European Journal of Radiology 96 (2017) 133–144

Contents lists available at ScienceDirect

European Journal of Radiology

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

Acute stroke differential diagnosis: Stroke mimics MARK

Pedro Vilela
Serviço de Neurorradiologia, Hospital Beatriz Ângelo – Loures, Avenida Carlos Teixeira, 3, 2674-514 Loures, Lisbon, Portugal

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

Keywords: Stroke mimics (SM) are non-vascular conditions that present with an acute neurological deficit simulating acute
Stroke mimic ischemic stroke and represent a significant percentage of all acute stroke hospital admissions. The most common
Acute ischemic stroke clinical SM includes conversion/functional (psychiatric disorder); seizures and postictal paralysis; toxic-
Seizures metabolic disturbances; brain tumours; infections, and migraine. Imaging is essential for SM recognition, being
Migraine
Diffusion weighted imaging (DWI), perfusion imaging and angiographic studies very useful. There are several
Transient periictal MRI abnormalities TPMA
Posterior Reversible Encephalopathy Syndrome
disorders that may have imaging features that simulate acute ischemic stroke, mainly presenting with cytotoxic
PRES oedema and/or perfusion deficits. The imaging features of the most frequent clinical and imaging stroke mimics
Reversible Cerebral Vasoconstriction Syndrome are reviewed.
RCVS

1. Introduction
Acute ischemic stroke (AIS) diagnosis is not always straightforward,
since there are several disorders, that presenting with an acute
neurological deficit imitates AIS, the stroke mimics. Stroke mimics
term is applied in a clinical evaluation, describing those non-vascular
conditions that simulate stroke, namely those presenting with an acute
neurological deficit, especially if the clinical deficit corresponds to a
hypothetical vascular distribution [1]. Stroke mimics correspond to the
false positive stroke cases. Additionally, it should also be emphasised
that several other vascular disorders may also present with acute
neurological deficits, such as transient ischemic attacks, cerebral
venous thrombosis, reversible vasoconstriction syndrome, posterior
reversible syndrome, and haemorrhagic stroke, among others.
Extending this concept to imaging, the imaging stroke mimics
would encompass those non-vascular disorders that may have an acute
phase imaging appearance resembling the most specific features of AIS,
such as brain cytotoxic oedema on DWI and Apparent Diffusion
Coefficient (ADC) mapping and perfusion deficits on Computed tomo-
graphy perfusion (CTP) – Perfusion-weighted imaging (PWI).
On the other hand, and more rarely, an acute ischemic stroke may
have an atypical clinical presentation that simulates other disorders;
these are termed stroke “chameleons” [2–4]. Stroke chameleons
correspond to the false negative stroke cases. Again, stroke “chame-
leons” is a term applied for clinical presentation. However, there are
also some unusual stroke imaging appearances that may lead us to an
erroneous diagnosis, being the “imaging stroke chameleons” [2–4].
The AIS initial imaging evaluation should be able not only to
identify and characterize the AIS, but also to exclude the stroke mimics
cases. In this paper the author reviews the imaging features of the most
common stroke mimics.
2. Clinical stroke mimics
The frequency of stroke mimics admissions in the emergency rooms
(ER) varies extensively, ranging from 1 to 2% to 30% of all strokes,
being lower in hospitals with higher neurological expertise and/or
stroke units [5–7].
Careful clinical assessment (clinical history and neurological exam-
ination) in association with laboratory evaluation is important for
depicting the stroke mimics. However, it is not always possible to
obtain an accurate clinical history because the patients may not provide
it, due to impaired speech or altered mental status, and/or the clinical
episode was not witnessed. An important clinical clue is the rapidity of
onset; sudden onset is typically present in AIS, with some few
exceptions in vertebro-basilar strokes, which can have a more progres-
sive course. There are no specific clinical signs and/or symptoms to
identify stroke mimics. However, decreased level of consciousness is
associated with a higher likelihood of stroke mimic, being found in
toxic-metabolic disturbances, postictal and epileptic statuses, and
infections [5]. Brain imaging is essential for the correct diagnosis of
AIS and stroke mimic exclusion. With the use of the clinical, laboratory
data and computed tomography (CT) evaluation the admission inci-
dence of stroke mimics declines to 4–6.5% [2,6,8–13]. The use of
magnetic resonance imaging (MRI), specially with DWI, reduces it even
further to 0–1.3% [2,6,8–13]

E-mail address: ferrovilela@sapo.pt.

http://dx.doi.org/10.1016/j.ejrad.2017.05.008
Received 3 May 2017; Accepted 4 May 2017
0720-048X/ © 2017 Elsevier B.V. All rights reserved.
P. Vilela
Table 1
Common causes of stroke mimics.
Psychogenic
Seizures
Migraine
Metabolic: hypo/hyperglycemia; hepatic wernicke’s encephalopathy
Infection: encephalitis; brain abscess
Tumor: CNS tumor, metastasis
Hypertensive encephalopathy/Posterior reversible constriction syndrome
Drug toxicity
The most common adult stroke mimic causes are conversion/
functional (psychiatric disorder); seizures and postictal paralysis;
toxic-metabolic disturbances; brain tumours; infections and migraine
(Table 1).
In the paediatric population, the causes of stroke mimics are similar
to the adults, such as migraine, psychogenic (in older children),
metabolic stroke (hypoglycaemia and mitochondrial disorders), sei-
zures and postictal phase [14]. Other common causes include acute
demyelinating disorders, tumours, musculoskeletal disorders and infec-
tions [14].
One important concern is the safety of IV rTPA administration in
patients with stroke mimic misdiagnosed as AIS. This has been
addressed in several papers that have shown a low rate of intracranial
and/or systemic haemorrhage and no mortality [7,13,15–19]. The rate
of symptomatic intracranial haemorrhage (ICH) in stroke mimics is very
low (0–2%), similar to the symptomatic ICH rate in those patients
treated with IV tPA for acute myocardial infarction [20] and the overall
outcome is favourable, with 85–96% of patients achieving a mRS 0–1 at
30 days [7,16–19]. In a multicentric study of 5581 patients treated with
IV rTPA, the haemorrhage rate varied between 1 and 2% for the stroke
mimic group, significantly lower compared to the rate in (5.5–7.9%)
patients with AIS, and without fatal cases [7].
2.1. Clinical stroke mimics: non-vascular disorders
Among non-vascular disorders simulating stroke, there are some
clinical and imaging presentations, such as those associated with
seizures, migraine, and metabolic disturbances, which represent diffi-
cult diagnostic challenges.
Seizures, postictal phase and epileptic statuses, especially noncon-
vulsive status epilepticus, represent a major diagnostic challenge, for
both clinicians and neuroradiologists. The first seizure, especially if not
witnessed, seizures associated with AIS, which may occur during the
first hours after stroke, patients with chronic strokes and seizures, and
the rare inhibitory seizures are challenging diagnosis. The neurological
deficits during the postictal phase are usually short lasting, but they
may last up to 48 h after the convulsion and brain imaging is crucial for
the correct diagnosis. Perfusion evaluation may allow the distinction
between AIS and epileptic disorder, demonstrating the absence of AIS
typical findings of reduced cerebral blood flow (CBF) and volume (CBV)
(Figs. 1 and 2).
The acute MR imaging features of seizures are named transient
periictal MRI abnormalities (TPMA). These are reversible brain lesions,
occurring during the acute or immediately postictal phase of seizures
(more commonly seen in association with status epilepticus), not having
a particular vascular distribution but rather being topographically
associated with the epileptic focus and surrounding tissue and also
affecting the ipsilateral thalamus [21–26]. These lesions are hyperin-
tense on T2WI and exhibit cytotoxic oedema on the DWI-ADC maps
(with cerebral cortical location with homolateral thalamus involve-
ment) and may exist some degree of cortical/pial contrast enhancement
[22–27]. The subcortical white matter may show vasogenic or cytotoxic
oedema. 1 [22–27] Perfusion studies will show a typical CBV increase
(hyperperfusion) at the epileptogenic area, which occurs simulta-
neously with restricted diffusion, during the ictal phase and a hypo-
134
European Journal of Radiology 96 (2017) 133–144
perfusion in the postictal phase [22–24,26,28,29] (Fig. 3). On MR
spectroscopy the most constant pattern is the lactate peak increase and
the NAA peak decrease [21,24].
After imaging abnormalities reversion, is crucial to rule out an
underlying focal pathology responsible for the seizure/epileptic status,
such as cortical malformations, tumoural or infectious diseases.
Besides the lesion reversibility on follow-up studies, important
imaging clues for the diagnosis of TPMA are the absence of a typical
vascular territory lesion distribution; the perfusion parameters (CBF/
CBV) being normal or increased; the gyral enhancement occurring
earlier than expected for AIS; and the diffusion abnormalities having a
mixed appearance with simultaneous acute cytotoxic cortical oedema
and vasogenic subcortical oedema.
Migraine accounts for up to 10% of stroke mimics and is especially
important among young patients [7,30]. Up to 25% of migraine
patients, namely migraine with aura and hemiplegic migraine, may
present with focal neurological deficits, which are commonly reversible
[31]. The pathophysiology of migraine is not well understood being
suggested that both neuronal and vascular factors interplay and that
cortical spreading depression could cause the neurological deficits
[31–33]. Familial hemiplegic migraine (FHM) is a rare migraine
variant, extremely difficult to diagnose in the first attack setting.
FHM is characterized by hemiparesis, which may be associated with
other neurological symptoms, such as visual disturbances and dyspha-
sia [33]. Young age, familiar history and headache should raise the
clinical suspicion of migraine [33]. On imaging, migraine may present
with brain areas of reversible cytotoxic oedema (restriction on DWI-
ADC maps) and increased CBV values [30–36]. On rare cases, these
migraine patients may suffer a “migrainous” infarction, with irrever-
sible neurological deficits and permanent brain lesions [30–36] (Fig. 4).
This accounts for 0.5–1.5% of all strokes (10–14% in young patients)
being more frequent in patients with migraine with aura and long
standing migraine [30–36]. Clinical presentation is an “aura that does
not reverse” generally a homonymous hemianopia due to the predilec-
tion for the posterior cerebral artery circulation. The outcome is
generally good and there is a low rate of recurrence [30–36].
Among toxic-metabolic disorders that simulate AIS, glucose blood
level fluctuations (hypogliceamia and hyperglycaemia) are the most
common. A careful laboratory evaluation will facilitate the diagnosis
and the neuroradiologist should also review the laboratory findings in
atypical stroke cases.
Hypoglycaemia is common in paediatric population, especially in
newborns. In adults, is more frequent in alcoholic and diabetic patients.
The symptoms generally begin with glycaemia below 45 mg/dl and
resolve after blood glucose level normalization [37,38]. The most
common clinical manifestations of hypoglycaemia are seizures, auto-
nomic symptoms/signs and decreased level of consciousness [37–39].
In less than 5% of cases, it also presents with acute focal neurological
deficit, resulting from focal brain lesions, being visual disturbances
(with unilateral or bilateral occipital lesions) and hemiparesis that can
be associated with aphasia (with frontal and parietal lesions) the most
frequent manifestations [37,38]. The simultaneous presence of auto-
nomic symptoms should raise the clinical suspicion of glycaemia
disturbance [37,38]. Imaging is also challenging, since in these
disorders the presence of cytotoxic oedema mimics AIS. During the
acute phase, the imaging signs of hypoglycaemia include cortical
necrosis with gyral swelling and sulci effacement associated with high
T2 signal and cortex diffusion restriction on the DWI-ADC maps, most
commonly located at the parieto-occipital cortex [21,37,38,40]. Other
possible lesion locations include the basal ganglia and thalamus,
hippocampi and amygdalae [21,37,38]. The absence of a clear vascular
distribution and the presence of bilateral lesions should raise the
suspicion of metabolic disorder [21,37,38] (Fig. 5).
Acute hyperglycaemia associated with hyperglycaemia hyperosmo-
lar syndrome (HHS) (more commonly) and diabetes ketoacidosis
syndrome (DKS), generally presents with confusion/decreased level of
P. Vilela
Fig. 1. CT postictal stroke mimic. 68 years old male presenting with acute left hemiparesis, resulting from postictal deficit. (a) Axials CT. Right inferior frontal encephalomalacia area
corresponding to a chronic brain lesion. (b) MTT CT perfusion map. Diffuse right cerebral hemisphere MTT reduction. (c) CBV CT perfusion map. Diffuse cortical right cerebral
hemisphere CBV increase with striking thalamic involvement.
consciousness, movement disorder symptoms, such as hemichorea-
hemiballism, and seizures [41–43]. On imaging, there may be unilateral
or bilateral asymmetric lesions of the basal ganglia, more commonly
affecting the putamen and/or caudate (contralateral to the side of the
patient's presenting symptoms) [41–43]. On CT there lesions are
slightly and spontaneously hyperdense and on MRI they are hyper-
intense on T1 WI, hypointense on T2 WI and may exhibit DWI-ADC
restriction [43]. A confounding feature may be associated with the
rapid correction of the hyperosmolar state inducing osmotic demyeli-
nation that superimposes another type of imaging appearance.
Other common metabolic conditions that may simulate AIS are
hypo/hypernatremia and acute hepatic encephalopathy [44]. Patients
with acute hepatic encephalopathy may present with acute neurological
deficits [45,46]. This disorder is caused by acute hyperammonemia
(hyperammonemic encephalopathy) and the patients are usually en-
cephalopathic [45,46]. Seizures and gradual decrease of consciousness
progressing to coma are other clinical manifestations [45,46]. On
imaging there may be a bilateral cortical oedema, with gyrus swollen
and/or cytotoxic oedema. MRI shows bilaterally symmetric T2/FLAIR
hypersignal on the insular cortex, cingulate gyri, and basal ganglia,
135
European Journal of Radiology 96 (2017) 133–144
generally sparing the perirolandic and occipital regions and the
subcortical white matter [47–49]. MR spectroscopy may be useful,
showing an elevation of the glutamate-glutamine peak at short echo
times [47–49].
Mitochondrial Encephalopathy with Lactic Acidosis and Stroke
(MELAS) is an important cause of stroke mimics especially in young
adults and children. Typically, these patients have multiple lesions
affecting the basal ganglia and the cerebral cortex (the parietal and
occipital areas are more frequently affected) spreading into the under-
lying white matter, with cortical oedema and swelling, high T2 WI/
FLAIR signal, and variable DWI-ADC appearance [50] (Fig. 6). Cortical/
pial contrast-enhancement may be present and haemorrhage is gen-
erally absent [50]. The DWI and perfusion changes associated with
MELAS are variable and a temporal evolution has been suggested,
namely with: a preclinical phase with increased CBF; an acute phase
with increased CBF and variable ADC values (increased, normal or
decreased); a subacute phase with a progressive CBF decrease; and
finally a chronic phase with CBF decreased and brain atrophy [50–55].
Psychiatry disturbances, such as the functional disorders, are
common stroke mimics. A neurological exam showing neurological
P. Vilela European Journal of Radiology 96 (2017) 133–144

Fig. 2. CT postictal stroke mimic. 77 years old male with acute left hemiparesis after generalized tonic-clonic seizure. (a) Axials CT. No acute and/or chronic focal brain lesion was
present. (b) MTT CT perfusion map. Diffuse right cerebral hemisphere MTT increase with no vascular territory distribution. (c) CBV CT perfusion map. Normal CBV map with symmetric
CBV distribution on both cerebral hemispheres.

inconsistencies and the absence of abnormalities on imaging, especially abrupt onset of both anterograde and retrograde transitory amnesia,
with the use of CT/CTP or MRI/DWI-MRI, and angiographic studies generally reversible within less than 24 h. Although the pathophysiol-
usually provides sufficient information for the diagnosis. ogy is still uncertain, it results from a hippocampus/parahippocampus
Transient global amnesia is a clinical condition characterized by lesion. Different aetiologies have been proposed, such as transient

136
P. Vilela European Journal of Radiology 96 (2017) 133–144

Fig. 3. Transient periictal MRI abnormalities (TPMA). 64 year-old female that over the last 4 days presented with progressive onset headache, nausea, and somnolence. Left hemianopia,
and left visual and tactile neglect were depicted at neurological examination. The EEG confirmed a non convulsive epilepticus status. (a) Axial T2 dark fluid MRI. Right temporal, occipital
and parietal cortical high T2 signal associated with cortical swelling, ipsilateral thalamic and less severe subcortical white matter involment. Concomitant moderate small vessel white
matter lesions (leukoaraiosis). (b) DWI MRI and corresponding ADC map. Cortical cytotoxic edema in association with subcortical vasogenic edema at the acute lesion areas. (c) Perfusion
ASL MRI map. Increase cortical CBF at the temporal, occipital and parietal lobes without a specific vascular territory. (d–f) 2 weeks follow up MRI performed after resolution epileptic
activity and on anti-epileptic drug teraphy. (d) Axial T2 dark fluid MRI, (e) DWI MRI, (f) Perfusion ASL MRI map CBV. Reversion of the transient periictal MRI abnormalities (TPMA).

ischemic attack (TIA) with CBF decrease; venous congestion (venous
ischemia – stroke); hippocampus epileptic discharge (seizures); or
spreading depression of cortical electrical activity (migraine variant)
[56–59]. CT is always normal and four MRI patterns have been
described. A normal pattern with no pathologic signal change in both
T2 WI/FLAIR and DWI; transient abnormalities pattern with pathologic
signal change in T2 WI/FLAIR and DWI that disappears during follow-
up; diffusion positive pattern with pathologic signal change in DWI and
no change in T2WI/FLAIR and finally T2 WI/FLAIR and diffusion
positive pattern with permanent abnormal signal change on both T2
and DWI [56–59].
Other nonvascular stroke mimics include brain tumours and extra-
axial collections, demyelinating disorders, infections (local or systemic)
that generally have evident clinical and imaging presentations and
rarely represent an imaging diagnosis concern.
2.2. Clinical stroke mimics: vascular diseases
Several vascular diseases may present with an acute neurological
deficit, including haemorrhagic stroke, cerebral venous thrombosis,

137
 P. Vilela

138
Fig. 4. Migraine. 29 years old female with a long-standing migraine with visual aura, presenting with a nonreversible hemianopia and right hemihypoesthesia. (a) Axial T2 WI. Cortical subcortical left medial occipital high T2 signal with a posterior
cerebral artery (PCA) territory distribution. (b) Axial DWI and corresponding ADC map. Corresponding cortical cytotoxic oedema. (c) 3D TOF MRA. Left PCA irregularities with focal areas of constriction with reduced diameter (vasospasm-like). (d)
Follow up axial T2 dark fluid MRI. Partial reversion of the lesion with small occipital brain infarct squeal.
European Journal of Radiology 96 (2017) 133–144
P. Vilela
Fig. 5. Hypoglicemia. Female newborn with difficulties in breast feeding (no breast
suction); several episodes of abnormal mouth and eye movements and hypoglicemia. (a)
Axial T2 WI. Slight bilateral and symmetrical medial occipital cortex high T2 signal with
the affected cortex appearing absent (“missing cortex” sign). (b) Axial DWI and
corresponding ADC map. Corresponding cortical cytotoxic oedema.
arteriovenous pial malformations, arteriovenous dural fistulae, aneur-
ysms and cavernomas among others. Generally, these disorders do not
represent a significant imaging challenge. There are two increasingly
recognised vascular disorders that represent a significant clinical and
imaging challenge: Posterior Reversible Encephalopathy Syndrome
(PRES) and Reversible Cerebral Vasoconstriction Syndrome (RCVS).1
In up to 38% of cases there is an overlap or a coexistence of these two
conditions [60–63].
PRES is an acute neurotoxic syndrome defined by clinicoradiologic
features, resulting from a cerebral vasoregulation dysfunction. It is
characterized by reversible subcortical vasogenic brain oedema in
patients presenting with variable acute neurological symptoms, includ-
ing headache, encephalopathy, seizures, visual disturbances and other
focal neurological deficits [64]. PRES results from acute and severe
blood pressure increase and/or from direct effect of cytokines on the
endothelium causing blood–brain barrier dysfunction, impaired cere-
bral autoregulation and brain oedema [62–64]. PRES is generally
reversible, both clinically and on imaging, and has a favourable
prognosis [64]. PRES was initially described in association to acute
hypertension [65] but it can also be associated with several other
medical conditions, such as eclampsia/pre-eclampsia, sepsis, immuno-
1
Also known as: Call or Call-Fleming syndrome; Postpartum angiopathy Eclampsia
associated vasoconstriction; Migraine ‘angiitis’; Thunderclap HA with reversible ‘vasos-
pasm’; Drug induced ‘angiitis’; CNS ‘pseudovasculitis’; Benign angiopathy of the CNS
(BACNS).
139
European Journal of Radiology 96 (2017) 133–144
suppressive agents/chemotherapy, infection and sepsis, autoimmune
diseases, and renal failure, among others [62–64,66,67]. On imaging
there is a typical bilateral symmetrical distribution pattern of vasogenic
oedema with posterior cerebral (parieto-occipital) parenchyma distri-
bution, involving mainly the subcortical white matter. Three major
patterns may be seen: dominant parietal-occipital pattern; superior
frontal pattern, with involvement of frontal lobes near the mid and
posterior aspect of superior frontal sulcus and holohemispheric wa-
tershed pattern, with frontal, parietal, and occipital lobes watershed
areas involvement. The cerebral cortex and other brain locations, such
as the anterior part of the frontal lobes, the cerebellum, the brain stem,
and the spinal cord may also be affected [62–64,68]. In up to 43% of
cases, contrast enhancement is present, which is not associated with
clinical or imaging severity, or with the final patient outcome [69].
Vascular abnormalities may be seen on angiographic studies in up to
one third of cases, more commonly with distal arterial vasoconstriction
pattern, or focal areas of vasoconstriction and/or vasodilatation (“string
of bead appearance”) [62–64]. Perfusion studies generally reveal
hypoperfusion on the brain lesions areas with decreased cerebral blood
volume and cerebral blood flow [70]. Typically, PRES lesions are
completely reversible, but cytotoxic oedema and irreversible lesions
may be present in 15–30% of cases [64]. Intracranial haemorrhage
(brain haemorrhage or subarachnoid haemorrhage) is seen in 10% of
cases [64]. The presence of any of these two atypical features should
not exclude the diagnosis of PRES, but the presence of cytotoxic
oedema, haemorrhage and/or extensive vasogenic oedema is associated
with worst outcome [71] (Fig. 7).
RCVS is a group of diverse conditions characterized by reversible
segmental and multifocal constriction of the cerebral arteries, present-
ing with severe headaches, namely thunderclap headache (in up to 95%
of cases) and recurrent headaches (in up to 75–87%) that may or may
not be associated with other neurological findings (seizures, transient
or persistent focal deficits) and that resolves within 1–3 months
[60,61,72]. Headache may be the only symptom in up to 75% of
patients, but the absence of headache does not exclude the diagnosis of
RCVS [72,73]. The long-term outcome is favourable: the vast majority
of patients (97.5% approximately) become functionally independent,
up to half the patients continue to have headache but in the majority
(88% approximately) will be less severe [74]. The recurrence rate of
this disorder is low, 1.71 per 100 patient-years [72,75]. There is a
female predominance and the peak incidence is between 20 and 50
years of age [72]. In up to 60% of cases, a predisposing factor may be
depicted, such as trauma, hypertension, cerebral tumours, nonaneur-
ysmal subarachnoid haemorrhage, pregnancy and postpartum, vasoac-
tive sympathomimetic or serotoninergic medications, illicit drug, such
as marijuana, cannabis, cocaine, ecstasy [72]. RCVS is characterized by
an arterial cerebral vasospasm, resolving over the following days to
weeks, and responding to vasodilator drugs, such as nimodipine. Up to
25% of RCVS patients also have migraine, which makes the clinical
diagnosis more difficult [76]. RCVS differs from migraine since brain
angiogram is generally normal in migraine patients, migraine patients
will have recurrent headache attacks over time and RCVS is generally a
single event [76].
The diagnosis of RCVS includes clinical, laboratory, and imaging
features. The diagnosis is made by exclusion of other causes of
haemorrhagic and ischemic stroke and by the presence of reversible
vascular abnormalities on imaging studies. These vasospasm-like
changes are characterized by multiple areas of arterial constriction
and dilation (beading), in different arterial territories (anterior and
posterior), with centripetally progression, affecting mostly large-med-
ium size arteries [72,76–81]. The vascular abnormalities are generally
reversible during the first 12 weeks after the acute presentation, with
full reversion in 73–76% of cases; partial reversion in 21–26% of cases;
and being suggested that a very small group of patients might exhibit no
reversion (1.5–2.4% of cases) [72,76–81] (Fig. 8). Brain imaging (brain
CT and/or MRI) is normal for the majority of cases (up to 70% of cases).
P. Vilela
Fig. 6. MELAS. 27 year-old female with MELAS disease diagnosed since the age of 17, admitted with subacute fluctuating global aphasia. (a) Axial DWI. Diffuse and bilateral cerebral
cortical and subcortical white matter high signal. (b) Corresponding ADC map. Demonstrating predominant vasogenic cortical and subcortical oedema with small and focal areas of
cortical cytotoxic oedema. (c) Perfusion ASL MRI map (fusion with the T2WI images). No CBF perfusion abnormalities were depicted.
However, reversible oedema (PRES-Like), cortical subarachnoid hae-
morrhage, infarcts (more commonly at watershed areas) and brain
haemorrhage have been described in RCVS [72]. The perfusion studies
may demonstrate multifocal areas of hypoperfusion at the cerebral
watershed zones that can progress to infarction [61].
3. Imaging stroke mimics
The most important imaging mimics in AIS imaging are those
conditions associated with brain cytotoxic oedema on DWI-ADC studies
and false penumbra on perfusion studies.
Although typically associated with AIS, brain cytotoxic oedema may
also be present in other disorders, such as metabolic strokes, seizures,
migraine, infectious diseases, intoxications (namely carbon monoxide
and methanol intoxications), demyelinating diseases, trauma (diffuse
axonal injury), among others [21].
Several clinical situations may present with an penumbra pattern on
CT perfusion, such as extracranial and intracranial stenosis, non acute
brain ischemia, venous congestion, vascular disregulation and anatomic
variants, like arterial hypoplasia/agenesis. There are also some techni-
cal pitfalls that can affect the perfusion parametric maps, such as the
head position during CT acquisition [82].
The differential diagnosis between AIS, TPMA, PRES, RCVS and
migraine, can be very challenging. All of these conditions may present
with cytotoxic oedema, but TPMA and migraine are associated with
hyperperfusion (increase CBF or CBV values) and/or vasodilation;
RCVS and AIS are associated with hypoperfusion (decrease CBF or
CBV values) and/or vasoconstriction or vessel occlusion; and PRES can
140
European Journal of Radiology 96 (2017) 133–144
present, more commonly, with vasogenic oedema (mostly subcortical)
and/or seldom with cytotoxic oedema (with a watershed distribution)
and there may be hypoperfusion on the border zones.
4. Stroke chameleons
Stroke “chameleons” also represent a clinical and imaging challenge
in the acute stroke setting. Atypical AIS presentations include vertigo,
seizures, mental status fluctuations, confusional states or delirium,
abnormal movements typically acute and unilateral, such as acute
hemiballism, unilateral dyskinesis and several types and locations of
pain.
Isolated vertigo is not common in AIS stroke, but the association
with other neurological symptoms, such as hearing loss, headache, or
brain stem neurological symptoms should raise the suspicion of a
vertebrobasilar AIS. The limbic cortex and the orbitofrontal regions
lesions may be related with mental status changes, the subthalamic
nucleus lesions may be associated for the abnormal movement pre-
sentations; and the thalamic or parietal lobe lesions with pain as
important clinical presentation [83,84].
5. Conclusions
Acute ischemic stroke remains a clinical and imaging challenge.
Stroke mimics may correspond up to 30% of stroke emergency room
admissions. Brain imaging is the cornerstone for the correct diagnosis
identifying the stroke mimics and preventing these cases from receiving
unnecessary or erroneous treatments. However, IV rTPA administration
P. Vilela European Journal of Radiology 96 (2017) 133–144

Fig. 7. Atypical (haemorrhagic) Posterior Reversible Encephalopathy Syndrome (PRES). Postpartum 35 years/old female with sepsis secondary to E Coli urinary tact infection, presenting
with decreased level of consciousness, cortical blindness and high arterial blood pressure (MRA and MRV − not shown – were normal). (a–d) Axial CT. Bilateral and symmetrical parieto-
occipital subcortical hypodense lesions associated to a subcortical acute right parietal hematoma. (e and f) Axial T2 dark fluid MRI. Bilateral and symmetrical parieto-occipital subcortical
high T2 lesions with a subcortical acute right parietal hematoma. 7 g Coronal T2*MRI: showing two subcortical brain parietal hematomas. 7 h Axial DWI and the corresponding ADC map.
Showing the vasogenic oedema type of the brain lesions.

141
P. Vilela European Journal of Radiology 96 (2017) 133–144

Fig. 8. Reversible Cerebral Vasoconstriction Syndrome (RCVS) Postpartum 30 year-old female presenting with thumberclap headache without other neurological symptoms or signs
(brain MRI – not shown – was normal). (a–c) 3D TOF MRA. Multiple areas of arterial constriction in the anterior and posterior arterial territories, affecting mostly the basilar artery,
posterior cerebral arteries, supraclinoid ICA segments, M1 and M2 middle cerebral arteries segments, anterior cerebral artery. (d–f) Follow up CTA showing the reversal of the arterial
abnormalities.

is not unsafe in stroke mimics patients, and the risk-benefit analysis
favours thrombolysis if there is any doubt of being a true ischemic
stroke. MRI, with the use of DWI, is the most reliable imaging method
to depict stroke mimics and to confirm the presence of acute ischemic
stroke.
References
[1] E.C. Jauch, J.L. Saver, H.P. Adams, A. Bruno, J.J.B. Connors, B.M. Demaerschalk,
et al., Guidelines for the early management of patients with acute ischemic stroke: a
guideline for healthcare professionals from the American Heart Association/
American Stroke Association, Stroke 44 (2013) 870–947, http://dx.doi.org/10.
1161/STR.0b013e318284056a.
[2] J.S. Huff, Stroke differential diagnosis – mimics and chameleons J. stephen huff,
MD, Emerg. Med. Clin. North Am. 20 (2002) 1–16, http://dx.doi.org/10.1016/
s0733-8627(02)00012-3.
[3] Brendan G. Magauran, Meaghan Nitka, Stroke mimics, Emerg. Med. Clin. N. Am. 30
(3) (2012) 795–804, http://dx.doi.org/10.1016/j.emc.2012.06.006 ISSN 0733-
8627.
[4] V.B. MD, Outpatient neuroimaging of stroke, Neurol. Clin. NA 27 (2009) 139–170,
http://dx.doi.org/10.1016/j.ncl.2008.09.009.
[5] R.B. Libman, E. Wirkowski, J. Alvir, T.H. Rao, Conditions that mimic stroke in the
emergency department: implications for acute stroke trials, Arch. Neurol. 52 (1995)
1119–1122, http://dx.doi.org/10.1001/archneur.1995.00540350113023.
[6] S.J. Allder, A.R. Moody, A.L. Martel, P.S. Morgan, G.S. Delay, J.R. Gladman, et al.,
Limitations of clinical diagnosis in acute stroke, Lancet 354 (1999) 1523–1531,
http://dx.doi.org/10.1016/S0140-6736(99)04360-3.
[7] S.M. Zinkstok, S.T. Engelter, H. Gensicke, P.A. Lyrer, P.A. Ringleb, V. Artto, et al.,
Safety of thrombolysis in stroke mimics: results from a multicenter cohort study,
Stroke 44 (2013) 1080, http://dx.doi.org/10.1161/STROKEAHA.111.000126.
[8] H. Ay, F.S. Buonanno, G. Rordorf, P.W. Schaefer, L.H. Schwamm, O. Wu, et al.,
Normal diffusion-weighted MRI during stroke-like deficits, Neurology 52 (1999)
1784, http://dx.doi.org/10.1212/WNL.52.9.1784.
[9] H. Ay, F.S. Buonanno, G. Rordorf, P.W. Schaefer, L.H. Schwamm, O. Wu, et al.,
Normal diffusion-weighted MRI during stroke-like, Neurology 1999 52 (2013) 1–2,
http://dx.doi.org/10.1212/wnl.52.9.1784.
[10] R.U. Kothari, T. Brott, J.P. Broderick, C.A. Hamilton, Emergency physicians:
accuracy in the diagnosis of stroke, Stroke 26 (1995) 2238–2241, http://dx.doi.org/
10.1161/01. STR.26.12.2238.
[11] A.M. Nor, J. Davis, B. Sen, D. Shipsey, S.J. Louw, A.G. Dyker, et al., The Recognition
of Stroke in the Emergency Room (ROSIER) scale: development and validation of a
stroke recognition instrument, Lancet Neurol. 4 (2005) 727–734, http://dx.doi.org/
10.1016/S1474-4422(05)70201-5.

142
P. Vilela
[12] P.C.A.J. Vroomen, M.K. Buddingh, G.-J. Luijckx, J. De Keyser, The incidence of
stroke mimics among stroke department admissions in relation to age group, J.
Stroke Cerebrovasc. Dis. 17 (2008) 418–422, http://dx.doi.org/10.1016/j.
jstrokecerebrovasdis.2008.06.007.
[13] A. Förster, M. Griebe, M.E. Wolf, K. Szabo, M.G. Hennerici, R. Kern, How to identify
stroke mimics in patients eligible for intravenous thrombolysis? J. Neurol. 259
(2012) 1347–1353, http://dx.doi.org/10.1007/s00415-011-6354-9.
[14] R.A. Shellhaas, S.E. Smith, E. O'Tool, D.J. Licht, R.N. Ichord, Mimics of childhood
stroke: characteristics of a prospective cohort, Pediatrics 118 (2006) 704–709,
http://dx.doi.org/10.1542/peds.2005-2676.
[15] O.Y. Chernyshev, S. Martin-Schild, K.C. Albright, A. Barreto, V. Misra, I. Acosta,
et al., Safety of tPA in stroke mimics and neuroimaging-negative cerebral ischemia,
Neurology 74 (2010) 1–6, http://dx.doi.org/10.1212/wnl.0b013e3181dad5a6.
[16] D.T. Winkler, F. Fluri, P. Fuhr, S.G. Wetzel, P.A. Lyrer, S. Ruegg, et al.,
Thrombolysis in stroke mimics: frequency, clinical characteristics, and outcome,
Stroke 40 (2009) 1522–1525, http://dx.doi.org/10.1161/STROKEAHA.108.
530352.
[17] J.A. Chalela, C.S. Kidwell, L.M. Nentwich, M. Luby, J.A. Butman, A.M. Demchuk,
et al., Magnetic resonance imaging and computed tomography in emergency
assessment of patients with suspected acute stroke: a prospective comparison,
Lancet 369 (2007) 293–298, http://dx.doi.org/10.1016/s0140-6736(07)60151-2.
[18] P.A. Scott, R. Silbergleit, Misdiagnosis of stroke in tissue plasminogen activator-
treated patients, Ann. Emerg. Med. 42 (2003) 611–618, http://dx.doi.org/10.1016/
s0196-0644(03)00443-8.
[19] J.L. Saver, W.G. Barsan, Swift or sure?: The acceptable rate of neurovascular mimics
among IV tPA-treated patients, Neurology 74 (2010) 1336–1337, http://dx.doi.org/
10.1212/wnl.0b013e3181dbe0ad.
[20] GUSTO investigators, An international randomized trial comparing four thrombo-
lytic strategies for acute myocardial infarction, N. Engl. J. Med. 329 (September
(10)) (1993) 673–682 PubMed PMID: 8204123.
[21] R. Forghani, P.W. Schaefer, Clinical applications of diffusion, in: S.H. Faro,
F.B. Mohamed, M. Law, J.T. Ulmer (Eds.), Functional Neuroradiology, Springer, US,
Boston, MA, 2011, pp. 13–52, , http://dx.doi.org/10.1007/978-1-4419-0345-7_2.
[22] A.J. Cole, Status epilepticus and periictal imaging, Epilepsia 45 (2004) 72–77,
http://dx.doi.org/10.1111/j.0013-9580.2004.04014.x.
[23] C. Di Bonaventura, F. Bonini, J. Fattouch, F. Mari, S. Petrucci, M. Carnì, et al.,
Diffusion-weighted magnetic resonance imaging in patients with partial status
epilepticus, Epilepsia 50 (2009) 45–52, http://dx.doi.org/10.1111/j.1528-1167.
2008.01970.x.
[24] R.S. Briellmann, R.M. Wellard, G.D. Jackson, Seizure-associated abnormalities in
epilepsy: evidence from MR imaging, Epilepsia 46 (2005) 760–766, http://dx.doi.
org/10.1111/j.1528-1167.2005.47604.x.
[25] G. Bauer, T. Gotwald, J. Dobesberger, N. Embacher, S. Felber, R. Bauer, et al.,
Transient and permanent magnetic resonance imaging abnormalities after complex
partial status epilepticus, Epilepsy Behav. 8 (2006) 666–671, http://dx.doi.org/10.
1016/j.yebeh.2006.01.002.
[26] S. Rupprecht, M. Schwab, C. Fitzek, O.W. Witte, C. Terborg, G. Hagemann,
Hemispheric hypoperfusion in postictal paresis mimics early brain ischemia,
Epilepsy Res. 89 (2010) 355–359, http://dx.doi.org/10.1016/j.eplepsyres.2010.02.
009.
[27] M.G. Lansberg, M.W. O'Brien, A.M. Norbash, M.E. Moseley, M. Morrell,
G.W. Albers, MRI abnormalities associated with partial status epilepticus,
Neurology 52 (1999) 1021, http://dx.doi.org/10.1212/WNL.52.5.1021.
[28] G. Leonhardt, A. de Greiff, J. Weber, T. Ludwig, H. Wiedemayer, M. Forsting, et al.,
Brain perfusion following single seizures, Epilepsia 46 (2005) 1943–1949, http://
dx.doi.org/10.1111/j.1528-1167.2005.00336.x.
[29] M.S. Mathews, W.S. Smith, M. Wintermark, W.P. Dillon, D.K. Binder, Local cortical
hypoperfusion imaged with CT perfusion during postictal Todd’s paresis,
Neuroradiology 50 (2008) 397–401, http://dx.doi.org/10.1007/s00234-008-
0362-1.
[30] S. Sacco, R. Ornello, P. Ripa, F. Pistoia, A. Carolei, Migraine and stroke: a
hemorrhagic meta-analysis, Stroke 44 (2013) 3032–3038, http://dx.doi.org/10.
1161/STROKEAHA.113.002465.
[31] M.-G. Bousser, K.M.A. Welch, Relation between migraine and stroke, Lancet Neurol.
4 (2005) 533–542, http://dx.doi.org/10.1016/s1474-4422(05)70164-2.
[32] F. Cutrer, Pathophysiology of migraine, Semin. Neurol. 30 (2010) 120–130, http://
dx.doi.org/10.1055/s-0030-1249222.
[33] M.B. Russell, A. Ducros, Sporadic and familial hemiplegic migraine: pathophysio-
logical mechanisms, clinical characteristics, diagnosis, and management, Lancet
Neurol. 10 (2011) 457–470, http://dx.doi.org/10.1016/S1474-4422(11)70048-5.
[34] A. Alhazzani, R.P. Goddeau, Migraine and stroke: a continuum of association in
adults, Headache 53 (2013) 1023–1027, http://dx.doi.org/10.1111/head.12115.
[35] A. Bashir, R.B. Lipton, S. Ashina, M. Ashina, Migraine and structural changes in the
brain: a systematic review and meta-analysis, Neurology 81 (2013) 1260–1268,
http://dx.doi.org/10.1212/WNL.0b013e3182a6cb32.
[36] T. Bosemani, V.J. Burton, R.J. Felling, R. Leigh, C. Oakley, A. Poretti, et al.,
Pediatric hemiplegic migraine: role of multiple MRI techniques in evaluation of
reversible hypoperfusion, Cephalalgia 34 (2014) 1–2, http://dx.doi.org/10.1177/
0333102413509432.
[37] R.E. Malouf, J.C.M. Brust, Hypoglycemia: causes, neurological manifestations, and
outcome, Ann. Neurol. 17 (1985) 421–430, http://dx.doi.org/10.1002/ana.
410170502.
[38] W.E. Wallis, I. Donaldson, R.S. Scott, J. Wilson, Hypoglycemia masquerading as
cerebrovascular disease (hypoglycemic hemiplegia), Ann. Neurol. 18 (1985)
510–512, http://dx.doi.org/10.1002/ana.410180415.
[39] P.E. Cryer, L. Axelrod, A.B. Grossman, S.R. Heller, V.M. Montori, E.R. Seaquist,
143
European Journal of Radiology 96 (2017) 133–144
et al., Evaluation and management of adult hypoglycemic disorders: an endocrine
society clinical practice guideline, J. Clin. Endocrinol. Metab. 94 (2009) 709–728,
http://dx.doi.org/10.1210/jc.2008-1410.
[40] R. Andrade, V. Mathew, M.J. Morgenstern, R. Roberge, K. Rubin, D. Senekjian,
et al., Hypoglycemic hemiplegic syndrome, Ann. Emerg. Med. 13 (1984) 529–531.
[41] C.-Y.L. MD, J.-N.L. MD, Computed tomographic and magnetic resonance abnorm-
alities of basal ganglion secondary to nonketotic hyperglycemia in a patient with
stroke, Am. J. Emerg. Med. 31 (1292) (2013), http://dx.doi.org/10.1016/j.ajem.
2013.04.010 e3–1292.e4.
[42] F. Massaro, P. Palumbo, M. Falcini, G. Zanfranceschi, A. Pratesi, Generalized
chorea-ballism in acute non ketotic hyperglycemia: findings from diffusion-
weighted magnetic resonance imaging, Parkinsonism Relat. Disord. 18 (2012)
998–999, http://dx.doi.org/10.1016/j.parkreldis.2012.04.008.
[43] Z. Zaitout, CT and MRI findings in the basal ganglia in non-ketotic hyperglycaemia
associated hemichorea and hemi-ballismus (HC–HB), Neuroradiology 54 (2012)
1119–1120, http://dx.doi.org/10.1007/s00234-012-1021-0.
[44] S.F. Berkovic, P.F. Bladin, D.G. Darby, Metabolic disorders presenting as stroke,
Med. J. Aust. 140 (1984) 421–424.
[45] J.W. Atchison, M. Pellegrino, P. Herbers, B. Tipton, V. Matkovic, Hepatic
encephalopathy mimicking stroke. A case report, Am. J. Phys. Med. Rehabil. 71
(1992) 114–118.
[46] J. Cadranel, Focal neurological signs in hepatic encephalopathy in cirrhotic
patients: an underestimated entity? Am. J. Gastroenterol. 96 (2001) 515–518,
http://dx.doi.org/10.1016/s0002-9270(00)02345-5.
[47] A. Rovira, J. Alonso, J. Cordoba, MR imaging findings in hepatic encephalopathy,
Am. J. Neuroradiol. 29 (2008) 1612–1621, http://dx.doi.org/10.3174/ajnr.A1139.
[48] X.-D. Zhang, Multimodality magnetic resonance imaging in hepatic encephalo-
pathy: an update, World J. Gastroenterol. 20 (2014) 11262–11312, http://dx.doi.
org/10.3748/wjg.v20.i32.11262.
[49] M. Rosario, K. McMahon, P.F. Finelli, Diffusion-Weighted imaging in acute
hyperammonemic encephalopathy, Neurohospitalist 3 (2013) 125–130, http://dx.
doi.org/10.1177/1941874412467806.
[50] H. Ito, K. Mori, S. Kagami, Neuroimaging of stroke-like episodes in MELAS, Brain
Dev. 33 (2011) 283–288, http://dx.doi.org/10.1016/j.braindev.2010.06.010.
[51] C. Tzoulis, L.A. Bindoff, Serial diffusion imaging in a case of mitochondrial
encephalomyopathy, lactic acidosis, and stroke-like episodes, Stroke 40 (2009)
e15–e17, http://dx.doi.org/10.1161/STROKEAHA.108.523118.
[52] T. Tsujikawa, T. Yamamoto, M. Ikawa, M. Yoneda, H. Kimura, Crossed cerebellar
hyperperfusion after MELAS attack followed up by whole brain continuous arterial
spin labeling perfusion imaging, Acta Radiol. 53 (2012) 220–222, http://dx.doi.
org/10.1258/ar.2011.110274.
[53] T. Tsujikawa, M. Yoneda, Y. Shimizu, H. Uematsu, M. Toyooka, M. Ikawa, et al.,
Pathophysiologic evaluation of MELAS strokes by serially quantified MRS and CASL
perfusion images, Brain Dev. 32 (2010) 143–149, http://dx.doi.org/10.1016/j.
braindev.2008.12.003.
[54] M. Ikawa, M. Yoneda, T. Muramatsu, A. Matsunaga, T. Tsujikawa, T. Yamamoto,
et al., Detection of preclinically latent hyperperfusion due to stroke-like episodes by
arterial spin-labeling perfusion MRI in MELAS patients, Mitochondrion 13 (2013)
676–680, http://dx.doi.org/10.1016/j.mito.2013.09.007.
[55] H.-L. Yeh, Y.-K. Chen, W.-H. Chen, H.-C. Wang, H.-C. Chiu, L.-M. Lien, et al.,
Perfusion status of the stroke-like lesion at the hyperacute stage in MELAS, Brain
Dev. 35 (2013) 158–164, http://dx.doi.org/10.1016/j.braindev.2012.03.017.
[56] K. Sander, D. Sander, New insights into transient global amnesia: recent imaging
and clinical findings, Lancet Neurol. 4 (2005) 437–444, http://dx.doi.org/10.1016/
S1474-4422(05)70121-6.
[57] C. Agosti, B. Borroni, N.M. Akkawi, G. DeMaria, A. Padovani, Transient global
amnesia and brain lesions: new hints into clinical criteria, Eur. J. Neurol. 15 (2008)
981–984, http://dx.doi.org/10.1111/j.1468-1331.2008.02250.x.
[58] M. Toledo, F. Pujadas, E. Grive, J. Alvarez-Sabin, M. Quintana, A. Rovira, Lack of
evidence for arterial ischemia in transient global amnesia, Stroke 39 (2008)
476–479, http://dx.doi.org/10.1161/STROKEAHA.107.498303.
[59] C. Enzinger, F. Thimary, P. Kapeller, S. Ropele, R. Schmidt, F. Ebner, et al.,
Transient global amnesia: diffusion-weighted imaging lesions and cerebrovascular
disease, Stroke 39 (2008) 2219–2225, http://dx.doi.org/10.1161/STROKEAHA.
107.508655.
[60] T.R. Miller, R. Shivashankar, M. Mossa-Basha, D. Gandhi, Reversible cerebral
vasoconstriction syndrome, part 1: epidemiology, pathogenesis, and clinical course,
Am. J. Neuroradiol. 36 (2015) 1392–1399, http://dx.doi.org/10.3174/ajnr.A4214.
[61] T.R. Miller, R. Shivashankar, M. Mossa-Basha, D. Gandhi, Reversible cerebral
vasoconstriction syndrome, part 2: diagnostic work-up, imaging evaluation, and
differential diagnosis, Am. J. Neuroradiol. 36 (2015) 1580–1588, http://dx.doi.
org/10.3174/ajnr.A4215.
[62] W.S. Bartynski, Posterior reversible encephalopathy syndrome, part 1: fundamental
imaging and clinical features, Am. J. Neuroradiol. 29 (2008) 1036–1042, http://dx.
doi.org/10.3174/ajnr.A0928.
[63] W.S. Bartynski, Posterior reversible encephalopathy syndrome, part 2: controversies
surrounding pathophysiology of vasogenic edema, Am. J. Neuroradiol. 29 (2008)
1043–1049, http://dx.doi.org/10.3174/ajnr.A0929.
[64] J.E. Fugate, A.A. Rabinstein, Posterior reversible encephalopathy syndrome: clinical
and radiological manifestations, pathophysiology, and outstanding questions,
Lancet Neurol. 14 (2015) 914–925, http://dx.doi.org/10.1016/S1474-4422(15)
00111-8.
[65] J. Hinchey, C. Chaves, B. Appignani, J. Breen, L. Pao, A. Wang, et al., N. Engl. J.
Med. 334 (1996) 494–500, http://dx.doi.org/10.1056/NEJM199602223340803.
[66] C.J. Stevens, M.K.S. Heran, The many faces of posterior reversible encephalopathy
syndrome, Br. J. Radiol. 85 (2012) 1566–1575, http://dx.doi.org/10.1259/bjr/
P. Vilela
25273221.
[67] V. Cuvinciuc, A. Viguier, L. Calviere, N. Raposo, V. Larrue, C. Cognard, et al.,
Isolated acute nontraumatic cortical subarachnoid hemorrhage, Am. J. Neuroradiol.
31 (2010) 1355–1362, http://dx.doi.org/10.3174/ajnr.A1986.
[68] L.C. Marrone, W.A. Martins, J.P. Brunelli, H. Fussiger, G.F. Carvalhal, J.R. Filho,
R.B. Soder, M. Schuck, F.S. Viola, A.C. Marrone, J.C. da Costa, PRES with
asymptomatic spinal cord involvement. Is this scenario more common than we
know? Spinal Cord Ser. Cases 2 (January) (2016) 15001, http://dx.doi.org/10.
1038/scsandc.2015.1 eCollection 2016. PubMed PMID: 28053726; PubMed Central
PMCID: PMC5125063.
[69] S.J. Karia, J.B. Rykken, Z.J. McKinney, L. Zhang, A.M. McKinney, Utility and
significance of gadolinium-based contrast enhancement in posterior reversible
encephalopathy syndrome, Am. J. Neuroradiol. 37 (2016) 415–422, http://dx.doi.
org/10.3174/ajnr.A4563.
[70] L.M. Brubaker, J.K. Smith, Y.Z. Lee, W. Lin, M. Castillo, Hemodynamic and
permeability changes in posterior reversible encephalopathy syndrome measured
by dynamic susceptibility perfusion-weighted MR imaging, Am. J. Neuroradiol. 26
(2005) 825–830.
[71] A.D. Schweitzer, N.S. Parikh, G. Askin, A. Nemade, J. Lyo, S. Karimi, A. Knobel,
B.B. Navi, R.J. Young, A. Gupta, Imaging characteristics associated with clinical
outcomes in posterior reversible encephalopathy syndrome, Neuroradiology 59
(April (4)) (2017) 379–386, http://dx.doi.org/10.1007/s00234-017-1815-1 Epub
2017 Mar 13. PubMed PMID: 28289809.
[72] A. Sattar, G. Manousakis, M.B. Jensen, Systematic review of reversible cerebral
vasoconstriction syndrome, Expert Rev. Cardiovasc. Ther. 8 (2014) 1417–1421,
http://dx.doi.org/10.1586/erc.10.124.
[73] V. Wolff, A. Ducros, Reversible cerebral vasoconstriction syndrome without typical
thunderclap headache, Headache 56 (2016) 674–687, http://dx.doi.org/10.1111/
head.12794.
[74] S. John, A.B. Singhal, L. Calabrese, K. Uchino, T. Hammad, S. Tepper, et al., Long-
144
European Journal of Radiology 96 (2017) 133–144
term outcomes after reversible cerebral vasoconstriction syndrome, Cephalalgia 36
(2016) 387–394, http://dx.doi.org/10.1177/0333102415591507.
[75] S.-P. Chen, J.-L. Fuh, J.-F. Lirng, Y.-F. Wang, S.-J. Wang, Recurrence of reversible
cerebral vasoconstriction syndrome: a long-term follow-up study, Neurology 84
(2015) 1552–1558, http://dx.doi.org/10.1212/WNL.0000000000001473.
[76] A.B. Singhal, Reversible cerebral vasoconstriction syndromes, Arch. Neurol. 68
(2011) 1005–1008, http://dx.doi.org/10.1001/archneurol.2011.68.
[77] A. Ducros, Reversible cerebral vasoconstriction syndrome, Lancet Neurol. 11 (2012)
906–917, http://dx.doi.org/10.1016/S1474-4422(12)70135-7.
[78] L.H. Calabrese, D.W. Dodick, T.J. Schwedt, A.B. Singhal, Narrative review:
reversible cerebral vasoconstriction syndromes, Ann. Intern. Med. 146 (2007)
34–44.
[79] S.-P. Chen, J.-L. Fuh, S.-J. Wang, F.-C. Chang, J.-F. Lirng, Y.-C. Fang, et al.,
Magnetic resonance angiography in reversible cerebral vasoconstriction syndromes,
Ann. Neurol. (2009) NA, http://dx.doi.org/10.1002/ana.21951.
[80] K. Koopman, M. Uyttenboogaart, G.J. Luijckx, J. De Keyser, P.C.A.J. Vroomen,
Pitfalls in the diagnosis of reversible cerebral vasoconstriction syndrome and
primary angiitis of the central nervous system, Eur. J. Neurol. 14 (2007)
1085–1087, http://dx.doi.org/10.1111/j.1468-1331.2007.01830.x.
[81] S.I. Moskowitz, L.H. Calabrese, R.J. Weil, Benign angiopathy of the central nervous
system presenting with intracerebral hemorrhage, Surg. Neurol. 67 (2007)
522–527, http://dx.doi.org/10.1016/j.surneu.2006.07.026.
[82] A.C. Best, N.R. Acosta, J.E. Fraser, M.T. Borges, K.E. Brega, T. Anderson, et al.,
Recognizing false ischemic penumbras in CT brain perfusion studies, Radiographics
32 (2012) 1179–1196, http://dx.doi.org/10.1148/rg.324105742.
[83] J. Ghika, J. Bogousslavsky, Abnormal movements, in: J. Bogousslavsky, L.R. Caplan
(Eds.), Stroke Syndromes, ed second, Cambridge University Press, Cambridge,
2001, pp. 162–181.
[84] J.S. Kim, Sensory abnormality, in: J. Bogousslavsky, L.R. Caplan (Eds.), Stroke
Syndromes, Cambridge University Press, Cambridge, 2001, pp. 34–47.