaging, SWI - susceptibility weighted imaging, CT -
computed tomography, FLAIR - fluid-attenuated inversion recovery, WMLs -
white matter lesions, MS - multiple sclerosis, NMO - neuromyelitis optica, DAI -
diffuse axonal injury, CMBs - cerebral microbleeds.
area of hypointensity in the thrombosed cortical veins or sinuses. The
engorgement and prominent hypointensity of venous system may sug­
gest venous stasis and slow collateral flow. Signs of venous congestion
detected on SWI may direct attention to the diagnosis of CVT at the early
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Clinical Neurology and Neurosurgery 221 (2022) 107368
stage, before infarction or haemorrhage occurs (Fig. 19).
15. Discussion
In this review, we focused on the application of SWI in the wide
range of different neurological conditions, showing its great value in the
diagnostic process and differential diagnosis of CNS diseases, often rare
and posing a diagnostic challenge.
Table 2 summarizes SWI features and signs characteristic of selected
neurological disorders (Table 2).
In the context of novel neuroimaging and contribution to modern
clinical settings, it has been shown that SWI may indicate potentially
iatrogenic but hitherto overlooked CNS lesions. Xiong et al. described
CMBs seen on SWI as a novel evidence about a previously overlooked
type of brain lesion after TAVR (transcatheter aortic valve replacement)
[94]. Authors identified new CMBs in all examined patients after TAVR
and the lesions remained unchanged during follow-up MRI. Knowing
that CMBs have been associated with cerebrovascular events and
increased mortality, these findings suggest the need of further evalua­
tion. The authors considered that newly detected SWI lesions may begin
with the possible clinical sequelae as patient management might need
improvements [94].
Another example of a potential application of SWI in a novel clinical
setting is CMBs assessment in Alzheimer’s disease (AD) and mild
cognitive impairment progressing to AD (MCI-p). Basselerie et al.
showed that AD and MCI-p patients developed significantly more new
CMBs comparing to healthy control group and stable mild cognitive
impairment patients (MCI-s) during a 4-year MRI follow-up period [95].
This finding suggests that CMBs could be an valuable biomarker in AD,
especially in identifying MCI-p patients, as well as longitudinal MRI
follow-up could be valuable for monitoring disease progression by
identifying new CMBs [95,96].
Based on reports cited above, we assume that there might be more
CNS entities with previously overlooked brain lesions, which might be
important for novel clinical patient management, and obviously this
issue requires further evaluation.
The major advantage of SWI over T2 * gradient echo imaging is that
SWI uses a 3D acquisition technique (allowing thinner slices and smaller
voxel sizes to be obtained), whereas T2 * gradient echo imaging is a 2D
technique. Thus, structure details, as we show in this review, can be
missed by the T2 * gradient echo imaging due to the thicker slices of the
2D sequence [97]. Apart from that SWI is more sensitive than
T2 * -weighted gradient-recalled-echo imaging in detecting micro­
bleeds. It has also been reported that SWI MR imaging is better at
detecting brain cavernous malformation in the familiar form of the
disease, compared to conventional FSE T2W and T2W GRE MR se­
quences [98]. However, increased sensitivity of SWI sequence to local
field inhomogeneities may also contribute to an increased number of
false-positive CMBs as compared to T2 * GRE techniques [99]. More­
over, the longer SWI acquisition time may be potential cause of motion
artefacts whereas, in some cases, the simple T2 * GRE sequence could be
more easier to acquire. In addition, the SWI is more expensive, and is not
available on every scanner. In some institutions, the T2 * GRE may be
the only option to obtain the susceptibility weighted images.
It should be remembered that SWI has its intrinsic disadvantages.
Some magnetic susceptibility sources may cause undesired artifacts
occurring at air-tissue interfaces such as the areas adjacent to the tem­
poral bone and sinuses limit investigation of these regions [2]. Also the
blooming artifact may sometimes lead to extreme tissue signal nullifi­
cation and loss of anatomical borders [2100]. A limitation of the SWI
method in the context of iron measurement is that phase values are
influenced not only by the iron content but also by surrounding tissues
with a different magnetic susceptibility. Background field
low-spatial-frequency effects from tissue/bone and air/tissue interfaces
lead to unwanted phase information and must be removed by a
high-pass phase filter [101], which, in turn, may cause some loss of the
A. Rubin et al. Clinical Neurology and Neurosurgery 221 (2022) 107368

phase contrast for the structures of interest [101]. J. Radiol. Nucl. Med. 49 (2018) 165–171, https://doi.org/10.1016/j.
ejrnm.2017.12.008.
Despite SWI inherited limitations, we acknowledge the legitimacy of
[20] MS J, Assessing multiple sclerosis brain plaques using susceptibility-weighted
constantly increasing application of SWI in the routine neuroimaging imaging in comparison with T2W and FLAIR, Clin. Radiol. Imag. J..l 2 (2018)
protocols and its contribution to modern neuroimaging in the clinical 1–6, https://doi.org/10.23880/crij-16000122.
setting. SWI has proven to facilitate the correct diagnosis and assessing [21] R.J. Ward, F.A. Zucca, J.H. Duyn, R.R. Crichton, L. Zecca, The role of iron in brain
ageing and neurodegenerative disorders, Lancet Neurol. 13 (2014) 1045–1060,
the course of a wide range of CNS diseases. Nevertheless, further https://doi.org/10.1016/S1474-4422(14)70117-6.
investigation into the wider clinical applications of SWI in neuro­ [22] R. Zivadinov, B. Weinstock-Guttman, I. Pirko, Iron deposition and inflammation
vascular and neurodegenerative diseases, traumatic, non-traumatic and in multiple sclerosis. Which one comes first? BMC Neurosci. 12 (2011) 60,
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tumoral CNS pathologies is still needed. [23] K. Morgen, N.O. Jeffries, R. Stone, R. Martin, N.D. Richert, J.A. Frank, H.
F. McFarland, Ring-enhancement in multiple sclerosis: marker of disease severity,
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Conflict of interest [24] A. Ceccarelli, M. Filippi, M. Neema, A. Arora, P. Valsasina, M.A. Rocca, B.
C. Healy, R. Bakshi, T2 hypointensity in the deep gray matter of patients with
benign multiple sclerosis, Mult. Scler. 15 (2009) 678–686, https://doi.org/
All authors declare that have no conflicts of interests.
10.1177/1352458509103611.
[25] S.D. Brass, R.H.B. Benedict, B. Weinstock-Guttman, F. Munschauer, R. Bakshi,
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