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    Irm Cerebral in Avc

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    Vlad Stefanescu
    1. MRI sequences are important for evaluating the stages of an ischemic stroke, including the hyperacute, acute, and chronic stages. 2. Diffusion-weighted imaging shows cytotoxic edema in the hyperacute phase, while perfusion imaging can identify potentially reversible penumbra tissue. 3. In the acute phase from 12 hours to 3 days, T1-weighted imaging with contrast shows intravascular and meningeal enhancement and parenchymal changes. 4. In the subacute phase from 3 days to 6 weeks, contrast enhancement decreases while edema and mass effect resolve over time.

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    Irm Cerebral in Avc

    Uploaded by

    Vlad Stefanescu
    64 views3 pages
    1. MRI sequences are important for evaluating the stages of an ischemic stroke, including the hyperacute, acute, and chronic stages. 2. Diffusion-weighted imaging shows cytotoxic edema in the hyperacute phase, while perfusion imaging can identify potentially reversible penumbra tissue. 3. In the acute phase from 12 hours to 3 days, T1-weighted imaging with contrast shows intravascular and meningeal enhancement and parenchymal changes. 4. In the subacute phase from 3 days to 6 weeks, contrast enhancement decreases while edema and mass effect resolve over time.

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    irm cerebral in avc

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    1. MRI sequences are important for evaluating the stages of an ischemic stroke, including the hyperacute, acute, and chronic stages. 2. Diffusion-weighted imaging shows cytotoxic edema in the hyperacute phase, while perfusion imaging can identify potentially reversible penumbra tissue. 3. In the acute phase from 12 hours to 3 days, T1-weighted imaging with contrast shows intravascular and meningeal enhancement and parenchymal changes. 4. In the subacute phase from 3 days to 6 weeks, contrast enhancement decreases while edema and mass effect resolve over time.

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    64 views3 pages

    Irm Cerebral in Avc

    Uploaded by

    Vlad Stefanescu
    1. MRI sequences are important for evaluating the stages of an ischemic stroke, including the hyperacute, acute, and chronic stages. 2. Diffusion-weighted imaging shows cytotoxic edema in the hyperacute phase, while perfusion imaging can identify potentially reversible penumbra tissue. 3. In the acute phase from 12 hours to 3 days, T1-weighted imaging with contrast shows intravascular and meningeal enhancement and parenchymal changes. 4. In the subacute phase from 3 days to 6 weeks, contrast enhancement decreases while edema and mass effect resolve over time.

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    of 3

    IRM CEREBRAL IN AVC ISCHEMIC

    Secventele obligatorii pt tromboliza


    DWI sec -> 6 sapt
    FLAIR 4-6h -> toata viata
    TOF
    T2*
    +/- PWI

    STD SUPRAACUT (primele 12h)


    - HS T2, FLAIR (la 4-6h) edem citotoxic (s cenusie), apoi vasogenic (s alba)
    - T1 ef de masa disparitia santurilor intergirale
    - stergerea cisternei insulare
    - comprimarea VL
    - disparitia hsemn intravasc normal det de flx a rapid (ocluzie/viteza mica)
    - + civ -> enhancement intravasal, evidentiaza perfuzia de lux de la perif infarctului
    - DWI HS (prabusirea pompei Na/K, edem citotoxic, limit difuziei H2O); ADC
    hS = nucleul infarctului (lez irevers)
    - PWI (+civ) evaluarea perf in 1-2 min -> hperf
    arata lez reversibile (penumbra) + irevers
    PWI DWI = mismatch -> indic de tromboliza

    STD ACUT, DE NECROZA ISCH (12h 3 zile)


    - HS T2, hS T1, margini flu, terit a
    - efect de masa (max in z 3-6)
    - T1+civ -> enhancement intravazal
    meningeal
    parenchim giriform (alter BHE)
    - transf hemoragica T2 hS (dezoxiHb)

    STD SUBAC, DE RESORBTIE (z3 6s)


    4-7 z creste priza de civ masiv, pseudotum
    dispare cea intravasc si mening
    ef de masa moderat, in scadere
    transf hemoragica T1 HS metHb
    petesiala, cuprinzand pred s cenusie, cu aspect giriform la niv
    cortexului si petesial patat in nc bazali
    1-6 s scaderea edemului si a ef de masa
    persista civ parench moderat, giriform
    transf hemoragica HS T1
    infarct hS T1, HS T2, limita neta

    STD CR, ENCEFALOMALACIE (>6s)


    - cav porencefalica (encefalomalacica) semnal asem cu LCR, marginita de glioza
    (HS FLAIR)
    - fara ef de masa, ci ef retractil
    - fara priza de civ
    - transf hemoragica hS T2 (hemosiderina)
    - atrofie + degen walleriana retrograda a caii py

    IRM CEREBRAL IN AVC HEMORAGIC


    Std hemoragiei Tip de Hb T1 T2 Edem
    Supraacut (1- OxiHb ic hS (plasma) HS (plasma) -
    6h) (Diamagnetica)
    Ac (6h-4z) DezoxiHb ic Izo-hS hS (>=1T) +
    (Paramagnetica) izoS (< 1T)
    Subac (5z-s)
    Precoce MetHb ic HS hS +
    Tardiv MetHb ec HS HS +
    (puternic paramagnetica)

    Cronic (s-ani) Central cavitate hS HS


    Periferic hemosiderina
    hS - izoS hS

    DIVERSE:

    Arteriopatia Moya-Moya idiopatica


    - la tineri
    - AIT, AVC I, hemoragie cerebrala, epi
    - stenoza lent progresiva + ocluzia vaselor cercului Willis ->
    colaterale anormal de fragile

    Sdr Ac antiPL
    - avorturi spontane recurente
    - tromboze v
    - trombocitopenie

    MELAS = miopatia mitoc, encefalopatia, acidoza lactica, epis stroke-like

    Cauze de AVC I progresiv


    - edem cerebral citotoxic la infarct mare
    - tromboza avansata -> +/-Heparina
    - embolie recidiv -> Heparina
    - transf hemoragica
    deces 40%

    AVC I lacunar

    Hemisdr motor pur Caps int, punte


    Hemisdr senz pur Talamus, tr
    Hemip senz-mot Caps int, talamus
    Dizartrie + mana inabila Punte, rar cp striati
    Hemip ataxica Punte + pedunc crbl

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