Avc- Accident vascular cerebral prezentare
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ACCIDENTELE VASCULARE CEREBRALE
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DEFINITIE
• AVC: deficit neurologic cu debut brusc de cauza presupus vasculara
* deficitul neurologic este de obicei focal (hemipareza, tulb de limbaj…); rar este global (ex hemoragia subarahnodiana)
* durata deficitului motor: < 24 ore = AIT, > 24 ore = AVC constituit
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EPIDEMIOLOGIE
• A 3-a cauza de mortalitate in Europa (dupa infarct si cancer)
• Prima cauza de handicap• In Romania una din cele mai frecvente cauze de
deces si invaliditate
• Incidenta anuala 145 cazuri /100.000 locuit– 33000 cazuri / an
Gravitate: - 20 % deces precoce
- 40 % sechele severe
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CLASIFICARE AVC• AVC ISCHEMICE ~ 80%
* prin ocluzia unui vas cerebral (tromboza sau embolie)
• AVC HEMORAGICE ~ 20%* prin ruptura peretelui unui vas
cerebral (acumulare de sange in parenchimul cerebral = hemoragia intraparenchimatoasa (HIP) sau in spatiul subarahnoidian = hemoragia subarahnoidiana (HSA) )
* tromboza venoasa cerebrala (TVC)
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REPARTITIA AVC
80%
10%
5%5%
ISCHHIPH.S.A.TVC
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Tendinte actuale (2010)
• 91% AVC ischemice
• 9% hemoragii intracerebrale (4% subarahnoidiene)
↓ frecventa AVC hemoragice in tarile dezvoltate si ↑ in tarile cu venit mic (control inadecvat al HTA)
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• ANATOMIA CIRCULATIEI CEREBRALE
- SINDROAME NEUROVASCULARE
• FIZIOLOGIA CIRCULATIEI CEREBRALE
• AVC ISCHEMICE
• AIT (ATACURILE ISCHEMICE TRANZITORII)
• AVC HEMORAGICE (HIP SI HSA, MAV)
• TROMBOZELE VENOASE CEREBRALE
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ANATOMIA CIRCULATIEI CEREBRALE
• Sistemul carotidian / anterior (2 artere carotide) LF, LP, partial LT
• Sistemul vertebro-bazilar / posterior (2 artere vertebrale care se unesc in trunchiul bazilar) Partial LT, LO, trunchiul cerebral, cerebel
• Unite la baza creierului prin poligonul Willis (situat in spatiul subarahnoidian)
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Poligonul Willis
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A. Sistemul carotidian
• Artera carotida comuna:
* la nivelul vert C6 se bifurca
ACE (gat, fata, scalp)
ACI
** anastomoze ACI / ACE
orbita
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Ramurile ACI:
• Colaterala : a oftalmica
• Terminale: a. cerebrala anterioara (ACA)
a. cerebrala medie (sylviana) (ACM)
a. coroidiana anterioara
a. comunicanta posterioara (ACoP)
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A oftalmica a. centrala a retinei
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• Fiecare artera (ACA, ACM) are un teritoriu superficial (cortex + subcortical) si un teritoriu profund (subst alba, nc bazali, talamusul, caps interna) = art “perforante” (lenticulo-striate)
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ACA / unite prin ACoA
• Terit superf:- fata mediala a cortex cerebral (< sant P-O), zona de ~ 3 cm din partea super a fetei laterale a cortexului
• Terit profund:- parte din ggl bazali si caps int
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• Particularitate a terit superficial al ACA: la nivelul ariei motorii primare iriga partea responsabila de motilitatea membrului inferior, trunchiului si partii proximale a membrului superior
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ACM (a. sylviana)
• Terit superf:
- fata laterala a LF, LP (exceptie 3 cm din partea super)+ fata laterala a LT
• Terit profund:
- parte din ggl bazali si caps int
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• Particularitate a terit superficial al ACM: la nivelul ariei motorii primare iriga partea responsabila de motilitatea fetei si membrului superior
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B. Sistemul vertebro-bazilar
• A. vertebrala (AV): ramura din a. subclavie
- traiect ascendent prin gaurile apofizelor transverse ale C1-C6.
- se uneste cu AV de partea opusa la niv jonct bulbo-pontine trunchiul bazilar (TB)
● TB: urca pe fata anterioara a trunchiului cerebral; la nivel de pedunculi se bifurca in cele 2 ACP (artere cerebrale posterioare)
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Ramurile art vertebrale:
• A spinala anterioara si a spinale posterioare maduva cervicala
• A cerebeloasa postero-inferioara (PICA)
• Ram bulbare
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Ramurile tr bazilar
• Ramuri pontine (de tip perforant si de tip circumferential)
• A labirintica
• A cerebeloasa antero-inferioara (AICA)
• A cerebeloasa superioara (SCA)
• A cerebrala posterioara (ACP): ram terminala – se uneste cu ACoP pentru a inchide poligonul Willis
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• SCA (din TB)
• AICA (din TB)
• PICA (din AV)
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PICA (a “fosetei laterale a bulbului”)
• Cerebel: vermis, nuclei, p inf emisfere
• Bulb: reg postero-laterala
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ACP
• Terit superf:
- fata inf si mediala a LT, intreg LO
• Terit profund:
- mezenc, o parte din talamus si ggl bazali, c. geniculati, diencefal, hipocamp
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Teritorii vasculare cerebrale
• ACA
• ACM
• ACoroidAnt
• ACP
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SINDROAME NEURO-VASCULARE
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• Ocluzia fiecarei artere cerebrale realizeaza un tablou clinic specific (ce depinde de functia regiunii cerebrale afectate) = sindrom topografic vascular
• Sunt descrise in AVC ischemice sindroamele clinice ale ischemiei cerebrale
• Sindromul de a oftalmica cecitate monoculara tranzitorie
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Sindromul de ACA
• Complet: hemipareza contralaterala
• Partial: hemipareza predominant crurala
• + alte semne:
- abulie (lipsa de initiativa, apatie)
- dezinhibare
- aparitia reflexelor primitive (grasping..)
- tulburari de mers (de tip apraxie)
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AVC ACA drt
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Sindromul de ACM (teritoriu complet)
• Ocluzia ACM la origine: tablou clinic sever
- hemiplegie contralaterala
- devierea capului si ochilor spre leziune
- hipoestezie pe hemicorpul contralateral
- hemianopsie omonima de partea opusa
- afazie globala (emisfer Dom) / neglijenta spatiului contralateral (emisfer min)
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Infarct total ACM drt / ACM stg
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Semnul ACM hiperdense (=tromb)
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Sindromul de ACM (teritoriul superficial)
• Ocluzia ramurilor ascendente (LF, LP)
- hemipareza contralaterala predominant facio-brahiala
- hipoestezie pe hemicorpul contralateral
- afazie de tip expresiv (Broca) / neglijenta spatiului contralateral
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Sindromul de ACM (teritoriul superficial)
• Ocluzia ramurilor descendente (LT) :
- hemianopsie omonima de partea opusa
- afazie receptiva (Wernicke)
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AVC terit superf ACM stg - DWI
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Sindromul de ACM (teritoriul profund)
• Ocluzia ramurilor perforante (CI):
- hemipareza contralaterala egala (MS = MI) cu ataxia membrelor afectate
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AVC terit profund ACM stg
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Sindromul de ACP
• Hemianopsie omonima contralaterala
• In infarcte bilaterale de ACP apare cecitate corticala
• Sindrom talamic contralateral (ocluzia unei ramuri profunde din ACP): hipoestezie, durere “talamica” si ataxie pe hemicorpul opus
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AVC ACP stg / ACP drt
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AVC art coroidiana ant drt
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AVC in teritoriul vertebro-bazilar
• “sindrom altern”:
- de partea leziunii afectarea unui nerv cranian (ex: hipoestezie faciala, pareza de oculomotori..etc)
- de partea opusa leziunii semne de afectare a cailor lungi ce trec prin Tr cerebral (ex: hemipareza, hipoestezie
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Sindromul de ocluzie al PICA / art vertebrale = sdr Wallenberg
• De aceeasi parte: - hipoestezie la nivelul fetei (nc V)- sindrom cerebelos (ataxie)- sindrom Cl Bernard Honer
• De partea opusa:- hipoestezie pentru sensibilitatea
termo-algezica+ sdr vestibular + tulb de deglutitie
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AVC PICA stg
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Sindroame de ocluzie a arterelor cerebeloase (AICA, SCA)
• De aceeasi parte:
- sindrom cerebelos (ataxie)
• De partea opusa:
- hipoestezie pentru sens termo-algezica
- hemipareza (poate fi frusta sau lipsi)
• - vertij, nistagmus, greturi, varsaturi
• AVC extinse duc la alterarea starii de constienta (compres v IV)
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Sindromul de ocluzie a trunchiului bazilar (“locked-in”)
• Infarct bilateral partea anterioara a puntii:
- tetraplegie
- diplegie faciala de tip periferic- abolirea miscarilor laterale ale
ochilor
- imposibilitatea articularii sunetelor (“anartrie”)
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AVC LACUNARE
• Infarcte de mici dimensiuni (0.5-15 mm) produse prin ocluzia arteriolelor perforante care iriga regiunile profunde din creier, TC
• Sindroame clinice tipice “lacunare”:
- hemipareza “pura” / izolata (egala B si C)
- hipoestezie izolata a unui hemicorp
- hemipareza ataxica
- sindromul disartrie-mana inabila
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FIZIOLOGIA CIRCULATIEI CEREBRALE
• Creierul: organul cel mai activ metabolic; necesita 15-20% din debitul cardiac
• Debitul sanguin cerebral (DSC) – normal in jur de 50 ml/min/100g tesut
• > 55-60 ml/min/100g = HTIC
• < 20 ml/min/100 g = ischemie
• < 10 ml/min/100 g = necroza
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Autoreglarea circ cerebrale
• DSC mentinut constant prin autoreglarea circulatiei cerebrale:
* in functie de TA sistemica (vasele de calibru mare): ↑ TA VC
↓ TA VD
* in functie de conc CO2 din singele arterial (vasele de calibru mic):
↑ conc CO2 VD
↓ conc CO2 VC
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ACCIDENTELE VASCULARE CEREBRALE ISCHEMICE
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DEFINITIE
• sindrom clinic caracterizat prin instalarea brusca a unui deficit neurologic provocat de scaderea debitului sanguin intr-o anumita regiune cerebrala
- scadere de durata scurta, reversibila AIT
- scadere importanta, durata mare AVC constituit
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FACTORI DE RISC
• NEMODIFICABILI
- varsta
- sexul
- rasa/etnia
- AHC (familiale)
- fct genetici
- AVC/ AIT/ IMA in
antecedente
• MODIFICABILI
- HTA (↑riscul de 4-6 x)- Stenoze carotidiene asimptomatice- FiA, alte boli cardiace (CI, IC)- Diabetul zaharat- Dislipidemia- Fumatul / si cel pasiv- Consumul de alcool- Hiperfibrinogenemia / hiperhomocisteinemia- Sindromul anticorpilor antifosfolipidici- Contraceptive orale / tratament hormonal
postmenopauza- Obezitate- Sicklemie (anemie falciforma)- Sedentarism; conditie economica precara- Sindrom metabolic- Abuz de droguri
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ETIOLOGIE
• 1. Mecanismul atero-trombotic (boala ocluziva a vaselor mari)
• 2. Mecanismul (cardio)embolic
• 3. Boala vaselor mici cerebrale (lacunarism)
• 4. Mecanismul hemodinamic
• 5. Cauze rare: disectii, vasculite, coagulopatii, hipervascozitate….
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1. Boala ocluziva a vaselor mari
• Ateroscleroza determina stenoza vaselor de calibru mare sau mediu prin depunere de material lipidic sub tunica intima placa de aterom
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Localizarea ATS
• Extracranian:- originea ACI, sifon carot- originea AV, crosa Ao
!! Caucazieni • Intracranian:
- originea ACM- orig, termin TB
!! Asiatici, hispanici, negrii
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Aterotromboza
• Placile de aterom se pot complica (ulcerare, hemoragie..) atrage trombocitele care adera activare agregare (stabilizare cu retea de fibrina) => tromb
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• Aterotromboza produce AVC ischemic prin 3 mecanisme:
1. Ocluzia totala a vasului prin formarea unui tromb (ex. tromboza de carotida)
2. Desprinderea unor fragmente de tromb cu embolizarea si obstructia arterelor din distalitate = embolie arterio-arteriala
3. Scaderea fluxului sangvin post-stenotic
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ATS embolie arterio- ocluzie completa
arteriala prin tromb
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2. Embolia cardiaca
• Cardiopatii emboligene:
- fibrilatia atriala
- infarctul miocardic recent
- boala valvulara
- cardio-miopatiile dilatative
- DSA (ASIA)
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3. Boala vaselor mici cerebrale
• Peretele vaselor mici cerebrale (arterele “perforante”) sufera modificari datorita HTA, DZ, inflamatiei (vasculite), amiloidozei, etc…(arterio-scleroza, lipohialinoza,...) ocluzia sau tromboza arteriolei infarct cerebral de mici dimensiuni = “lacuna”
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4. Mecanismul hemodinamic
• se produce cand in circulatia cerebrala exista leziuni stenozante ale vaselor + scaderea debitului sanguin cerebral (hipoTA, aritmii, stop cardiac, perioperator, etc..)
• Localizate la limita dintre 2 teritorii vasculare invecinate = infarcte “de granita” (jonctionale, “watersheed”)
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AVC jonctionale dupa chir cardiaca
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5. Cauze rare de AVC
• Disectia arteriala: determina stenoza sau ocluzia vasului afectat prin hemoragia din peretele vascular (trauma, sport)
• Arterita (vasculite)
• Consumul de droguri: cocaina, heroina, amfetamine
• Coagulopatii
• Hipervascozitate sangvina (leucemii…)
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Disectie ACI drt
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Disectia ACI drt: zone de infarct
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FIZIOPATOLOGIA AVC ISCHEMIC
• ischemia neuronala ireversibla incepe cand DSC < 18 mL/100 mg/min; creierul nu are rezerve de glucoza
• “cascada ischemica”: oprirea glicolizei aerobe acumulare intraneuronala de Na+, Ca++, acidoza, producere de radicali liberi edem celular activarea lipazelor, proteazelor moarte neuronala
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3 zone in cadrul ischemieicerebrale:
• Zona de necroza (DSC <8 ml/100g/min): disfunctia membranelor si moarte neuronala; aici neuronii mor in primele minute de la debutul AVC
• Zona de penumbra (< 18 ml/100g/min): regiune de ischemie incompleta aflata in jurul zonei de ischemie completa; contine neuroni fara activitate electrica, dar inca viabili pentru cateva ore (prin circulatia marginala)
Necroza
Penumbra
Oligemia
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Debitul sanguin cerebral DSC
1 2 3
10
20
40
30
50
DSC
ml/mn/100g
Timp (h)
Permanent
Oligemie
Penumbra
Infarct
Normal
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■ Zona de “olighemie”, “perfuzie de mizerie” (DSC sub cel normal): contine neuroni nefunctionali, dar intacti structural
* In timp, zona de penumbra se transforma in zona de necroza (ischemie, excitotox, acidoza,…etc)
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• Scopul tratamentului trombolitic (iv sau ia) este recanalizarea vasului si restabilirea circulatiei salvarea neuronilor din zona de penumbra inaintea producerii injuriei ireversibile
• Neuroprotectia are ca scop conservarea viabilitatii neuronilor ischemici pentru a extinde fereastra terapeutica a trat trombolitic
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ATACUL ISCHEMIC TRANZITOR (AIT)
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Definitie
• Un episod tranzitor de disfunctie neurologica cauzata de ischemia focala a creierului sau retinei, fara evidenta de infarct acut (AHA/ ASA Guidelines, 2009)
• Definitia veche continea doar conditia de reversibilitate completa a simptomelor dupa 24 de ore
• Definitia din 2002 continea reversibilitatea simptomelor in decurs de 1 ora si absenta vreunei dovezi de infarct acut pe examinarile imagistice
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Durata AIT
• In general 5-20 minute ( ~ 8 min AIT in teritoriul V-B si ~ 14 min AIT carotidiene)
• Fiecare episod neurologic tranzitor, indiferent de durata, la care se constata leziuni ischemice pe RMN (secventa DWI) este considerat AVC
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Kidwell, Stroke 1999;30:1174
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Epidemiologie
• Incidenta 80 – 200 cazuri /100.000 locuit.• Incidenta AIT creste cu varsta !! • Este un factor de risc major pentru AVC
ischemic, dar si pt IMA• Dupa AIT, riscul de AVC este de 5% in
prima sapt, si de 20% in primele luni• 7-40% din pacientii cu AVC au avut un AIT• AIT “crescendo” (ca durata, frecventa
episoadelor, severitate) Iminenta AVC
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Cauzele AIT / fizipat
• Obstructia unui vas printr-un embol plachetar de dimensiuni mici, care va fi lizat rapid
• Embolul provenit din arterele carotide / vertebrale sau de la cord
• DSC este ↓ sau intrerupt intr-o anumita regiune cerebrala inhibarea reversibila a activitatii neuronale, fara moarte celulara
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Simptome in AIT
• AIT carotidian- Cecitare monoculara
tranzitorie (isch. retin)- Hemipareza contralat./
inabilitate a mainii- Hipoestezie contralat /
parestezii- Tulb de limbaj de tip
afazie- Combinatii
• AIT vertebro-bazilar- Tulburari de vedere
binoculare (HLO)- Deficit motor
(contralat, bilateral)- Hipoestezie /
parestezii (contralat sau bilat)
- Vertij, ataxie, diplopie, disartrie combinate
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• Nu sunt acceptate ca AIT urmatoarele simptome neurologice:
- pierderea starii de cunostinta
- ameteala
- starea de confuzie
- incontinenta sfincteriana
- vertijul, ataxia, diplopia sau disartria daca apar izolat
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Diagnosticul pozitiv in AIT
• Clinic:
- anamneza f importanta; uneori diagnosticul se pune retrospectiv
- examen obiectiv: deseori e normal, pacientul ajunge la Urgenta dupa ce simptomele s-au remis
• Investigatii complementare: identice ca in AVC ischemic constituit
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Evaluarea pacientului cu AIT
• Ex neuroimagistice: CT sau RMN cerebral fara contrast (secvente DWI) absenta de modificari ischemice acute pt dgn de AIT; excludere alte cauze (tu...)
• Cautarea cauzei AIT:- Eco Doppler carotido-vertebral
(stenoze? placa ATS instabila? disectie?)- ECG, Eco cord (FiA? Emboli ?)- angioRMN cerebral (stenoze
intracraniene?)- arteriografie (in caz de stenoze
stranse)
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Diagnosticul diferential in AIT
• Migrena cu aura
• Crize epileptice focale (motorii sau senzitive)
• Sincopa, pierderea starii de constienta
• Hipoglicemia
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Prognosticul AIT: scorul ABCD2
• Identifica pacientii AIT cu risc mare pt AVCA (Age): 1 pct pt varsta >60 ani, B (BP = TA): 1 pct pt val ↑ TA (si
anteced) C (clinica): 2 pct pt hemipareza
unilaterala, 1 pct pt tulb limbaj fara deficit motor
D (durata simpt); 1 pct pentru 10–59 min, 2 pct pt >60 min.
D (Diabet): 1 pct (si hiperglicemia)Scor 0-3 = risc scazut, scor 6-7 risc f inalt
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Tratamentul AIT
• Are ca scop prevenirea producerii de noi evenimente ischemice (= preventie secundara) – se suprapune peste trat AVC
• - trat antiagregant plachetar:
- ASA, clopidogrel, triflusal
- daca era deja pe antiagregant asociere de 2 (ASA + dipiridamol SR = Asasantine) sau schimbare ASA cu Clopidogrel
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• - trat anticoagulant – doar daca exista sursa emboligena cardiaca
- acenocumarol
- [warfarina]
- dabigatran, apixaban
● - trat hipotensor (HTA – princ factor de risc)
● - statinele (stabilizarea placilor de aterom)
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• Tratamentul stenozelor carotidiene stranse (> 75%): chirurgical prin endarterectomie / endovascular prin stentare
• Control al valorilor glicemice mari
• Renuntarea la fumat
• Schimbarea stilului de viata
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AIT = factor de risc major = urgenta !!
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ACCIDENTELE ISCHEMICE CONSTITUITE
(INFARCTELE CEREBRALE)
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Terminologie
• AVC “constituit”: deficit neurologic stationar timp de ore / zile
• AVC “in progresie”: instalare progresiva sau agravarea simptomelor neurologice in cursul primelor 24 – 48 h
• AVC “regresiv”: ameliorarea deficitului motor
• AVC remis clinic: disparitia in timp a simptomelor neurologice
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• Zona de necroza IRM – ADC (silentiul electric si energetic)
• Zona de penumbra IRM – DWI (apreciaza gradientele ionice trans-membranare, dependente de energie)
• Zona de oligemie IRM - PWI
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MAV: angiom cavernos pontin
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Hemor. in faza acuta: infarct hemoragic venos (v. corticale) in LLA
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Hemoragie lobara F stg: meta de melanom
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Hemor putam stg cu edem perilez si efect de masa : glioblastom
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Hemoragii dupa trat trombolitic
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Microhemoragii: depozite de hemosiderina - AAC
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Hemor putaminala stg
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Anevrism ACA drt: HSA
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Anevrism ACM drt: HSA
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Stentarea carotidiana