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Ischemic stroke

Ischemic stroke.ppt

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Ischemic stroke

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Objectives

Pathophysiology of ischemicstroke

• Imagistic aspects

• Etiology

• Clinical aspects

• Diagnosis

• Treatment

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Ischemic stroke = absence of the bflow

Consequences of the vascular occlusion depend on the dimensions oand on the presence and patency of the brain vessels anastomosis

• Cervical occlusion of ICA –  circulation can be compensated by ACoAExternal carotid artery can be another source of supply, through ophtor other anastomosis

• VA Occlusion  –compensatory flow can be provided by deep cervic

thyreocervical arteries or from the contralateral VA• MCA/ACA occlusion (outside the circle of Willis) – meningeal anastom

• In case of the occlusion of a big artery, the cerebral infarction can vary

0 – 100% of the area vascularized by the occluded vessel

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Neurovascular unitAfter the occlusion of th

•  lack of oxygen and glu

•  failure of energy prod

•  distruction of cell com

membranes•  cell death

Depending on the duratvessel obstruction and o

level of the blood flow, tchanges can be permanereversible

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Cerebral blood flow (CBF)• CBF = Cerebral blood volume (CBV)/Mean transit time (MTT)

• CBF level influences the dimension of stroke (cerebral infarction)

• Initial event : increase in MTT due to the occlusion or stenosis of a vessel• MTT is influenced by the place of the occlusion/stenosis and by the prese

collaterals

• In response to the increase of MTT the mechanisms of cerebral autoreguldetermine the vasodilation of the vessels distally from the site of occlusioincrease of oxygen extraction rate from the blood

• Vasodilation leads initially to an increase of CBF in order to maintain a conblood flow supply despite the obstruction of the vessel

• When the capacity of vasodilation is exhausted, the MTT will continue to cerebral blood volume will decrease and finally the CBF will decrease uptwhich are incompatible with survival

• Neuronal death (necrosis) will occur

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Hemodynamics

•  Normal CBF = 55 mL/100gr cerebral tissue /min

CBF < 10-12ml/100gr/min leads to infarction irrespective of the duratiothe occlusion

• Critical hypoperfusion = 23-12 mL/ 100gr/ min – neuronal function isabolished and the brain tissue is affected

• EEG shows slow waves

• Below this level the EEG becomes flat (iso-electric)

• CBF of 6-8 ml/100gr/min :

•   ATP depletion, ↑ K extracelular, ↑ Ca intracelular, celular acidosis histologic signs of necrosis

• Activation of phospholypases – distruction of neuronal membrane

• Accumulation of Prostaglandines, Leucotriens, Free radicals alteredintracelular enzymes and proteins

• „ neuronal balonization” cytotoxic edema

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Ischemic stroke = absence of the blflow

• Some of these processes are reversible (by re- vascularizatio

• In the center of the ischemic area the lesions are irreversiblcore)

• The margins of this area are hyperemic, being vascularized bcollaterals – in this area the neurons are „at risk”, but can bif the blood flow is re-established

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From pathophysiology timagistic aspects

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Magnetic resonance imagingDWI/PWI mismatch• Diffusion Weighted Imaging (DWI)

reflects biochemical compromise(core of infarction)

Changes are visible within the firsthour after vessel obstruction (in 3 h100% of patients will show hangeson DWI sequences)

• Perfusion Weighted Imaging (PWI)reflects hemodynamic compromise

• The differences between the twoareas represents the salvageabletissue (penumbra)

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MRI aspects• In the first hours, on T2 seq stroke is not

visible, but it can be seen on DWI (redarrow)

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Early signs

• Noncontrast CT of the head is thefirst-line imaging modality for theassessment of strokes todifferentiate ischemic fromhemorrhagic strokes and to ruleout other intracranial pathologies.It is very sensitive at detecting

intracerebral and subarachnoidhemorrhages, as well as subduralhematomas. Hemorrhage appearsas a readily identifiable hyperdensearea within the brain.

The CT reveals early signs of a m

cerebral artery stroke, with loss

definition of the gyri and grey w

boundary (arrow)

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Early signs

This CT scan was taken 24 h after a st

In ischemic strokes, an early head CT may be

grossly normal because edema andinfarction have not yet developed

adequately to be identified. However, other

subtle findings may include:

•  loss of the gray-white matter

differentiation (red arrow)

•obscuration of the lentiform nucleus(white asterisk)

•  sulcal asymmetry (yellow arrow)

•  an insular ribbon sign

• Hyperdense MCA

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Hyperdense MCA

M1 segment

M1 segment

M2 s

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Figure 4. A. Axial unenhanced CT image, obtained in a 73-year-old woman 21/2 hours af

onset of left hemiparesis, shows hypoattenuation and obscuration of the posterior part

right lentiform nucleus (white arrow) and a loss of gray matter  –white matter .

B. Normal aspect (I = insula, C= caudate nc, L= lentiform nc, IC = internal caps

M1 – M3 – arterial territory of MCA

Srinivasan A et al. Radiographics 2006;26:S75-S95

©2006 by Radiological Society of North America

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Sub- acute stroke

As the ischemic cascade progresses,more signs are visible on head CT. Effacementof the third ventricle (blue arrow), a midlineshift (yellow line), hypodense areas in avascular watershed pattern, and sulcaleffacement (red arrow) will develop overtime. Midline shift may be subtle and is best

determined by drawing a line from theanterior to posterior attachments of the falxcerebri and looking for any deviation. Thehead CT shown was taken on day 3 after anacute ischemic stroke.

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Hemorrhagictransformation

Presence of the blood (white arrow) in an area of

to late recanalization of some of the occluded ve

the blood into the brain parenchima through the a

barrier

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Old stroke

Old lesions are intensely hypodense, similar

(red arrows)

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Risk factors for stroke• Non- modifiable :

• Age

•Gender

• Family history of stroke

• Personal history of stroke

• Modifiable• Arterial hypertension

• Hypercholesterolemia

• Diabetes• Smoking

• Obesity

• Physical inactivity

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Clinical aspects

• Practically every neurological sign and symptom due to a dythe Central Nervous System can be caused by a transient orocclusion of a vessel

• If the signs and symptoms are transient and the imagistic stnot show a lesion of the brain, we call this a transient ischem(TIA) . The definition of the TIA admits a duration of the sym

but typical TIAs last ≤ 1 h. 

• If the occlusion is permanent, a cerebral infarction will occuthis an ischemic stroke

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The media campaign for increasing public awareness towards stroke included the most freque

stroke, and stressed out the importance of acting fast, because “time is brain” 

Facial paresis, decrease in force of the arm or leg, dysarthria or aphasia are present in almost

Other signs, like cerebellar signs, hemianopia, brainstem signs can occur if the affected vessel

vertebro-basilar territory (see also the lecture about brain arteries for the clinical signs of diffe

stroke)

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TIA transient ischemic attack• TIA is an emergency !

The patient must be evaluated rapidly and treated because this way we can prevent a permanent stroke

• Causes and mechanisms for stroke and TIAs are similar (wildetailed in the next slides)

• The clinical judgement of the case and the investigations are

for stroke and TIA• Treatment for the acute period and for secondary preventio

similar for stroke and TIA

• The ABCD2 score is a risk assessment tool design to predict term stroke risk (at 2 days) but also stroke risk at 90 days fro

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Even if the patient is not hospitalize

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Even if the patient is not hospitalizehe/she must be rapidly evaluated antreated

Stroke etiology

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Stroke etiology

The HeartSmall vessels

Blood

Big vessels

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The Heart

• Left atrium• Thrombi due to atrial fibrillation• Atrial mixoma

• Valves (Mitral valve, Aortic valve)• Prosthesis

• Mechanical (metallic)

• Biological

• Endocarditis• Infectious

• Non- infectious

• Marantic (para neoplastic)

• SLE (Liebman- Sachs)

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The Heart

• Ventricles

• Myocardial infarction

(hypokinesia, aneurysms andthrombi)

• Paradoxical embolism

• Persistent Foramen Ovale (PFO)

• Interatrial septal defect• Interatrial septal aneurysm

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 Atrial fibrillation

• The most common cause of

cardioembolic stroke• Any form of atrial fibrillation can

cause a stroke (paroxysmal orpermanent)

• AF is more frequent in men, but

strokes due to AF are morefrequent in women (reasons are

not clear )

• Prevalence of AF increases withage

• The majority of cases a

valvular AF, but AF canassociated with valvula(mitral stenosis)

• A person with AF and smust receive anticoagutherapy (unless there a

contraindications for looral anticoagulants)

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PFO

• In order to affirm a stroke due to

paradoxal embolism:• Presence of PFO

• Right to left shunt

• Presence of deep vein thrombosis

• Treatment :• Antiplatelet drugs/Anticoagulant

drugs (not enough data)• If under treatment, a recurrent

stroke occurs we can consider PFOclosure ( Amplazer device is themost popular)

Epitheli

Big vessels:

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Big vessels:I.  AtheromatosisII. Dissection

I . Atheromatosis

• Plaques

• Stenosis

• Occlusion

• Preferential sites: „ low shear stress regions” : ICA bulb, CCAbifurcation

Do not forget the aortic crosa !!! (sometimes, even if the ICA we can identify ateromatous plaques with thrombosis on the crosa by Trans Esophageal Ecocardiography)

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Big vessels : Atheromatosis

• Plaques• Accumulation of lipids (foam cells) in tunica media• Hyperplasia of smooth muscle cells

• Hypertrophy of smooth muscle cells

• Colagen fibers

• Neo- vascularization (sometimes these vessel bleed and intraplaque hemmaques the plaque unstable)

• Calcifications

• There is endothelial dysfunction and the endothelium above theprone to rupture (exposes the lipid core, and causes thrombosis

• Thrombosis in situ, with complete acute occlusion of the vessel

• Arterial embolism : thrombus will be fragmented and will occlude small

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 Atheromatous plaques

Atheromatous plaques can be visua

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 Atheromatous plaques can be visuaby Doppler Ultrasound examination

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 Atheromatosis: stenosis, occlusion• Stenosis

• High velocities inside

(Can determine the rupplaque and arterial em

• Combined with a decsystemic blood pressto hemodynamic infa

 flow infarction, wate

infarction  = infarcts tbetween superficial tmain vessels or betwsuperficial /deep terrmain vessel (ACA, MC

Doppler Ultrasound : extracranial (E

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pp (can visualize stenosis or occlusion(yellow arow)

Doppler ultrasound  – transcranial (T

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pp (Gives us information about the circleWillis

Transtemporal approach; through a go

“window “ one can easily visualize MCA

Watershed infarction

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Watershed infarction

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II. Dissection

Young patientsMinor trauma

Idiopatic

Extension from aortic dissection (rare)

Clinical aspects :Stroke or TIA

Lateral cervical pain

Claude Bernard – Horner Syndrome

Pulsatile Tinnitus

headache

Hypoglossus paralysis

Location : most frequent in the carotidchannel (the bone channel through whichthe ICA enters into the skull)

The mechanism : cleavage between intimaand media; blood enters between intima andmedia, can cause stenosis or occlusion;about 30% of dissections recanalize

Ecographic aspe

Small vessels

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Small vessels• Small arteries : diameter between 100 – 400

mcrons

• Arterioles: Vessels with a diameter < 100microns

The strokes will have small dimensions andare called lacunar infarcts (yellow arrow); aresituate in the subcortical white matter, basalganglia, brainstem (especially pons)

• Main causes:Arterial hypertension

Diabetes mellitus

VasculitisInflammatory

Isolated CNS vasculitisSecondary (infectious, in cancer, toxic origin,autoimmune disorders)

Non- inflammatory

Susac syndrome

Sneddon Syndrome

Post-partum angiopathy

Genetic disorders : CADASIL

CADASIL :Cerebral Autosomal DominantArteriopathy with Subcortical Infarction and

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 Arteriopathy with Subcortical Infarction andLeukoencephalopathy

• Genetic defect on Notch 3 gene(cromozome 19)

• Clinical phenotype - variablecombinations of:

• Migraine with aura

• Seizures

• Ischemic stroke

• Dementia

Fig. 1

Fig. 2

Fig. 1 MRI aspect of CADASIL. Typical white matter

lesions are seen as a hypersignal in FLAIR sequence-

white arrows

Fig. 2 : evolutive pattern of CADASIL (it is not

mandatory to have all the clinical manifestations but

the ma orit of atients finall will be demented

Blood

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Blood

Red cellsPolicytemia vera

Sickle cells disease

White cells

Leukemias (acute or chronic)

Lymphoma (there is a rare form of intravascular lymphoma)

Platelets

Thrombocytosis

Thrombocytopenia (i.e in thrombotic thrombocytopenic purpura)

Plasma

Waldenström Macroglobulinema

Thrombophilias

Hyperhomocysteinemia

Antiphospholipid antibodies

H di t k ?

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How we diagnose stroke ?• Anamnesis:

• Medical history (risk factors, associated diseases, age, family histo

Sudden onset (it is important to establish exactly the moment of othe time interval from the onset to the emergency room)

• Rapid progression of the clinical signs

• Altered consiousness or coma with focal neurological signs (in masor vertebro- basilar strokes)

• Clinical exam

From clinical point of vue, a sudden or a subacute onset can also be by:• Cerebral hemorrhage

• Subdural hematoma

• Necrosis or hemorrhage inside a brain tumor (primary tumor or a metastas

• Acute enkephalytis

H di t k ?

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How we diagnose stroke ?

• Clinical exam• Stroke mimics (ask about headache, seizures or psychiatric antecedents – i

migraine, a post seizure paresis (Todd paresis) or malingering)

• Cerebral CT scan (mandatory !)

• Can differentiate immediately between ischemic and hemorrhag

• Can differentiate ischemic stroke from other lesions (tumors, trau

In daily practice CT is usually enough for the diagnostic.• If there is a problem of differential diagnostic, CT with cont

MRI will be neccesary

Our patient has a stroke.

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Our patient has a stroke.Why did this happen?• If we know the cause, we will be more efficient in preventing a s

ischemic stroke• You keep in mind the list of possible etiologies (keep in mind the

there are many other causes ot inccluded on the slides)

• Start looking for the most frequent causes

• Continue by searching the less frequent

• Despite our extensive search arround 20% of strokes will remain

as „ undetermined etiology ” • Searching the cause can take several days, sometimes weeks. Th

will be treated from the beginning, according to general principltreatment for the ischemic stroke and the treatment will be adjuif it is neccessary the according to the results of the investigation

First line investigations (after we have performe

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First line investigations (after we have performe

scan (or MRI), and we know it is an ischemic stroke)

• Measure arterial blood pressure (ABP), heart rate, respiratory ra

oxymetry, body temperature• ECG

• Blood analysis (FBC, ESR, cogulation tests, glycemia, AST, ALT, BNcreatinine, LDL- cholesterol, HDL-chol, CK, CK- MB, LDH)

• Doppler ultrasound (ECD + TCD)

• Transthoracic ecocardiography (TTE), and in selected cases,transesophageal ecoardiography (TEE)

S d li i ti ti

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Second line investigations

• ECG continuous monitoring on 24 hours (purpose : to discover e

paroxysmal AF, or other rhythm disorders)• BP monitoring on 24 hours (purpose : to adjust the treatment)

• CTA, MRA (combined with Doppler can quantify stenoses)

• Angiography (can offer a precise measurement of stenosis, can cocclusion, may identify specific changes in small vessel vasculitis

Blood analysis for thrombophilias, vasculitis, certain infectious d(like shyphilis), dosage of alfa – galactosidase (for Fabry disease)

• Skin biopsy : osmiophilic garnulations (in CADASIL)

• And other...

CTA (computed tomography

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C (co puted to og ap yangiography)

Can visualize intracranial/

extracranial vessels :• Stenosis

• Occlusion

• Aneurysms

Arterio- venous malformation

Fig. 1 : stenosis of the internal carotid artery

F

Fig. 2 : Normal aspect of supraaortic

vessels (CCA, ICA, ECA, subclavian A,

VA, basilar artery

MRA (Magnetic resonance angiogra

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MRA (Magnetic resonance angiogra

Can visualize intracraniaextracranial vessels :

• Stenosis• Occlusion

• Aneurysms

• Arterio- venous malfor

MCA

ACA

ICA

PCA

Basilar artery

Vertebral artery

Fig. 1 : Circle of Willis

DSA Digital subtraction angiograph

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DSA. Digital subtraction angiograph

• The “gold standard “ for vessels` investigation

• A “four vessel” angiography should be performed (injection contrast substance through both ICA and both VA

• Image can be rotated so that the localization of an abnorma(stenosis, aneurysm) can be very precise

• Can differentiate between stenosis/occlusion

• Can visualize arterio-venous malformations (AVM) and idenfeeding arteries and drainage veins

• Can visualize specific changes in vasculitis (narrowing of sma

DSA (digital subtraction angiography

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DSA (digital subtraction angiography

MCAACA

Small infarctions in the basal ganglia and cortex (blue arrows) and focal narrowings of the sm(yellow arrows) in a case of postpartum angiopathy

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Management of stroke patients

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Management of stroke patients

• I. Primary prevention

• II. Acute stroke treatment

• III. Secondary prevention

• IV. Neurorehabilitation

Primary prevention

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Primary prevention• Treat the risk factors

• Arterial hypertension (the best results seem to be with ACE inhibitors +

• Diabetes mellitus: keep glycemia into normal ranges

• Dyslipidemia : use statins• Cholesterol dependent effects : they decrease LDL chol and triglycerides (use gu

the target level of LDL chol)

• Non- cholesterol dependent effects: statins improve endothelial dysfunction, stplaque, may determine the decrease of plaque dimensions)

• Change lifestyle : less food, less alcohol, more sports, no smokin

Use existing scores to calculate risk (i.e SCORE risk)• Do not use routinely Aspirin for primary prevention of stroke. It w

proven to be efficient. Use Aspirin when the patient has a high ristroke, like high grade carotid stenosis

• Use anticoagulants if the patient has a proven source of cardiac he/she has AF with a CHADS score ≥ 2 

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For AF use CHADS2 or CHADS- Va

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score

CHADS- vasc

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CHADS- vasc

• Attention !

• When a person alreadystroke we are speakingsecondary prevention

II Management of acute

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II. Management of acute • Admit the patient in the stroke unit

(monitoring, specialized personnel)

• Stabilize the vital functions• Intubate if necessary

• Give oxygen if needed• IV lines for hydration and medication

• Do not give Glucose iv (5 or 10%), unless youhave to correct hypoglycaemia because it willworsen acidosis

• Correct the glycaemia, electrolytes

•Treat cerebral edema with Mannitol 20%125 ml, iv perfusion, slow rhythm,maximum dose 6 perfusions/day

• Lower body temperature in case of fever *• * hypothermia (around 32◦ C can be an

important method for neuronal protection,but it is not a routine for the moment

• In the first 48 hours after stroblood pressure only if it exce

220/120 mm Hg• If the patient is a candidate f

thrombolysis, the cut-off valu

185/110 mm Hg

• Stroke is a stressful conditionpatient and blood pressure incompensatory reaction. Lowpressure will aggravate the pprognostic

• Do not lower fast the blood p

• Preferred drugs:• Labetalol

• Enalapril iv (when Labetalol i

Management of the acute stroke

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Thrombolysis• Criteria for thrombolysis:

Interval from stroke onset to thrombolysis ≤ 4.5 h • TA < 185/110 mm Hg

• Glycaemia > 50 mg/dL

• Platelets > 100.000/mmc

There are a lot of exclusion criteria, listed in a protocol, so that the pcan check everything, i.e:

- „wake –up „ stroke because there is no certainty about the moment of stro

- Surgical intervention in the last three weeks

- Hemorrhagic stroke in medical history

- Age < 18 years

- And others

Thrombolysis

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Thrombolysis• Check inclusion/exclusion criteria

• Cerebral CT scan

• Give 0.9 mg/kg body weight of rTpa (recombinant tromboplasminogen acbut no more than 90 mg in one hour, with an initial bolus of 10%

• The patient is monitored in the next 24 hours, especially for blood pressu

• The sooner we give rTpa the greater are the chances to recanalize the vesbrain); always try to gain time !

• Complications :• Bleeding (especially brain hemorrhage)•

Allergy to rTpa• Re- thrombosis after an initial recanalization (we can not repeat thrombolysis)

• Intravenous thrombolysis can be combined with intraarterial thrombolys

• In selected cases (especially in basilar occlusion) intrarterial thrombolysiscatheterism) may be the irst choice

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In a recent trial which compared thrombolysis/mechanical devices

thrombolysis was proved to be more efficient

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Management of acute stroke

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Management of acute stroke

• If the patient is not a candidate for thrombolysis treat all the com(stabilize vital functions, treat infections, feed the patient with ivor nasogastric tube, prevent pressure sores, prevent deep venouthrombosis); Of course we will treat all these also in thrombolyze

• Aspirin is the only drug proven to be efficient in acute stroke : 32

• Anticoagulants are indicated in cardioembolic stroke, but if the smassive, has a spontaneous risk of hemorrhagic transformation better to delay anticoagulation 48- 72 hours; Aspirin will be givetime interval

• After thrombolysis antiplatelet or anticoagulants can be given onhours.

III. Secondary prevention

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III. Secondary prevention

• Treat risk factors and associated diseases• For arterial hypertension the preferred combination is ACEI + Indapamid

• Change lifestyle

• Give oral anticoagulants in cardioembolic stroke (especially in AF• Acenocoumarol (Warfarin, Sintrom) : variable dosage, needs INR contro

least); in case of supradose or due to increase of the effect because of adrugs hemorrhage can occur.

The antidot: fresh frozen plasma

• Direct thrombin inhibitors (Dabigatran, 150 mg bid or 110 mg bid); do ncontrol, but Cr Clearance must be checked in case of dysfunction of the dosage must be decreased

• Inhibitors of Factor X activated (Rivaroxaban, Apixaban) – recently appro

Secondary prevention

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y p

• For all other strokes give antiplatelets

•Clopidogrel 75 mg/day

• Aspirin + Extended release Dipiridamol (Agrenox)

• Aspirin 75 mg/day

• If the patient is treated with Aspirin and has a recurrent stroAspirin will be replaced by Clopidogrel

• The association of Clopidogrel + Aspirin increases the risk ofhemorrhages and should be reserved to selected cases

Secondary prevention

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y p

Revascularization procedures

If a stroke occurs in the distribution territory of the internal cartery and ICA has a stenosis of 70%, this stenosis is considersymptomatic.

If no stroke occured and the discovery of the stenosis is incidestenosis is considered asymptomatic

Asymptomatic stenosis must not be re- vascularized routinely

Symptomatic stenosis > 70% must be re-vascularizedThe best results are obtained if the procedure is performed in the firafter stroke

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Ac

r

A

S

Revascularization

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• Endarterectomy

• Proven efficacy in 2 large trials(NASCET, ECST)

• Possible complications:• Hypoglossus paresis

• Complications related toanesthesia

• Acute thrombosis afterendarterectomy

• restenosis

• Angioplasty with stenti

• Increased efficay afterimprovement of technith use of protective filt

• Possible complications:• Arterial hypotension

Acute stent thrombosis• Restenosis

Patients with carotid stenting should rece

least 30 days after the procedure a combi

Clopidogrel 75 mg/day + Aspirin 75 mg/d

Patients with endarterectomy should

receive one antiplatelet drug, Clopidogrel

or Aspirin

Carotid Stenting

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ICA stenosis (white arrow), revascularization after introduction of the stent (red arrow), and

stent inside the vessel (yellow arrow)

IV Neurorehabilitation

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• It is very important for the recovery of normal functions, for social andinsertion of the patient

• Should be started very early, in the post – acute period• The neurorehabilitation team should include:

• Neurologist, physiotherapist, logopedist, occupationl therapist, social worker

• Every aspect should be assessed: motor function, spasticity, equilibrumdeglutition, speech, cognitive disorders

Cognitive disorders are an important aspect in stroke patients. It is not c

diagnose dementia immediatey after stroke, but the patients should beand re- evaluated because incidence of dementia is 9 fold increased in year after stroke

Depression also has an increased incidence and should be diagnosed anbecause if untreated it influences negatively the rehabilitation process