European Journal of Radiology 96 (2017) 133–144

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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 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
Acute ischemic stroke (AIS) diagnosis is not always straightforward, common stroke mimics.
since there are several disorders, that presenting with an acute
neurological deficit imitates AIS, the stroke mimics. Stroke mimics 2. Clinical stroke mimics
term is applied in a clinical evaluation, describing those non-vascular
conditions that simulate stroke, namely those presenting with an acute The frequency of stroke mimics admissions in the emergency rooms
neurological deficit, especially if the clinical deficit corresponds to a (ER) varies extensively, ranging from 1 to 2% to 30% of all strokes,
hypothetical vascular distribution [1]. Stroke mimics correspond to the being lower in hospitals with higher neurological expertise and/or
false positive stroke cases. Additionally, it should also be emphasised stroke units [5–7].
that several other vascular disorders may also present with acute Careful clinical assessment (clinical history and neurological exam-
neurological deficits, such as transient ischemic attacks, cerebral ination) in association with laboratory evaluation is important for
venous thrombosis, reversible vasoconstriction syndrome, posterior depicting the stroke mimics. However, it is not always possible to
reversible syndrome, and haemorrhagic stroke, among others. obtain an accurate clinical history because the patients may not provide
Extending this concept to imaging, the imaging stroke mimics it, due to impaired speech or altered mental status, and/or the clinical
would encompass those non-vascular disorders that may have an acute episode was not witnessed. An important clinical clue is the rapidity of
phase imaging appearance resembling the most specific features of AIS, onset; sudden onset is typically present in AIS, with some few
such as brain cytotoxic oedema on DWI and Apparent Diffusion exceptions in vertebro-basilar strokes, which can have a more progres-
Coefficient (ADC) mapping and perfusion deficits on Computed tomo- sive course. There are no specific clinical signs and/or symptoms to
graphy perfusion (CTP) – Perfusion-weighted imaging (PWI). identify stroke mimics. However, decreased level of consciousness is
On the other hand, and more rarely, an acute ischemic stroke may associated with a higher likelihood of stroke mimic, being found in
have an atypical clinical presentation that simulates other disorders; toxic-metabolic disturbances, postictal and epileptic statuses, and
these are termed stroke “chameleons” [2–4]. Stroke chameleons infections [5]. Brain imaging is essential for the correct diagnosis of
correspond to the false negative stroke cases. Again, stroke “chame- AIS and stroke mimic exclusion. With the use of the clinical, laboratory
leons” is a term applied for clinical presentation. However, there are data and computed tomography (CT) evaluation the admission inci-
also some unusual stroke imaging appearances that may lead us to an dence of stroke mimics declines to 4–6.5% [2,6,8–13]. The use of
erroneous diagnosis, being the “imaging stroke chameleons” [2–4]. magnetic resonance imaging (MRI), specially with DWI, reduces it even
The AIS initial imaging evaluation should be able not only to 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 European Journal of Radiology 96 (2017) 133–144

Table 1 perfusion in the postictal phase [22–24,26,28,29] (Fig. 3). On MR

Common causes of stroke mimics. spectroscopy the most constant pattern is the lactate peak increase and
the NAA peak decrease [21,24].
Psychogenic
Seizures After imaging abnormalities reversion, is crucial to rule out an
Migraine underlying focal pathology responsible for the seizure/epileptic status,
Metabolic: hypo/hyperglycemia; hepatic wernicke’s encephalopathy such as cortical malformations, tumoural or infectious diseases.
Infection: encephalitis; brain abscess Besides the lesion reversibility on follow-up studies, important
Tumor: CNS tumor, metastasis
Hypertensive encephalopathy/Posterior reversible constriction syndrome
imaging clues for the diagnosis of TPMA are the absence of a typical
Drug toxicity 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
The most common adult stroke mimic causes are conversion/ mixed appearance with simultaneous acute cytotoxic cortical oedema
functional (psychiatric disorder); seizures and postictal paralysis; and vasogenic subcortical oedema.
toxic-metabolic disturbances; brain tumours; infections and migraine Migraine accounts for up to 10% of stroke mimics and is especially
(Table 1). important among young patients [7,30]. Up to 25% of migraine
In the paediatric population, the causes of stroke mimics are similar patients, namely migraine with aura and hemiplegic migraine, may
to the adults, such as migraine, psychogenic (in older children), present with focal neurological deficits, which are commonly reversible
metabolic stroke (hypoglycaemia and mitochondrial disorders), sei- [31]. The pathophysiology of migraine is not well understood being
zures and postictal phase [14]. Other common causes include acute suggested that both neuronal and vascular factors interplay and that
demyelinating disorders, tumours, musculoskeletal disorders and infec- cortical spreading depression could cause the neurological deficits
tions [14]. [31–33]. Familial hemiplegic migraine (FHM) is a rare migraine
One important concern is the safety of IV rTPA administration in variant, extremely difficult to diagnose in the first attack setting.
patients with stroke mimic misdiagnosed as AIS. This has been FHM is characterized by hemiparesis, which may be associated with
addressed in several papers that have shown a low rate of intracranial other neurological symptoms, such as visual disturbances and dyspha-
and/or systemic haemorrhage and no mortality [7,13,15–19]. The rate sia [33]. Young age, familiar history and headache should raise the
of symptomatic intracranial haemorrhage (ICH) in stroke mimics is very clinical suspicion of migraine [33]. On imaging, migraine may present
low (0–2%), similar to the symptomatic ICH rate in those patients with brain areas of reversible cytotoxic oedema (restriction on DWI-
treated with IV tPA for acute myocardial infarction [20] and the overall ADC maps) and increased CBV values [30–36]. On rare cases, these
outcome is favourable, with 85–96% of patients achieving a mRS 0–1 at migraine patients may suffer a “migrainous” infarction, with irrever-
30 days [7,16–19]. In a multicentric study of 5581 patients treated with sible neurological deficits and permanent brain lesions [30–36] (Fig. 4).
IV rTPA, the haemorrhage rate varied between 1 and 2% for the stroke This accounts for 0.5–1.5% of all strokes (10–14% in young patients)
mimic group, significantly lower compared to the rate in (5.5–7.9%) being more frequent in patients with migraine with aura and long
patients with AIS, and without fatal cases [7]. standing migraine [30–36]. Clinical presentation is an “aura that does
not reverse” generally a homonymous hemianopia due to the predilec-
2.1. Clinical stroke mimics: non-vascular disorders tion for the posterior cerebral artery circulation. The outcome is
generally good and there is a low rate of recurrence [30–36].
Among non-vascular disorders simulating stroke, there are some Among toxic-metabolic disorders that simulate AIS, glucose blood
clinical and imaging presentations, such as those associated with level fluctuations (hypogliceamia and hyperglycaemia) are the most
seizures, migraine, and metabolic disturbances, which represent diffi- common. A careful laboratory evaluation will facilitate the diagnosis
cult diagnostic challenges. and the neuroradiologist should also review the laboratory findings in
Seizures, postictal phase and epileptic statuses, especially noncon- atypical stroke cases.
vulsive status epilepticus, represent a major diagnostic challenge, for Hypoglycaemia is common in paediatric population, especially in
both clinicians and neuroradiologists. The first seizure, especially if not newborns. In adults, is more frequent in alcoholic and diabetic patients.
witnessed, seizures associated with AIS, which may occur during the The symptoms generally begin with glycaemia below 45 mg/dl and
first hours after stroke, patients with chronic strokes and seizures, and resolve after blood glucose level normalization [37,38]. The most
the rare inhibitory seizures are challenging diagnosis. The neurological common clinical manifestations of hypoglycaemia are seizures, auto-
deficits during the postictal phase are usually short lasting, but they nomic symptoms/signs and decreased level of consciousness [37–39].
may last up to 48 h after the convulsion and brain imaging is crucial for In less than 5% of cases, it also presents with acute focal neurological
the correct diagnosis. Perfusion evaluation may allow the distinction deficit, resulting from focal brain lesions, being visual disturbances
between AIS and epileptic disorder, demonstrating the absence of AIS (with unilateral or bilateral occipital lesions) and hemiparesis that can
typical findings of reduced cerebral blood flow (CBF) and volume (CBV) be associated with aphasia (with frontal and parietal lesions) the most
(Figs. 1 and 2). frequent manifestations [37,38]. The simultaneous presence of auto-
The acute MR imaging features of seizures are named transient nomic symptoms should raise the clinical suspicion of glycaemia
periictal MRI abnormalities (TPMA). These are reversible brain lesions, disturbance [37,38]. Imaging is also challenging, since in these
occurring during the acute or immediately postictal phase of seizures disorders the presence of cytotoxic oedema mimics AIS. During the
(more commonly seen in association with status epilepticus), not having acute phase, the imaging signs of hypoglycaemia include cortical
a particular vascular distribution but rather being topographically necrosis with gyral swelling and sulci effacement associated with high
associated with the epileptic focus and surrounding tissue and also T2 signal and cortex diffusion restriction on the DWI-ADC maps, most
affecting the ipsilateral thalamus [21–26]. These lesions are hyperin- commonly located at the parieto-occipital cortex [21,37,38,40]. Other
tense on T2WI and exhibit cytotoxic oedema on the DWI-ADC maps possible lesion locations include the basal ganglia and thalamus,
(with cerebral cortical location with homolateral thalamus involve- hippocampi and amygdalae [21,37,38]. The absence of a clear vascular
ment) and may exist some degree of cortical/pial contrast enhancement distribution and the presence of bilateral lesions should raise the
[22–27]. The subcortical white matter may show vasogenic or cytotoxic suspicion of metabolic disorder [21,37,38] (Fig. 5).
oedema. 1 [22–27] Perfusion studies will show a typical CBV increase Acute hyperglycaemia associated with hyperglycaemia hyperosmo-
(hyperperfusion) at the epileptogenic area, which occurs simulta- lar syndrome (HHS) (more commonly) and diabetes ketoacidosis
neously with restricted diffusion, during the ictal phase and a hypo- syndrome (DKS), generally presents with confusion/decreased level of

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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- generally sparing the perirolandic and occipital regions and the
hemiballism, and seizures [41–43]. On imaging, there may be unilateral subcortical white matter [47–49]. MR spectroscopy may be useful,
or bilateral asymmetric lesions of the basal ganglia, more commonly showing an elevation of the glutamate-glutamine peak at short echo
affecting the putamen and/or caudate (contralateral to the side of the times [47–49].
patient's presenting symptoms) [41–43]. On CT there lesions are Mitochondrial Encephalopathy with Lactic Acidosis and Stroke
slightly and spontaneously hyperdense and on MRI they are hyper- (MELAS) is an important cause of stroke mimics especially in young
intense on T1 WI, hypointense on T2 WI and may exhibit DWI-ADC adults and children. Typically, these patients have multiple lesions
restriction [43]. A confounding feature may be associated with the affecting the basal ganglia and the cerebral cortex (the parietal and
rapid correction of the hyperosmolar state inducing osmotic demyeli- occipital areas are more frequently affected) spreading into the under-
nation that superimposes another type of imaging appearance. lying white matter, with cortical oedema and swelling, high T2 WI/
Other common metabolic conditions that may simulate AIS are FLAIR signal, and variable DWI-ADC appearance [50] (Fig. 6). Cortical/
hypo/hypernatremia and acute hepatic encephalopathy [44]. Patients pial contrast-enhancement may be present and haemorrhage is gen-
with acute hepatic encephalopathy may present with acute neurological erally absent [50]. The DWI and perfusion changes associated with
deficits [45,46]. This disorder is caused by acute hyperammonemia MELAS are variable and a temporal evolution has been suggested,
(hyperammonemic encephalopathy) and the patients are usually en- namely with: a preclinical phase with increased CBF; an acute phase
cephalopathic [45,46]. Seizures and gradual decrease of consciousness with increased CBF and variable ADC values (increased, normal or
progressing to coma are other clinical manifestations [45,46]. On decreased); a subacute phase with a progressive CBF decrease; and
imaging there may be a bilateral cortical oedema, with gyrus swollen finally a chronic phase with CBF decreased and brain atrophy [50–55].
and/or cytotoxic oedema. MRI shows bilaterally symmetric T2/FLAIR Psychiatry disturbances, such as the functional disorders, are
hypersignal on the insular cortex, cingulate gyri, and basal ganglia, common stroke mimics. A neurological exam showing neurological

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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

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

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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 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
Fig. 5. Hypoglicemia. Female newborn with difficulties in breast feeding (no breast patients, but the absence of headache does not exclude the diagnosis of
suction); several episodes of abnormal mouth and eye movements and hypoglicemia. (a)
RCVS [72,73]. The long-term outcome is favourable: the vast majority
Axial T2 WI. Slight bilateral and symmetrical medial occipital cortex high T2 signal with
of patients (97.5% approximately) become functionally independent,
the affected cortex appearing absent (“missing cortex” sign). (b) Axial DWI and
corresponding ADC map. Corresponding cortical cytotoxic oedema. up to half the patients continue to have headache but in the majority
(88% approximately) will be less severe [74]. The recurrence rate of
arteriovenous pial malformations, arteriovenous dural fistulae, aneur- this disorder is low, 1.71 per 100 patient-years [72,75]. There is a
ysms and cavernomas among others. Generally, these disorders do not female predominance and the peak incidence is between 20 and 50
represent a significant imaging challenge. There are two increasingly years of age [72]. In up to 60% of cases, a predisposing factor may be
recognised vascular disorders that represent a significant clinical and depicted, such as trauma, hypertension, cerebral tumours, nonaneur-
imaging challenge: Posterior Reversible Encephalopathy Syndrome ysmal subarachnoid haemorrhage, pregnancy and postpartum, vasoac-
(PRES) and Reversible Cerebral Vasoconstriction Syndrome (RCVS).1 tive sympathomimetic or serotoninergic medications, illicit drug, such
In up to 38% of cases there is an overlap or a coexistence of these two as marijuana, cannabis, cocaine, ecstasy [72]. RCVS is characterized by
conditions [60–63]. an arterial cerebral vasospasm, resolving over the following days to
PRES is an acute neurotoxic syndrome defined by clinicoradiologic weeks, and responding to vasodilator drugs, such as nimodipine. Up to
features, resulting from a cerebral vasoregulation dysfunction. It is 25% of RCVS patients also have migraine, which makes the clinical
characterized by reversible subcortical vasogenic brain oedema in diagnosis more difficult [76]. RCVS differs from migraine since brain
patients presenting with variable acute neurological symptoms, includ- angiogram is generally normal in migraine patients, migraine patients
ing headache, encephalopathy, seizures, visual disturbances and other will have recurrent headache attacks over time and RCVS is generally a
focal neurological deficits [64]. PRES results from acute and severe single event [76].
blood pressure increase and/or from direct effect of cytokines on the The diagnosis of RCVS includes clinical, laboratory, and imaging
endothelium causing blood–brain barrier dysfunction, impaired cere- features. The diagnosis is made by exclusion of other causes of
bral autoregulation and brain oedema [62–64]. PRES is generally haemorrhagic and ischemic stroke and by the presence of reversible
reversible, both clinically and on imaging, and has a favourable vascular abnormalities on imaging studies. These vasospasm-like
prognosis [64]. PRES was initially described in association to acute changes are characterized by multiple areas of arterial constriction
hypertension [65] but it can also be associated with several other and dilation (beading), in different arterial territories (anterior and
medical conditions, such as eclampsia/pre-eclampsia, sepsis, immuno- 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
1
full reversion in 73–76% of cases; partial reversion in 21–26% of cases;
Also known as: Call or Call-Fleming syndrome; Postpartum angiopathy Eclampsia
associated vasoconstriction; Migraine ‘angiitis’; Thunderclap HA with reversible ‘vasos-
and being suggested that a very small group of patients might exhibit no
pasm’; Drug induced ‘angiitis’; CNS ‘pseudovasculitis’; Benign angiopathy of the CNS reversion (1.5–2.4% of cases) [72,76–81] (Fig. 8). Brain imaging (brain
(BACNS). CT and/or MRI) is normal for the majority of cases (up to 70% of cases).

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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- present, more commonly, with vasogenic oedema (mostly subcortical)
morrhage, infarcts (more commonly at watershed areas) and brain and/or seldom with cytotoxic oedema (with a watershed distribution)
haemorrhage have been described in RCVS [72]. The perfusion studies and there may be hypoperfusion on the border zones.
may demonstrate multifocal areas of hypoperfusion at the cerebral
watershed zones that can progress to infarction [61]. 4. Stroke chameleons

3. Imaging stroke mimics Stroke “chameleons” also represent a clinical and imaging challenge
in the acute stroke setting. Atypical AIS presentations include vertigo,
The most important imaging mimics in AIS imaging are those seizures, mental status fluctuations, confusional states or delirium,
conditions associated with brain cytotoxic oedema on DWI-ADC studies abnormal movements typically acute and unilateral, such as acute
and false penumbra on perfusion studies. hemiballism, unilateral dyskinesis and several types and locations of
Although typically associated with AIS, brain cytotoxic oedema may pain.
also be present in other disorders, such as metabolic strokes, seizures, Isolated vertigo is not common in AIS stroke, but the association
migraine, infectious diseases, intoxications (namely carbon monoxide with other neurological symptoms, such as hearing loss, headache, or
and methanol intoxications), demyelinating diseases, trauma (diffuse brain stem neurological symptoms should raise the suspicion of a
axonal injury), among others [21]. vertebrobasilar AIS. The limbic cortex and the orbitofrontal regions
Several clinical situations may present with an penumbra pattern on lesions may be related with mental status changes, the subthalamic
CT perfusion, such as extracranial and intracranial stenosis, non acute nucleus lesions may be associated for the abnormal movement pre-
brain ischemia, venous congestion, vascular disregulation and anatomic sentations; and the thalamic or parietal lobe lesions with pain as
variants, like arterial hypoplasia/agenesis. There are also some techni- important clinical presentation [83,84].
cal pitfalls that can affect the perfusion parametric maps, such as the
head position during CT acquisition [82]. 5. Conclusions
The differential diagnosis between AIS, TPMA, PRES, RCVS and
migraine, can be very challenging. All of these conditions may present Acute ischemic stroke remains a clinical and imaging challenge.
with cytotoxic oedema, but TPMA and migraine are associated with Stroke mimics may correspond up to 30% of stroke emergency room
hyperperfusion (increase CBF or CBV values) and/or vasodilation; admissions. Brain imaging is the cornerstone for the correct diagnosis
RCVS and AIS are associated with hypoperfusion (decrease CBF or identifying the stroke mimics and preventing these cases from receiving
CBV values) and/or vasoconstriction or vessel occlusion; and PRES can unnecessary or erroneous treatments. However, IV rTPA administration

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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.

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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.

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