StrokeMimics Stroke Mimics - esnr.org

16.10.2019

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Stroke Mimics

Carolina Tramontini, M.D.Neuroradiologist

Clínica Universitaria Colombia, BogotáNeuroradiology Professor

Fundación Universitaria Sanitas, Bogotá

ECNR Rovinj, October 16th, 2019

Disclosure: I have nothing to disclose

Stroke Mimics

• Introduction

• Topographic distribution patterns

• Imaging approach in stroke mimics

• Take home messages

Stroke Mimics

• Introduction




Stroke Mimics

• Stroke is a clinical diagnosis

• For the clinician it is not always an easy Dx

Introduction

Dupre et all, J Stroke Cerebrovasc Dis, 2017Boulter TJ,Schaeffer PW, Seminars in Radiology 2014

Two different types of diagnostic error

Two different types of diagnostic error

Conditions resembling strokebut are no real stroke

Conditions resembling strokebut are no real stroke

Presentations sugestinganother condition but are

stroke

Presentations sugestinganother condition but are

stroke

STROKE MIMICS STROKE CHAMELEON

• Stroke mimics in

– 9‐31% of suspected strokes

– 2.8‐17% of strokes treated with IV‐tPA

• Many different causes

• Imaging facilitates diagnosis

• But brain imaging, even DWI, are not infallible

Introduction

Kamalian S et all. Applied Radiology, 2015Hand PJ et all. Stroke, 2006Boulter TJ,Schaeffer PW, Seminars in Radiology 2014

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• Cognitive impairment

• Abnormal signs in othersystems

• Loss of consciousness orseizures at onset

• Complete abscence of neurological signs

Predictor for Stroke and Mimics

• Exact time of onset

• Definite focal symptoms

• Abnormal vascular findings

• Presence of neurological signs

• Being able to lateralize the signsto left or right side of the brain

• Being able to determine a clinical stroke subclassification

StrokepredictorsStroke

predictorsMimic

predictorsMimic

predictors

Hand PJ et all. Stroke, 2006Liberman AL, Prabhakaran S. Curr Neurol Neurosci Rep 2017

Most frequent causes are:

Causes of stroke Mimics

Kamalian S et all. Applied Radiology, 2015Hand PJ et all. Stroke, 2006.

21%‐ 17%

17%‐13%

13%‐ 11%

15%‐9%

9%

SeizureSeizure

SepsisSepsis

Toxic/metabolicToxic/metabolic

Space occupying lesionsSpace occupying lesions

SyncopeSyncope

• 57% of mimics were neurological conditions

• In +18% of mimics neurological conditions were in the DDX

Causes of stroke Mimics

Hand PJ et all. Stroke, 2006.

Many had normal brainimaging

Most had abnormalbrain imaging

• 75% of mimics withneurological conditions

• 42% of mimics hadprevious stroke

• Stroke mimics account for 2 to 17% of Iv‐tPA treatedpatients

• Incidence of sICH

– Stroke mimics 0.5‐ 1%

– Confirmed stroke patients 4‐ 7.9%

• Median excess cost was approximately US$ 5400 per admission

Stroke Mimics and Thrombolysis

Daniere F et all. Journal of Neuroradiology 2014Zinkstok SM et all, Stroke 2013

“The benefit of rapid treatment with tPA likelyoutweighs the minimal risk of complications associatedwith tPA in stroke mimics”

“The benefit of rapid treatment with tPA likelyoutweighs the minimal risk of complications associatedwith tPA in stroke mimics”

Liberman AL, Prabhakaran S. Curr Neurol Neurosci Rep 2017Goyal N, Journal of Stroke and Cerebrovascular Diseases, 2015

• Introduction




Stroke Mimics Approach based on topographicdistribution patterns

Large artery territoryinfarction

Large artery territoryinfarction

Perforating vessel infarctionPerforating vessel infarction

Border zone patternBorder zone pattern

Hypoxic ischemicencephalopathyHypoxic ischemicencephalopathy

Ischemic white matterdisease

Ischemic white matterdisease

Central embolizationCentral embolization

Regional grey and whitematter

Regional grey and whitematter

Deep grey matter and brain stem

Deep grey matter and brain stem

Vascular watershedborder zones

Vascular watershedborder zones

Cortical and deep gray matter

Cortical and deep gray matter

White matterWhite matter

Scattered fociScattered foci

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• Regional grey and white matter

• Cortical and deep gray matter

• Deep grey matter

• White matter

• Scattered foci

• Border zone pattern

Approach based on topographicdistribution patterns

Regional grey and white matterLarge artery territory infarct

SeizuresSeizures

MigraineMigraine

Brain tumorsBrain tumors

Herpes simplex encephalitisHerpes simplex encephalitis

HypoglicemiaHypoglicemia

Transient global amnesiaTransient global amnesia

MELASMELAS

Venous infarctionsVenous infarctions

• One‐third of strokemimics are due to seizures or postictaldeficits

• Seizures may cause T2 hyperintensity and restricted diffusion

• Distinguishing features– Nonvascular distribution

– Earlier edema and gyral enhancement

– Normal or elevated perfusion

– Absence of vascular occlusion

– Sometimes simultaneous restricted cortical and elevated subcortical diffusion

Regional grey and white matterSeizures

Boulter TJ,Schaeffer PW, Seminars in Radiology 2014Milligan T et all, Seizure 2009Daniere F et all, Journal of Neuroradiology, 2014

Three patterns of diffusion restriction:

• Hypocampus: Ipsilateral to side of seizure onset

• Cortical: Hypoxia, reduced energy suply, cytotoxic edema

• Splenial: excitotoxic damage due to status epilepticus

Seizures

Milligan T et all, Seizure 2009

• Causes 5‐10% of strokemimics

• May show restricted diffusion

• Distinguishing factors– Long history of migraines

– Involvement of multiple arterial territories

– Absence of vascular occlusion

• Perfusion decreases in acute‐onset aura

• Perfusion is normal or elevated in prolonged episodes

• The lesions are usually reversible

Regional grey and white matterMigraine

But remember : 15% of strokes in patients younger than 45 years of age are due to migraineBut remember : 15% of strokes in patients younger than 45 years of age are due to migraine

Regional grey and white matterBrain tumors

• May present with acute neurologic deficits

• Low‐grade glial tumor– Mildmass effect

– Cortical involvement

– May be confused with subacute infarction

• High‐grade gliomas with hemorrhage

– Can show areas of restricted diffusion

– Heterogeneous enhancement

– Mass effect

– May be confused with subacute infarction

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Brain tumors Brain tumors

Distinguishing features

Nonvascular distributionNonvascular distribution

Lack of significant restricteddiffusion

Lack of significant restricteddiffusion

Lack of gyral enhancementLack of gyral enhancement

• Most common cause of viral encephalitis

• Predilection for the limbic system

• Restricted diffusion is observed in early stages

Irreversible neuronal damage

• Cause of restricted diffusion: glutamate excitotoxic pathway

Regional grey and white matterHerpes simplex encephalitis

Kamalian S et all. Applied Radiology, 2015Boulter TJ,Schaeffer PW, Seminars in Radiology 2014

Herpes simplex encephalitis

• Hyperintense on FLAIR images• Frequently hemorrhagic transformation• DWI shows concurrent areas with decreased

and increased diffusivity

• Can present with focal neurologic deficits

• Restricted diffusion may be seen in the cerebral cortex (occipital lobes), corona radiata and centrum semiovale

• Basal ganglia, hippocampi, internal capsules and splenium maybe involved

• Cerebellum, brain stem and hypothalamus are usually spared

Regional grey and white matterHypoglicemia

Kang, AJNR, 2010

Hypoglicemia

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Hypoglicemia

Cause of diffusion restriction:

Energy failure due to lack of glucose

Energy failure due to lack of glucose

Excitotoxic edemaExcitotoxic edema

Asymmetric cerebral bloodflow

Asymmetric cerebral bloodflow

Cortical and deep gray matterHypoxic‐ischemic encephalopathy

Wernicke’s encephalopathy Wernicke’s encephalopathy

Hepatic encephalopathyHepatic encephalopathy

Creutzfeldt‐Jakob disease Creutzfeldt‐Jakob disease

Eastern equine encephalitisEastern equine encephalitis

• In alcoholics and other malnourished patients with thiaminedeficiency

• Clinically presents with:

– Altered mental status

– Memory impairment

– Ophthalmoplegia

– Ataxia

Cortical and deep gray matterWernicke’s encephalopathy

Wernicke’s encephalopathy

Symmetric T2/FLAIR hyperintensity in :• Mammillary bodies• Hypothalami• Medial thalami• Tectal plate and periaqueductal area• Cerebral cortex may also be involved


• Early stages: restricted diffusion due to cytotoxic edema• Later stages: no diffusion restriction

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• Neuropsychiatric abnormalities, potentially reversible

• In chronic and acute hepatic failure

• Clinical severity: West Haven Criteria grades 1‐4

• Diffuse cortical involvement can be reversible, but is associated

with an increased risk of permanent neurologic sequela

• Decrease in ADC values due to the excitotoxic injury and osmotic

disturbance in astrocytes due to ammonia

Cortical and deep gray matterHepatic encephalopathy

McKinney et all AJNR 2010Rovira et all AJNR 2008

Mild case: symmetric T1

hyperintensity in globus pallidus

Hepatic encephalopathy

Hepatic encephalopathy

McKinney et all AJNR 2010Rovira et all AJNR 2008

Severe case: T2 hyperintensity and restricted diffusion

in the cortex (especially the cingulate gyri and insula),

basal ganglia, and thalami

Case courtesy: Fabricio Goncalvez

Cortical and deep gray matterCreutzfeldt‐Jakob disease

• Transmissible and fatal neurodegenerative disease caused by a misfolded prion protein

• Sporadic, familiar and acquired (iatrogenic and variant) forms

• Patients present with a rapidly progressive dementia

• Involvement of the basal ganglia (symmetric)

• Involvement of the cortex (symmetric or assymetric)

• DWI is more sensitive than FLAIR orT2WI

• Decreased ADC Wada R, Kucharczyk W. Neuroimag Clin 2008Boulter TJ, Schaeffer PW. Seminars in Radiology 2014

Creutzfeldt‐Jakob disease

Sporadic CJD• EEG with period sharp wave complexes• 14‐3‐3 protein positive in CSF• sCJD has not pulvinar and hockey stick signs seen in vCJD

Deep gray matter

Perforating vessel infarction

Carbon monoxide poisoning Carbon monoxide poisoning

Osmotic demyelination syndromeOsmotic demyelination syndrome

Vigabatrin toxicity Vigabatrin toxicity

Nonketotic hyperglycemiaNonketotic hyperglycemia

Radiology Assistant.com

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• Delayed encephalopathy :

– Bilateral confluent periventricular white matterT2 hyperintensity

– Areas of restricted diffusion

• Restricted diffusion

– Acute phase : cytotoxic edema

– Delayed phase: demyelination

Deep gray matterCarbon monoxide poisoning

MildMild

Restricted diffusionGPRestricted diffusionGP

T2 hyperintenseGPT2 hyperintenseGP

SevereSevere

Basal ganglia, thalamiBasal ganglia, thalami

Cerebral cortex and wmCerebral cortex and wm

Corpus callosumCorpus callosum

Carbon monoxide poisoning

• Due to rapid correction of hyponatremia

• Can be seen with malnourishment, chronic alcoholism, hyperosmolar conditions, liver transplant

• Patients typically present with pseudobulbar palsy and spasticquadriplegia

Deep gray matterOsmotic demyelination syndrome

Osmotic demyelinationsyndrome

Osmotic demyelinationsyndrome

Central pontineCentral pontine ExtrapontineExtrapontine

• Pontine lesion : centrally located and spares the corticospinal tracts

• Extrapontine lesions : thalamus, basal ganglia, lateral geniculate body

and cerebellar white matter

• T2 hyperintensity may lag up to 2 weeks

Osmotic demyelination syndrome

• Restricted diffusion appears within the first 24 hours and

may persist up to 3 weeks

Osmotic demyelination syndrome

Howard SA et all. RadioGraphics 2009

Howard SA, RadioGraphics

IschemicWhite Matter Disease

White matter

Metronidazole toxicityMetronidazole toxicity

Metrotexate toxicityMetrotexate toxicity

Heroin induced leukoencephalopathyHeroin induced leukoencephalopathy

Multiple sclerosisMultiple sclerosis

Infectious cerebritis and abscessInfectious cerebritis and abscess

thelancet.com

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• Inflammatory demyelinating disorder

• Can present with sudden acute deficits similar to acutestroke

• Acute demyelinating lesions (2‐7 days) may show transientrestricted diffusion

• Cytotoxic edema : Excitotoxic injury to oligodendrocytes, myelin sheaths and axons

White matterMultiple sclerosis

Differentiating factors:

• Typical MRI

• Multiple periventricular, deep and juxtacorticalT2/FLAIR hyperintense lesions

• Combination of clinical features and short‐term follow‐up imaging

Multiple sclerosis

Differentiating factors:

• Typical MRI

• Multiple periventricular, deep and juxtacorticalT2/FLAIR hyperintense lesions

• Combination of clinical features and short‐term follow‐up imaging

Multiple sclerosis

Small vessel disease

Multiple sclerosis

Scattered punctate fociCentral embolism

Diffuse axonal injuryDiffuse axonal injury

Fat embolismFat embolism

MetastasesMetastases

• Disruption of axons

• Caused by rapid deceleration or rotational forces

• Severe head trauma

• Multiple foci of restricted diffusion and/or hemorrhage

• Restricted diffusion for days to weeks

Scattered punctate fociDiffuse axonal injury

• Located at gray‐white matter interface and along the cerebral white matter fiber tracts, corpus callosum and brainstem

• Differentiating features:

– Nonvascular distributions and sparing of cortex

– Presence of early hemorrhage

– Clinical context of head trauma

Diffuse axonal injury

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• Secondary to spread of fat globules that reach the systemiccirculation and lung

• Setting of a recent long bone fracture or orthopedic procedure

• Can also occur following pulmonary contusion, cardiac surgeryor liposuction

• Patients present with– Changes in the respiratory pattern

– Neurologic deficits

– Petechial rash

• Not a clear knownmechanism, toxic intermediaries proposed

Scattered punctate fociFat embolism

Kamalian S et all. Applied Radiology, 2015 Boulter TJ,Schaeffer PW, Seminars in Radiology 2014

Endothelial injury and microhemorrhages

Fat embolism

• Punctate foci of restricted diffusion in white and gray matter

• Multiple hypointense foci on SWI

• Highly cellular metastases (small cell lung carcinoma)

– Can show restricted diffusion

– May be confused with subacute central embolic infarcts

• Features favoring metastases

– Presence of vasogenic edema surrounding the larger lesions

– Ring‐pattern enhancement

– Additional sites of disease

– Absence of large infarcts due to more proximal emboli

Scattered punctate fociMetastases

Differentiating factors

• Vasogenic edema

• Ring‐pattern enhancement

• Additional sites of disease

• Absence of large infarctsdue to more proximal emboli

Metastases

Boulter TJ,Schaeffer PW, Seminars in Radiology 2014

Border zone patternBorder zone infarction

Severe carotid stenosis,Moya Moya, RCVS

Posterior reversible encephalopathy syndrome (PRES) Posterior reversible encephalopathy syndrome (PRES)

Cerebral hyperperfusion syndromeCerebral hyperperfusion syndrome

Manga et all. Radiographics 2011Radiology Assistant.com

• Posterior reversible encephalopathy syndrome

• Loss of vascular autoregulation and capillary leakage leads to vasogenic edema

• Clinical presents with headaches, cortical visual symptoms, seizures, and confusion

• Triggered by

– Hypertension

– Eclampsia/ pre‐eclampsia

– Critical medical illness

– Immunosuppressants

Border zone patternPRES

Petrovic, Radiol Clin N Am ,2011

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• T2‐FLAIR hyperintensity with elevated diffusion

• Bilateral occipital and parietal lobes

• Borderzone distribution between the anterior and middle cerebral arteries

• Restricted diffusion in 10–25% patients

• Intraparenchymal hemorrhage in 15% of cases

PRES

• Introduction




Stroke Mimics

Approach to MRI and CT in StrokeMimics

Regional grey and white matter



Deep grey matterDeep grey matterCortical and deep

gray matterCortical and deep

gray matter

Border zonepattern

Border zonepattern








gray matter

Border zonepattern

Border zonepattern


Border zoneinfarction

Central embolismIschemicWhite Matter Disease

Perforating vessel

infarction

Hypoxic‐ischemic

encephalopathy

Large arteryterritory infarct







gray matter

Border zonepattern

Border zonepattern




Perforating vessel

infarction

Hypoxic‐ischemic

encephalopathy


Central embolism







gray matter

Border zonepattern

Border zonepattern




Perforating vessel

infarction

Hypoxic‐ischemic

encephalopathy


Posterior reversible encephalopathy syndrome (PRES) Posterior reversible encephalopathy syndrome (PRES)

Cerebral hyperperfusion syndromeCerebral hyperperfusion syndrome

Diffuse axonal injury

Fat emboli

Metastases

Metronidazole toxicityMetronidazole toxicity

Metrotexate toxicityMetrotexate toxicity

Heroin induced leukoencephalopathyHeroin induced leukoencephalopathy

Multiple sclerosisMultiple sclerosis

Infectious cerebritis and abscessInfectious cerebritis and abscess


Hepatic encephalopathyHepatic encephalopathy

Creutzfeldt‐Jakob disease Creutzfeldt‐Jakob disease

Eastern equine encephalitisEastern equine encephalitis

Carbon monoxide poisoning Carbon monoxide poisoning

Osmotic myelinolysisOsmotic myelinolysis

Vigabatrin toxicity Vigabatrin toxicity

Nonketotic hyperglycemiaNonketotic hyperglycemia

SeizuresSeizures

MigraineMigraine

Brain tumorsBrain tumors

Herpes simplex encephalitisHerpes simplex encephalitis

HypoglicemiaHypoglicemia

Transient global amnesiaTransient global amnesia

MELASMELAS

Venous infarctionsVenous infarctions

Central embolism

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• Introduction




Stroke Mimics Take home messages

• Up to 30% of suspected strokes are strokemimics

• Most frequent causes of strokemimics are:

– Seizures, sepsis, toxic/metabolic, space occupying lesions, syncope

• Inaccurate Dx can lead to unnecessary administration of

thrombolytic therapy or delays in appropriate therapy

Take home messages

• Review the clinical records of the patients

• Have an adequate knowledge of the vascular territories and evolution of images on stroke

• Remember there are different causes of diffusion restriction

• Always keep alternate diagnoses in mind when you are lookingat the images

• Use a careful pattern based approach

StrokeMimics Stroke Mimics - esnr.org

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