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Stroke Dr.amarnath

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    IMAGING IN ISCHEMICSTROKE

    DR.C.AMARNATH,MD,DNB,FRCR

    ASSOCIATE PROFESSOR & HOD,STANLEY MEDICAL COLLEGE

    Consultant radiologist, SCANS WORLD

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    ACKNOWLEDGEMENTS

    ORGANISERS

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    Sudden onset of neurological deficit

    caused by impaired blood supply to the

    brain

    Defining stroke

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    STROKETypes of Ischemic Stroke

    1. TIA Transient Ischemic Attack

    A sudden neurological disturbance lasting for more than 15

    minute but with complete resolution with in 24 hours.

    35% of these patients may develop major stroke in 12 months

    of initial incident

    2. RIND reversible Ischemic Neurological Deficit RIND is a deficit

    that persist for more than 24 hours but complete recovery

    within 3 weeks

    3. PRIND Progressive Reversible Ischemic Neurological Deficit

    4. Stroke in evolution

    5. Complete Stroke

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    STROKEOccurrence Rate according to the Type

    Ischemic Stroke

    83-85%

    Hemorrhagic Stroke

    15-17%

    Thrombotic

    51.5%

    Embolic

    31.5%

    Intracerebral

    Hemorrhage

    10%

    Subarachnoid

    Haemorrhage

    7%

    All Stroke 100%

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    STROKE ETIOLOGIES :

    TYPE OF STROKE PERCENT (% )

    INFARCTION (80 % )

    large vessel occlusion 40-50

    small vessel (lacunar ) infarcts 25

    Cardio-embolic 15

    Blood disoders 5Vasculitis 5

    PRIMARY ICH (15 % )

    HTN 40-60

    amyloid 15-25vascular malformations 10-15

    NON-TRAUMATIC SAH (5 % )

    aneurysm 75-80

    vascular malformation 10-15

    Non-aneurysmal SAH 5-15

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    DIFFUSION / PERFUSION MISMATCHDIFFUSION / PERFUSION MISMATCH

    Modified from Kidwell et al. Stroke 2003

    ml/100g

    m/minRegional CBF 55

    GM 65-75

    WM 15-20

    Electricaldysfunction 10-20

    Neuronal

    death

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    Pathophysiology:Pathophysiology:

    Ischemic penumbraIschemic penumbra the area surrounding the primary injury CBF is 10-20 ml/100g of brain/min

    Electrical silence but irreversible damage has

    not yet occurred Animal studies:

    reversible neurologic deficit if cerebral vesselocclusion lasts less than 2h

    after 6h of occlusion: irreversible neurologic deficit Thus the 2-6 hour therapeutic window for

    thrombolysis

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    The ischemic brain

    Central infarcted core dead non salvageable tissue

    Penumbra surrounding salvageable stunned brain tissue

    Time is Brain ` < 3 hours postictus

    IV thrombolysis

    `3- 6(?9) hours postictus

    IA thrombolysis

    ` > 6(?9) hours postictus

    Usually not a

    thrombolysis candidate

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    Hyperacute -0-6 hrs

    Acute 6-24 hrs Subacute 24 hrs 2 weeks

    Chronic - > 2 weeks

    11

    Stroke characterization-time

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    ACUTE STROKE IMAGINGACUTE STROKE IMAGING

    PRIMARY GOAL :

    1.STROKE TYPE ?

    2.STROKE MIMIC ?

    SECONDARY GOAL :1.PROGNOSTIC .

    2.ISCHAEMIC VIABLE TISSUE VS INFARCTED TISSUE

    3.DETECTION & LOCALIZATION OF ARTERIAL OCCLUSION .

    FOR PATIENT SELECTIONINDIVIDUALIZE Tt

    EXTEND THERAPEUTIC WINDOW

    IMPROVE Tt OUTCOME .

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    Techniques CT - MRI

    Nonenhanced CT

    CT perfusion

    CT Angiography

    Conventional MR

    GRE

    Diffusion MR

    Perfusion MR

    MRA

    13

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    Non contrast CT

    Primary imaging modality

    To reveal early direct or indirect signs of

    brain infarction To exclude lesions that mimic stroke

    intracranial hemorrhage, subdural

    hematoma, cerebritis, migraine, tumorsSensitivity 45 - 88% (mean 55.3%)

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    ACUTE INFARCTS

    HYPERACUTE (

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    Insular ribbon sign

    F, 732 hours

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    Obscuration of lentiform nuclei

    17

    Non enhanced CTEarly ischemic

    changes

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    Hyper dense MCA/vessel sign

    18

    Non enhanced CTEarly ischemic

    changes

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    Disappearing basal ganglia sign

    Caused by MCA

    M1 segment

    occlusion

    proximally tolenticulostriate

    arteries

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    Disappearing basal ganglia sign

    F,58, 6 hours

    Setting of variable window width to accent the graywhite matter contrast

    window width80 HU

    center level 20

    HU

    W 8 HU

    C 32 HU

    Narrow

    window

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    22

    Quantification of ischemia-

    The ASPECTS systemEach MCA region score 1

    Deduct one score for each region involved

    ALBERTA STROKE PROGRAMME EARLY CTSCORE

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    Quantification of ischemia-

    The ASPECTS systemDiffuse ischemia score 0

    Normal score 10

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    SUBACUTE INFARCTS

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    STROKE OR TUMOUR

    Sudden onset

    Grey and white matter

    involved

    Wedge shaped

    Typical distribution

    Gradual onset

    Preferentially involves

    white matter

    Round/infilterating

    Not confined to any

    vascular territory

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    CTA-MCA occlusion

    Vessel occlusion or cutoff related to

    thromboemboli

    Delayed (antegrade) flow

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    CTA ICA stenosis

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    CTA-Aneurysm MCA

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    CT Perfusion -Technique

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    CT Perfusion

    rMTT(sec)

    > 145%

    aCBV

    (ml/100g)

    < 2.0

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    CT perfusion

    Advantages : Quantification and resolution

    Arterial input function

    Disadvantages: Limited coverageIonizing radiation

    Iodinated contrast

    Complex postprocessingCBF/CBV mismatchStroke

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    Hemorrhage

    Estimate area of ischemia

    Determine infarct core

    Determine penumbra

    Status of vessels

    Conclusions from CT

    Nonenhanced CT

    (primary goal)

    Secondary goal

    CT perfusion

    CT Angiography

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    No hemorrhage

    Involvement of 7

    Penumbra >20 % infarct

    Intravenous Thrombolysis Based

    on Advanced CT Imaging

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    Conventional MR Anatomy

    DW MR -Hyper acute irreversible

    ischemia(core)

    GRE /Susceptibility MR - Hemorrhage.

    MRA-neck and intracranial vessels

    Diffusion Perfusion mismatch - penumbra.

    34

    MRI

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    Sagittal T1-weighted

    Axial DW

    Axial GRE

    Axial FLAIR

    MR Perfusion

    MR angiography (MRA)

    35

    MR- Emergent protocol

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    Diffusion Imaging in Stroke

    Goals

    1. To visualize the ischemic penumbra

    2. To identify at an early time the difference between

    salvageable, nonsalvageable and undamaged tissue

    3. This will help in selecting proper cases for intervention

    4. Prediction of outcome of intervention

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    DWI-Hyperintense in ischemia

    ADC-hypointense in ischemia

    Hyperintense tissue on DWI-irreversibly infarcted

    tissue(core)

    Diffusion weighted MRI

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    Large artery infarction

    Small vessel or lacunar infarction

    Cardioembolic infarctions multiple vascular

    territories

    Watershed infarctions-Border zones

    Global ischemia

    38

    TOAST classification

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    DWI-Large arterial territory

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    DWI-Lacunar infarct

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    DWI-Embolic

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    DWI-Watershed

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    Endogenous spin arterial labelling

    Exogenous tracer-commonly used

    Signal loss due to T2* shortening

    MR Perfusion-Technique

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    PWI-DWI DISCONCORDANCE :

    TYPE 1: PWI >>> DWI

    TYPE 2 : PWI = DWI

    TYPE 3 : PWI

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    PATTERN 1 : PI>DWI

    Proportion of PI>DWI patterns decreased with

    scan delay,

    constituting 75.0% before 6 hours,which in the following6-hour periods decreased

    to71.4%, 50.0%, and 44.4% .

    The greater efficacy of thrombolytic treatment.

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    Salvage of mismatch region with thrombolytic

    therapy.

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    PATTERN 2 OR 3 :PATTERN 2 OR 3 :

    (MATCHED OR PWI

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    DWI CBV CO-REGISTERED

    NO MISMATCH

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    PATTERN 4: Isolated DWIThe reperfusion:

    Strongly suggests that the initial

    proximal occlusion has been lysed .

    PATTERN 5: Only PI deficit .Represents tissue at risk but not committed to

    infarction . Spontaneous resolution of clinical and

    perfusion deficits or may progress to infarction .

    - TIA

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    DIFFUSION WEIGHTED MR

    PWI > DWI - Neuroprotective agents and / or

    Thrombolysis is beneficial

    PWI = DWI

    PWI < DWI

    Not beneficial

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    MRA-Extracranial vessels

    3 D TOF MRA CE MRA

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    MRA-Intracranial vessels

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    8 HOURS 2 DAY 1 WEEK

    Contrast-enhanced T1-weighted images show intravascular

    enhancement over the infarct on the first and second days and

    moderate cortical and subcortical enhancement 1 week after stroke.

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    Absolute contraindications

    Intracranial hge ,mass lesions

    >1/3rd MCA

    3 hrs for IV thrombolysis

    Ictus >6 hrs for IA thrombolysis

    Criteria for thrombolysis

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    ` Favourable factors

    Proximal MCA or basilar tip occlusion

    Diffusion perfusion mismatch or penumbra on CTP

    Unfavourable factors

    Microbleeds on GRE

    Early parenchymal enhancement

    Larger DWI abn volume

    Very low CBF

    Criteria for thrombolysis

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    61%

    35%

    11%

    Recanal. rate

    Rate of recanalization after tPA and site

    of occlusion

    ACI M1 M2-M3

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    NECT/MRI+DWI

    No hemorrhage

    0-3 hourspost ictal

    IV thrombolytics

    3-6 hrs post ictal

    CTA +CTP/DWI+MRP

    Thrombus withpenumbra

    IA thrombolytics

    No penumbra +/-thrombus

    No IA thrombolytics

    Hemorrhage

    No Rx

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    Is There a Hemorrhage?

    MR=CT for parenchymal hge

    CT better than MR for SAH

    Is there a penumbra?

    MRP provides more brain coverage than CTP

    MRP only qualitative but CTP is quantitative

    Recap ; MR or CT

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    Is a Large Vessel Occluded?

    CTA =MRA

    MRA prone to artifacts due to motion in emergent

    situation

    ` Time?

    CT fast to perform ,post processing and reporting

    difficult

    MR difficult to perform,easy to report

    Recap: MR or CT

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    Time is brain

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    Both CT and MR equally efficacious for imaging

    acute stroke

    Using individual modality is according to

    availability, logistics and preference

    Penumbra is the most important thing to imageafter 3 hrs and CTP and MR DW P mismatch

    both excellent to detect

    Conclusion

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    Thank you


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