Ischemic stroke

ACUTE CEREBRAL ISCHEMIAINFARCTION

Terminology
Interrupted blood flow to
brain resulting in cerebral
ischemia/infarction with
variable neurologic deficit

ACUTE CEREBRAL ISCHEMIAINFARCTION

Imaging
Major artery (territorial) infarct
Generally wedge-shaped; both GM, WM involved
Embolic infarcts
Often focal/small, at GM-WM interface
NECT
Hyperdense vessel (high specificity, low sensitivity)
"Dense MCA" sign: Acute thrombus in artery
Loss of GM-WM distinction in 1st 3 hours (50-70%)
"Insular ribbon" sign: Loss of gray-white
differentiation of insular cortex

CT Findings :NECT
Hyperdense vessel (high specificity, low
sensitivity)
Represents acute thrombus in cerebral
vessel(s)
Hyperdense Ml MCA in 35-50%
"Dot" sign: Occluded MCA branches in
sylvian fissure (16-17%)
Loss of GM-WM distinction in 1st 3 hours
(50-70%)
Obscuration of deep gray nuclei

CT Findings:NECT
Parenchymal hypodensity

If> 1/3 MCA territory initially,

larger lesion usually develops later

Temporary transition to isodensity

(up to 54%) at 2-3 weeks post-ictus
(CT "fogging")
Gyral swelling, sulcal effacement 1224 hours
"Hemorrhagic transformation" in 1545%

CECT
Enhancing cortical vessels: Slow flow
or collateralization acutely
Absent vessels: Occlusion
Perfusion CT (pCT): Assess ischemic
core vs. penumbra; identify patients
who benefit most from
revascularization
pCT calculates cerebral blood flow
(CBF),cerebral blood volume (CBV),
time to peak (TIP); deconvolution
can give mean transit time (MTI)

CECT
Cortical gyral enhancement after 4872 hours
CTA: Identify occlusions, dissections,
stenoses, status of collaterals

ACUTE CEREBRAL ISCHEMIAINFARCTION

ACUTE CEREBRAL ISCHEMIAINFARCTION

ACUTE CEREBRAL ISCHEMIAINFARCTION

ACUTE CEREBRAL ISCHEMIAINFARCTION

ACUTE CEREBRAL ISCHEMIAINFARCTION

SUBACUTE CEREBRAL
INFARCTION
Terminology
Subacute infarction
approximately 2-14 days
following initial ischemic event

CT Findings :NECT
Wedge-shaped area of decrease
attenuation involving gray and white
matter
Mass effect initially increase, then
decrease by 7-10 days; often less than
expected given lesion size as acuity
resolves
HT of initially ischemic infarction
occurs in 15-20% of MCA occlusions,
usually by 48-72 hours
Common are basal ganglia and

CECT
Enhancement typically patchy or gyral
Appear as early as 2-3 days after
ictus, persists up to 8-10 weeks
"2-2-2" rule = enhancement begins at
2 days, peaks at 2 weeks, disappears
by 2 months

CTA
Evidence of subacute occlusion
correlates strongly,independently with
poor clinical outcome
Significantly worse discharge
National Institutes of Health Stroke
Scale (NIHSS) score
CT perfusion
More useful in acute> subacute stroke
Helpful in predicting tissue outcome
Significant difference between infarct
and peri-infarct tissue for both

SUBACUTE CEREBRAL
INFARCTION

SUBACUTE CEREBRAL
INFARCTION

SUBACUTE CEREBRAL
INFARCTION

SUBACUTE CEREBRAL
INFARCTION

SUBACUTE CEREBRAL
INFARCTION

DIFFERENTIAL DIAGNOSIS

Neoplasm
DWl: Vasogenic ("tumoral") edema instead of cytotox
edema
Enhancing mass instead of patchy, gyral enhanceme
Will not regress on follow-up imaging
Encephalitis/ Cerebritis
Gyriform, ring-enhancing patterns (late cerebritis)
Nonvascular distribution
Different clinical presentation

DIFFERENTIALDIAGNOSIS
Venous Infarction
Non arterial distribution
Venous instead of arterial occlusion, typically
major dural sinus
Commonly hemorrhagic, affecting white
matter of cortex
Different clinical presentation/setting
(trauma,hypercoagulable states, pregnancy,
dehydration)

CHRONIC CEREBRAL INFARCTION

Etiology
Prolonged cerebral ischemia
Duration and severity of ischemic
insult determines cellular viability
Results of CI vary with sensitivity of
individual cell types to ischemia

CT Findings
NECT
Focal, well-delineated low-attenuation areas in
affected vascular distribution
Adjacent sulci become prominent; ipsilateral
ventricle enlarges
Wallerian degeneration may be present
Dystrophic Ca++ may very rarely occur in
infarcted brain

CECT:No enhancement
CTA:May see lack of flow in affected
vessel

DIFFERENTIAL DIAGNOSIS
Porencephalic Cyst
Congenital cyst typically seen in younger age
groups
Also lined by gliotic white matter

Arachnoid Cyst
No gliotic margins
Usually in locations atypical for vascular
territory
Intact gray matter lining brain, displaced by
cyst

DIFFERENTIAL DIAGNOSIS
Postoperative/Post -Trau matic
Encephalomalacia
History and associated findings help to
distinguish
May see leptomeningeal cyst in posttraumatic setting
Low-Attenuation Tumors
Typically shows mass effect
Usually slightly hyperdense/intense
compared to CSF

CHRONIC CEREBRAL INFARCTION

CHRONIC CEREBRAL INFARCTION

CHRONIC CEREBRAL INFARCTION

CHRONIC CEREBRAL INFARCTION

CHRONIC CEREBRAL INFARCTION

ACA CEREBRAL INFARCTION

Terminology
Ischemia/infarct in part or all of ACA vascular
territory
Imaging
CT: Hypodensity/loss of GM/WM differentiation in
cortical ACA distribution
Hypodensity in caudate head, anteromedial
putamen/globus pallidus, anterior limb of internal
capsule (lenticulostriate arteries)
Perfusion CT shows decrease CBF/CBV, increase TTP
in medial cerebral hemisphere

Top Differential Diagnoses

Cerebral edema
Herpes encephalitis
Subdural effusion, empyema

ACA CEREBRAL INFARCTION

ACA CEREBRAL INFARCTION

MCA CEREBRAL INFARCTION

Terminology
Occlusion of middle cerebral artery (MCA)resulting in
ischemia and infarct
Imaging
Best imaging clue: Abnormal perfusion or diffusion in
MCA territory
CT: Hypodensity in frontal, parietal, &/or temporal
lobes +/- basal ganglia (BG)
CT perfusion and CTA in acute setting
CBFand CBVcan help predict ischemic core /penumbra
CTA can identify occlusion

MCA CEREBRAL INFARCTION

DWl MR: Restricted diffusion in MCA
territory
> 95% sensitive for hyperacute stroke
detection

Middle cerebral artery comprised of 4

segments:
Horizontal (Ml), insular (M2), opercular
(M3),cortical (M4) segments

MCA CEREBRAL INFARCTION

MCA CEREBRAL INFARCTION

Top Differential Diagnoses

Traumatic cerebral edema
Herpes encephalitis

PCA CEREBRAL INFARCTION

Imaging
Best imaging clue: CT hypodensity or
DWl/FLAIR/T2 hyperintensity in PCA vascular
distribution
Occipital or inferior temporal lobes commonly
Also includes thalamus, hypothalamus,
geniculate bodies, internal capsule posterior
limb, upper midbrain, choroid plexus
PCA ischemia may arise from anterior circulation
emboli if PCA of fetal-origin is present

PCA CEREBRAL INFARCTION

Segmental anatomy of PCA
PI (precommunicating segment)
P2 (ambient segment)
P3 (quadrigeminal segment)
P4 (calcarine or cortical segment)

PI and P2: Primarily supply inferolateral temporal lobes

and occipital lobes
Perforators and posterior choroidal arteries also supply
thalamus, hypothalamus, internal capsule posterior limb,
midbrain, choroid plexus

P3 and P4: Supply posterior 1/3 of brain along

interhemispheric fissure, lower parietal, occipital and
temporal lobe

PCA CEREBRAL INFARCTION

PCA CEREBRAL INFARCTION

Top Differential Diagnoses

Herpes encephalitis
Low-grade diffuse astrocytoma
Traumatic cerebral edema
Acute hypertensive encephalopathy,
PRES

CHOROIDAL ARTERY CEREBRAL

INFARCTION
Terminology
Infarct of anterior choroidal or
medial/lateral
posterior choroidal arteries

Imaging
Best diagnostic clue: Acute ischemia in
choroidal artery distribution
NECT: Hypodensity in medial temporal
lobe,thalamus, or lateral midbrain
MR: DWI/T2/FLAIR hyperintensity in choroidal
artery territory

Anatomy

Anterior choroidal artery arises from ICA

Supplies optic tract, lateral midbrain,
uncus, thalamus, and posterior limb of
internal capsule
Medial/lateral posterior choroidal arteries
arise from P2 segment of PCA
Supply pulvinar, part of thalamus, medial
temporal lobe, splenium, and choroid
plexus

CHOROIDAL ARTERY CEREBRAL

INFARCTION

CHOROIDAL ARTERY CEREBRAL

INFARCTION

Top Differential Diagnoses

Mesial temporal sclerosis
Herpes encephalitis
Low-gradediffuse astrocytoma

Top of basilar cerebral infarction

Terminology
Infarct of rostral brainstem and
cerebral hemispheres supplied by
distal basilar artery
Clinically recognizable syndrome
characterized by visual, oculomotor,
and behavioral abnormalities.

Basilar thrombosis cerebral

infarction
Terminology
Infarct of pons + midbrain secondary to basilar
artery occlusion; may result in locked in
syndrome
Imaging
Best imaging clue CTA with basilar artery filling
detect + hypodensity/hyperintensity of pons
CT imaging: May see hyperdense basilar artery
NECT: Low attenuation in pons, + hemorrhage
CTA: Occlusion, filling defect, dissection, or stenosis of
basillar artery

Basilar perforating artery

cerebral infarction
Terminology
Focal infarct in pons or pontomedullary
junction secondary to pontine perforator or
basilar branch artery ischemia
Pontine perforating or basilar branch arteries
usually produce unilateral paramedian, lateral
pontine, or pontine tegmental infarcts

Basilar perforating artery

cerebral infarction

Imaging
Best imaging clue: DWI/FLAIR/T2
hyperintensity in pons, typically
respects midline
NECT: Focal hypodensity in medial,
paramedian, or lateral pons
Rule out basilar artery occlusion or
stenosis with MRA or CTA

Superior cerebellar artery

cerebral infarction
Terminology
Infarct of superior cerebellum + upper
pons, supplied by superior cerebellar
artery (SCA)
Imaging
Best imaging clue: T2/FLAIR
hyperintensity in superior cerebellum
+ uppper lateral pons

AICA Cerebellar infarction

Imaging
Best diagnostic clue: DWI/T2/FLAIR
hyperintensity in anterior inferior
cerebellar artery (AICA) territor.
NECT findings of early ischemia may
be masked by beam harderning
artifact in posterior fossa.

PICA Cerebellar infarction

Terminology
Ishemia in posterior inferior cerebellar
artery (PICA) distribution.
Inferior cerebellar hemispheres,
lateral medulla, inferior vermis,
tonsils.

PICA Cerebellar infarction

Imaging
Best imaging clue: Diffusion restriction
of PICA territory, typically lateral
medulla and majority of lower
cerebellar hemispheres.
PICA: Supplies inferir cerebellar
hemispheres, lateral medulla, inferior
vermis, tonsils, choroid plexsus.

Lacunar infarction
Definitions
Small, deep cerebral infarcts typically
located in basal gaglia (BG) and
thalamus, < 15 mm in size.
lacuna used to describe small focus
of encephalomalacia, mostly in basal
ganglia

Lacunar infarction

General Features
Best diagnostic clue
Small , well-circumscribed areas of
parenchymal abnormality (encephalomalacia
in BG, thalamus.
Location
Commonly deep gray nuclei, especially
putamen, thalamus, caudate nuclie : interna
capsule, pons

Lacunar infarction
General Features
Size
Ranges from microscopic to 15 mm.
Majority < 8 mm.
Morphology
Typically round or ovoid.

Lacunar infarction
CT Finding
NECT
Because the small size, most true lacunar
infarcts are not seen on CT scans.
Visible lacunes are seen as small, wellcircumscribed areas of low (CSF) attenuation.
Usually seen in setting of more extensive white
matter disease; typically multiple.
CECT
May enhance if late acute/early subacute.

Thank for your

attention

Reference