IMAGING IN STROKE

DEFINITION

ETIOLOGY

STROKE

ISHEMIC HEMORRHAGIC

ARTERIAL VENOUS

EVOLUTION OF HEMORRHAGE

ARTERIAL ISCHEMIC STROKE

ASCO phenotypic system. TOAST classification system.

In acute stroke, there is a central, irreversibly infarcted tissue core surrounded by a peripheral region of stunned cells called the penumbra that receives a collateral blood supply from uninjured arterial and leptomeningeal territories .

The cells in the penumbra are potentially salvageable with early recanalization.

CHRONOLOGY OF STROKE

Early hyperacute-0-6 hrs Late hyperacute-6-24 hrs Acute-24 hrs-1 week Subacute -1-3 weeks Chronic -> 3weeks

CBV is defined as the volume of blood in a given amount of brain tissue, most commonly milliliters of blood per 100 g of brain tissue.

CBF is defined as the volume of blood passing through a given amount of brain tissue per unit of time, most commonly milliliters of blood per minute per 100g of brain tissue.

Mean transit time (MTT) corresponds to the average time, in seconds, that red blood cells spend within a determinate volume of capillary circulation.

MTT = cerebral blood volume (CBV) / cerebral blood flow

IMAGING MODALITIES

Computed tomography, Magnetic Resonance Imaging, Duplex sonography.

COMPARISON B/W IMAGING MODALITIES

IMAGING IN STROKE

<6hrs <24hrs >72hrs

MRI SE 50% 80% 100%

DWI 70% 100% 100%

CT 30% 50% 95%

SENSITIVITY

GOALS OF IMAGING Parenchyma Pipes Perfusion Penumbra

NECTCT AngiographyPerfusion CT & CT angiographyPerfusion CT & CT angiography

HYPER ACUTE & ACUTE STROKE

In 50-60% cases imaging helpsNECT- Dense MCA sign Blurring with indistinctness of GM-WM junction Insular ribbon sign Disappearing basal ganglia sign Wedge shaped parenchymal hypodensity with

indistinct GM-WM borders & sulcal effacement Malignant MCA infarct

ASPECTS infarct scoring system Two NECT slices Ten regions One point is detected for each area involved <7 indicates > 1/3 MCA territory.

CECT- Intravascular enhancement is noticed

CT Angiography- To assess intra& extra cranial circulation for occlusion Triple rule out p CT –CBV,CBF,MTT are calculated Color coding is done based on perfusion Well perfused GM- red/yellow, WM- blue Ishemia – blue/ purple Non perfused – black For MTT, the slower the transit time the closer to the red

end of the scale

CTA shows an abrupt “cutoff” with a meniscus of contrast in the proximal left MCA. Contrast in the distal M2 and M3 segments is caused by slow retrograde collateral flow from pial branches of the ACA across the watershed to M4 (cortical) branches .

NECT shows hypodensity of the right basal ganglia compared to the normal. pCT was performed CBV shows markedly reduced blood volume in the right basal ganglia compared to the normal left side . CBV in the cortex overlying the basal ganglia infarct appears relatively normal.

MRIExpedited protocol with only FLAIR,T2*,DWI T1WI- normal in first 3-6 hrs. subtle gyral swelling & hypointensity-12-24 hrs loss of flow void T2WI-positive after 12-24 hrs FLAIR- 30-50% positive with in 4 hours& positive in all

cases by 7 hrs intraarterial hyperintensity early sign T2* - Blooming hypointensity In older patients look for blooming black dots as

they pose for subsequent anti-coagulant related hemmorhage

DWI- Positive in > 95% cases within minutes Hyperintense on DWI Hypointense on ADC mappingMismatch between FLAIR & DWI – PENUMBRADWI negative strokes p MR - for at risk penumbra. DSA- For patients undergoing intraarterial

thrombolysis or mechanical thrombectomy.

SUBACUTE STROKE 2 days - 2 weeks

Increased edema , mass effect , hemorrhagic transformation occurs

NECT- Wedge shaped hypodensity becomes well defined Mass effect increases & then decreases with in 7- 10 days Hemorrhagic transformation is seen as gyriform or Cortical or basal ganglia hyperintensity -HT

CECT- 2-2-2 rule patchy or gyriform hyperintensity at 2

days peaks at 2 weeks disappears at 2 months

MRI-

T1WI-hypointensity (NH) or isointensity(HT) + mass effect + sulcal effacement

T2WI- Hyperintensity to isointensity ( T2 fogging effect)

FLAIR-Hyperintensity.

T2*-blooming foci in HT

T1C+ - Leptomeningeal enhancement

DWI-restriction with hyperintensity on DWI & hypointensity on ADC which gradually reverses.

DD: Neoplasms – no restriction on DWI & do not regress

with time Infections –no defined vascular distribution

FLAIR (left) and GRE (right) in the same case show HT in this example of subacute stroke

Axial T1WI at 2 weeks after stroke onset shows hemorrhagic BG transformation , persisting gyral swelling with sulcal effacement

T1 C+ FS scan in the same patient shows intense enhancement characteristic of subacute infarction

CHRONIC INFARCTSVolume loss with gliosis NECT- Well defined wedge shaped

hypodensity that involves both the GM & WM confined to the vascular territory of the involved artery

Ipsilateral sulci are prominent & ventricle may be dilated

CECT- non enhancing MRI- CSF equivalent signal intensity on all

sequences with gliosis being hyperintense on FLAIR & ADC

Encephalomalacia in the left MCA distribution . Basal ganglia were spared.

T2WI shows hyperintensity in the same distribution. (R) FLAIR shows the difference between encephalomalacia , gliosis

MULTIPLE EMBOLIC INFARCTS

Involves terminal cortical branches GM-WM interface most commonly effectedIMAGINGNECT: Low attenuation foci in wedge shaped

distribution. Calcification in atherosclerotic emboli. Hemorrhage in septic infarcts.CECT: Multiple ring enhancing lesions.

MRI: Multiple peripheral T2/FLAIR hyperintensities. Blooming on T2* sequences. Multiple punctate enhancing foci on T1C+. Small peripheral foci of diffusion restriction in

several different vascular distributions on DWI.

NECT scan in a patient with infected mitral valve, decreasing mental status shows 2 hemorrhagic foci at the GM-WM junctions of both occipital lobes. (Right) Scan through the corona radiata shows additional hemorrhagic foci . Findings suggest multiple septic emboli. DWI shows multiple foci of restricted diffusion at the GM-WM junctions of both hemispheres.

LACUNAR INFARCTS Secondary to lipohyalinosis & atherosclerotic

occlusion of perforating branches that arise from the circle of Willis & peropheral cortical arteries

Most commonly seen around the basal ganglia,thalami, internal capsule, deep cerebral white matter & pons.

IMAGING FINDINGS Acute infarcts (< 1 week) may not be visible on NECT Chronic lacunae may appear as well-defined CSF like

holes . Acute lacunae may be visible only on T2W images. On T1W decreased signal intensity & on T2W

increased signal intensity is noted. On FLAIR fluid is suppressed where as the peripheral

gliosis gives a higher signal intensity Blooming is noticed on T2* if associated with chronic

hypertension. Acute lacunar infarcts restrict on DWI & may

enhance on T1C+.

Axial T1WI in a 43-year-old woman with a long history of drug abuse shows multiple hypointensities in the basal ganglia, thalami, and deep cerebral white matter .

Axial T2WI in the same patient demonstrates the characteristic hyperintensity and irregular shape of typical lacunar infarcts

FLAIR scan in the same patient shows that older lacunae suppress completely whereas more recent lesions have a hyperintense rim of gliotic tissue surrounding a hypointense center that is not yet completely CSF-like. T2* GRE scan shows no evidence of hemorrhage

WATERSHED INFARCTS Occur at the junction between the two

nonanastamosing distal arterial distributionsExternal watershed zones: Frontal cortex( b/w ACA & PCA junction) Parietoocipital cortex ( b/w MCA & PCA junction) Paramedian subcortical white matter near the

vertex.Internal watershed zones: Junction b/w penetrating branches & major

cerebral vessels.

Axial FLAIR scan demonstrates typical findings of bilateral external (cortical) watershed infarcts

Nearly symmetric confluent and punctate deep white matter hyperintensities are seen above and behind the lateral ventricles .FLAIR scan just above the previous image shows distinct bilateral rosary-like white matter hyperintensities

ADC DWI FLAIR T1 T1 C T2

Early hyperacute

Low High Variable

Isointense Arterial enhancement f/b parenchymal

Isointense Loss of flow void

Late hyperacute

Low High High Low after 16 hrs

Arterial f/b parenchymal & meningeal enhancement

Variable ;High after 8 hrs

Acute Low High High Low ;hyperintense if cortical necrosis

Arterial f/b parenchymal & meningeal enhancement

High

Subacute Low f/b pseudonormalisation f/b high

High then iso to hypo then hyper

High Low Parenchymal enhancement

High

Chronic High Variable

Low Low Parenchymal High

VENOUS INFARCT Secondary to venous obstruction which may be

due to cerebral venous thrombosis(M.C) ,trauma ,post surgical ligation.

Increased venous pressure due to any cause leads to vasogenic edema ,if the process continues it may lead to arterial infarction.

THROMBOSED AREA INFARCTED AREASagittal sinus Para sagittal areaLabbe s vein Temporal lobeDeep venous system B/L or U/L involvement

of thalami , basal ganglia , internal capsule

IMAGING MODALITIES

CT MRI

CT: 30% sensitiveNECT Hyperdensity of involved vein – cord sign Thrombosis of posteior portion of SSS –filled

delta sign/ dense triangle sign Ishemic area that crosses the arterial territory ,

involvement of subcortical area with sparing of cortical areas with or with out hemorrhagic component .

CECT Enhancement of the dural lining with the filling

defect. Central hypodensity due to slow or absent flow

surrounded by contrast enhancement in posterior aspect of SSS- EMPTY DELTA SIGN

CT VENOGRAPHY: Direct visualization of thrombus as filling defect.

CORD SIGN

MRI Loss of flow void which is best depicted on T2,FLAIR. MR venography

Age T1 T2/FLAIR Other sAcute Isointense Hypointense Enlarged &

convex margins

Subacute Hyperintense

Hyperintense

Chronic Isointense Isointense Collateral drainageDura-arachnoid thickening

ACUTE THROMBUS IN RT TS

SUBACUTE STAGE

HEMORRHAGIC STROKE

Spontaneous (nontraumatic) primary intracranial hemorrhage (pICH) causes about 15% of strokes.

GOALS OF IMAGING:1. Detect & locate the bleed.2. Age the bleed.3. Determine the underlying etiology

ARTERIAL INFARCT VENOUS INFARCTDon’t cross arterial territories Crosses arterial territoryInvolves both grey & white matter

Spares grey

HYPERTENSIVE ICH

Acute manifestation of nontraumatic ICH secondary to systemic hypertension (HTN)

The putamen/external capsule (striatocapsular hemorrhages) is MC f/b thalamus,pons & cerebellum

Lobar hemorrhages-5-10%.

CEREBRAL AMYLOID ANGIOPATHY

1% of all strokes and 15-20% of primary intracranial bleeds in patients over the age of 60 years.

Mean age at onset is 73 years. Patients with CAA are usually normotensive and

moderately demented. Distribution of hemorrhages in CAA is typically lobar

and peripheral.

SUMMARY Imaging plays a key role in diagnosing the stroke It also plays a key role in guiding the further

management. MRI is more sensitive than CT in detecting the early

changes which are often subtle on CT. Expedite MRI protocol which includes FLAIR ,T2*,DWI

will answer the all questions needed in an acute settting.

THANK YOU