IMAGING IN

ACUTE STROKE

Dr Anoop.K.RAsst professor

General MedicineMMCH,Calicut

Vascular territories of the brain

Left ACA territory

Right ACA territory

Right MCA territory

Diffusion-weighted MRI of the brain showing a large-vessel ischemic stroke of the left middle cerebral artery (MCA) territory

Left PCA territory

PICA Infarction

Sharp midline delineation

SCA territory

Right AChA territory

Right lateral lenticulostriate artery territory

Watershed zones

The term stroke is most accurately used to describe a clinical event that consists of the sudden onset of neurologic symptoms.

Cerebral infarction, by contrast, is a term that describes a lethal tissue-level ischemic event that may or may not cause symptoms.

• In the absence of blood flow, available energy can maintain neuronal viability for 2-3 minutes

• In the brain, ischemia is incomplete, with collateral supply

• Cerebral ischemia = central irreversibly infarcted tissue core surrounded by peripheral region of stunned cells, the ‘penumbra’

• The penumbra is potentially salvageable with early recannalization

Cerebral infarction accounts for approximately 85% of all stroke.

-- which may be arterial ( large vessel or small vessel ) or venous

Primary cerebral hemorrhages account for most of the remainder.

The goals of an imaging evaluation for acute stroke are to:

•Establish a diagnosis as early as possible

•Guide appropriate treatment

•Assess location and size of territory involved

•Rule out hemorrhage and stroke mimics

•Obtain accurate information about the intracranial vasculature and brain perfusion for guidance in selecting the appropriate therapy

• Parenchyma: – Assess early signs of acute stroke, rule out hemorrhage

• Pipes – Assess extracranial circulation (carotid and vertebral

arteries of the neck) and intracranial circulation for evidence of intravascular thrombus

• Perfusion – Assess cerebral blood volume, cerebral blood flow, and

mean transit time• Penumbra

– Assess tissue at risk of dying if ischemia continues with out re-canalization of intravascular thrombus

The speed, widespread availability, low cost, and accuracy in detecting subarachnoid and intracranial hemorrhage have led CT scanning to become the first-line diagnostic test for the emergency evaluation of acute stroke.

Head CT scans can detect ischemic brain regions within 6 h of stroke onset.

Importantly, the identification of ischemic brain tissue by CT not only defines regions likely to infarct, but also may predict outcome and response to intravenous (i.v.) or intra-arterial (i.a.) thrombolytic therapy.

CT is used to exclude parenchymal hemorrhage and significant established infarction.

Unenhanced CT findings can additionally,in some settings, help to predict hemorrhagic transformation of already necrotic tissue following arterial reperfusion.

Early ischemic signs

1. Focal parenchymal hypodensity– Of the insular ribbon – Of the lenticular nuclei

2. Cortical swelling with sulcal effacement

3. Loss of gray-white matter differentiation

4. Hyperdense MCA sign

Certain points to be kept in mind

• to maximize image quality – especially of the posterior fossa structures

• to minimize radiation dose

• to minimize helical artifact

• to minimize image noise

Hypointensities

Insular ribbon sign

Effect of patient position

Large MCA infarct

Hyperdense MCA sign

Physical basis of imaging findings

A 1% increase in net tissue water produces 2.5 HU decrease on NCCT

The finding of early (up to 6 h) parenchymal hypodensity has been hypothesized to be secondary to cytotoxic edema, caused by lactic acidosis and failure of cell membrane ion pumps due to an inadequate ATP supply.

This process may involve redistribution of tissue water from the extracellular to the intracellular space, but because there is little overall change in net tissue water, there is only minimal reduction in gray and white matter brain parenchymal Hounsfield attenuation.

When stroke-related edema is extensive and life-threatening, it is sometimes called malignant brain edema.

Life-threatening brain edema that is associated with stroke occurs most commonly in patients with extensive ischemia in the temtory of a middle cerebral artery (MCA).

Interesting phenomenon occurs in the subacute phase of stoke is the “CT fogging effect,” in which irreversibly infarcted regions “disappear” on unenhanced CT performed on older generation scanners, 2–6 weeks after stroke onset

Effect of narrowing window width

• The Alberta Stroke Programe Early CT Score (ASPECTS) is a 10-point quantitative topographic CT scan score used in patients with middle cerebral artery (MCA) stroke.

• Segmental assessment of MCA territory is made and 1 point is removed from the initial score of 10 if there is evidence of infarction in that region.

• caudate • putamen • internal capsule* • insular cortex • M1: "anterior MCA cortex," corresponding to frontal operculum • M2: "MCA cortex lateral to insular ribbon" corresponding to

anterior temporal lobe • M3: "posterior MCA cortex" corresponding to posterior temporal

lobe

•M4: "anterior MCA territory immediately superior to M1"

•M5: "lateral MCA territory immediately superior to M2"

•M6: "posterior MCA territory immediately superior to M3"

(M1 to M3 are at the level of the basal ganglia and M4 to M6 are at the level of the ventricles immediately above the basal ganglia)

An ASPECTS score less than or equal to 7 predicts worse functional outcome at 3 months as well as symptomatic haemorrhage.

Lacunar infarcts

• Lacunar infarcts are small infarcts in the deeper parts of the brain (basal ganglia, thalamus, white matter) and in the brain stem.

• Lacunar infarcts are caused by occlusion of a single deep penetrating artery.

• Lacunar infarcts account for 25% of all ischemic strokes.

• Atherosclerosis is the most common cause of lacunar infarcts followed by emboli.

NECT

• Because of their small size, most "true" lacunar infarcts not seen on CT scans

• Visible lacunes seen as small, well circumscribed areas of low (CSF) attenuation

• Usually seen in setting of more extensive white matter disease; typically multiple

MR Findings• Tl WI: Small, well circumscribed hypointense foci• T2WI: Small, well circumscribed hyperintense foci

• FLAIR:Typically increased in signal

• DWIo Restricted diffusion (hyperintense) if acute/subacuteo May show small lesions otherwise undetectable

• Tl C+: May enhance if late acute/early subacute

• MRA: Normal

Lacunes may be confused with other empty spaces, such as enlarged perivascular Virchow-Robin spaces (VRS).The VRS are extensions of the subarachnoid space that accompany vessels entering the brain parenchyma.

The goal of imaging in a patient with acute stroke is:

• Exclude hemorrhage • Differentiate between irreversibly affected

brain tissue and reversibly impaired tissue (dead tissue versus tissue at risk)

• Identify stenosis or occlusion of major extra- and intracranial arteries

CT SCAN

• CT has the advantage of being available 24 hours a day and is the gold standard for hemorrhage. Hemorrhage on MR images can be quite confusing. On CT 60% of infarcts are seen within 3-6 hrs and virtually all are seen in 24 hours.

CT SIGNS

1.Hypoattenuating brain tissue

• The diagnosis is infarction, because of the location (vascular territory of the middle cerebral artery (MCA) and because of the involvement of gray and white matter, which is also very typical for infarction.

2.Obscuration of the lentiform nucleus

• Obscuration of the lentiform nucleus, also called blurred basal ganglia, is an important sign of infarction.It is seen in middle cerebral artery infarction and is one of the earliest and most frequently seen signs.The basal ganglia are almost always involved in MCA-infarction.

3.Insular Ribbon sign

• This refers to hypodensity and swelling of the insular cortex. It is a very indicative and subtle early CT-sign of infarction in the territory of the middle cerebral artery. It has to be differentiated from herpes encephalitis.

4.Dense MCA sign

• This is a result of thrombus or embolus in the MCA.

Hemorrhagic infarcts15% of MCA infarcts are initially hemorrhagic.

???

CTA

MRI

• On T2WI and FLAIR infarction is seen as high SI.These sequences detect 80% of infarctions before 24 hours.They may be negative up to 2-4 hours post-ictus!

• High signal on conventional MR-sequences is comparable to hypodensity on CT.It is the result of irreversible injury with cell death.So hyperintensity means BAD news: dead brain.

Diffusion Weighted Imaging (DWI)• DWI is the most sensitive sequence for stroke

imaging.DWI is sensitive to restriction of Brownian motion of extracellular water due to imbalance caused by cytotoxic edema.Normally water protons have the ability to diffuse extracellularly and loose signal. High intensity on DWI indicates restriction of the ability of water protons to diffuse extracellularly.

This is why DWI is called 'the stroke

sequence'

MRI VS TIME

• In the acute phase T2WI will be normal, but in time the infarcted area will become hyperintense.

• The hyperintensity on T2WI reaches its maximum between 7 and 30 days. After this it starts to fade

MRI VS TIME

• DWI is already positive in the acute phase and then becomes more bright with a maximum at 7 days.

• DWI in brain infarction will be positive for approximately for 3 weeks after onset (in spinal cord infarction DWI is only positive for one week!).

MRI VS TIME

• ADC will be of low signal intensity with a maximum at 24 hours and then will increase in signal intensity and finally becomes bright in the chronic stage.

INFARCT??

CHRONIC INFARCT

VENOUS INFARCTS

CT Angiographyand

CT Perfusion

• For assessment of intracranial and extracranial circulation

• Can demonstrate thrombi

• Timed bolus of contrast for vessel enhancement

• Can guide decision regarding intraarterial or mechanical thrombolysis by quantifying clot burden

Normal CT Angiography

Case

CT Perfusion

• With CT and MR-diffusion we can get a good impression of the area that is infarcted.

• But, we cannot preclude a large ischemic penumbra (tissue at risk).

• With perfusion studies we monitor the first pass of an iodinated contrast agent bolus through the cerebral vasculature.

• Areas of decreased perfusion will tell us which area is at risk.

Used to measure the following parameters:

– Cerebral Blood Flow (CBF)• The volume of blood per unit brain tissue (N = 4-5 mL/100g)

– Cerebral Blood Volume (CBV)• The volume of blood flow per unit of brain tissue per minute

(N = 50-60 mL/100g/min in gray matter)– Mean Transit Time (MTT)

• Time difference between arterial inflow and venous outflow– (Time to Peak Enhancement:

• Time from beginning of contrast injection to max concentration in ROI)

• Infarct shows: – Severely decreased CBF (< 30%) and CBV (<40%) with

increased MTT

• Penumbra shows either: – Increased MTT, moderately decreased CBF and normal

or increased CBV– Increased MTT, markedly decreased CBF and

moderately reduced CBV

Core and Penumbra

Normal ??

CT Perfusion

Dissection

Diffusion Weighted Imaging (DWI)

DWI is the most sensitive sequence for stroke imaging.

DWI is sensitive to restriction of Brownian motion of extracellular water due to imbalance caused by cytotoxic edema.

Normally water protons have the ability to diffuse extracellularly and loose signal.

High intensity on DWI indicates restriction of the ability of water protons to diffuse extracellularly.

• Acute stroke causes excess intracellular water accumulation or “cytotoxic edema”, with an overall decreased rate of water molecular diffusion within the affected tissue.

• Tissues with a higher rate of diffusion undergo a greater loss of signal in a given period of time than do tissues with a lower diffusion rate.

• Therefore, areas of cytotoxic edema, in which the motion of water molecules is restricted, appear brighter on diffusion-weighted images because of lesser signal losses.

• Hyperintense restriction from cytotoxic edema

• DWI improves hyperacute stroke detection to 95%

• High signal can persist up to 57 days post-ictus, (after 10 days, T2 effect may predominate over low ADC = "T2 shine-through")

• Corresponding low signal on ADC maps- May normalize after tissue reperfusion, Note: Hyperintensity on ADC map (T2 "shine-through") may mimic diffusion restriction

• Distinguishes cytotoxic from vasogenic edema in complicated cases; especially helpful for evaluation of new deficits following tumor-resection

Territories in DWI

Normal ??

Left Frontal diffusion restriction

Identification of Ischemic Penumbra

MR Findings

• Tl WI: Early cortical swelling & hypointensity, loss of gray-white borders

• T2WIEarly cortical swelling, hyperintensity in affected distributionMay normalize 2-3 weeks post-ictus = MR "fogging"

• FLAIR

May be positive (hyperintense) when other sequences normal (as early as 6 hrs post-ictus)

MR intra-arterial signal on FLAIR= early specific signof major vessel occlusion

• Occasionally, the territories of supply of the lenticulostriate arteries may be the only regions that undergo infarction in MCA stroke .

• When occlusion of the MCA occurs distal to the MI segment (and thus distal to the origins of the lenticulostriatearteries), infarction in the cortical territory of the MCA may occur without infarction of the basal ganglia.

Post Gadolinium study

Parenchymal enhancement associated with ischemic stroke, by comparison, is most commonly seen in thesubacute time frame is seen to some degree in most

patients by 7 days following an ischemic stroke

Venous infarcts in brief

Venous drainage

Venous territories

Venous territories

Deep veins

Venous thrombi

• Dural sinus thrombosis

• Cortical venous thrombosis

• Deep cerebral venous thrombosis

• Thrombus initially forms in dural sinus

• Clot propagates into cortical veins

• Venous drainage obstructed, venous pressureelevated

• Blood-brain barrier breakdown with vasogenicedema, hemorrhage

• Venous infarct with cytotoxic edema ensues

Venous ischemia

• Type 1: No abnormality

• Type 2: High signal on T2WI/FLAIR; no enhancement

• Type 3: High signal on T2WI/FLAIR; enhancement present

• Type 4: Hemorrhage or venous infarction

Empty delta sign

Cord sign

Thank you