CerebrovascularCerebrovasculardisorders: disorders:

strokestroke

What is stroke?

• Suddenly (acutely) developing neurological deficit of vascular origin that lasts longer than 24 hours

• 80-85% ischemic

Stroke subtypes

Albers G et al. Chest. 2001; 119 (suppl): 300S.

Ischemic stroke ~ 80%

Haemorrhagic stroke~20%

Other5%

Unknown30%

Cardiogenembolisation

20%

Small artery disease

25%

Atherothrombotikucstroke

20%

Prognosis of stroke

• Slight disabilities 57 %• Moderate disabilities 9 %• Severe disabilities 18 %• Deceased 15 %

Grau AJ, et al. Stroke 2001

Transient ischamic attack (TIA)

• Sudden onset of (any kind) focal neurological sign that disappears within 24 hours

• anything (weakness, numbness, dizziness, aphasia, visual disturbance (amaurosis fugax), double vision

TIA symptoms

• Sudden onset, usual duration is 5-20 min.• Carotid artery symptoms:

– Ipsilateral monocular visual loss (amaurosisfugax)

– Contralat. paresis, sensory loss– Aphasia, agnosia, apraxia (dominant

hemisphere)– Combination of the above

TIA symptoms

• Vertebrobasilar arteries:– Binocular visual loss

– Vertigo, ataxia– Dysarthria, dysphagia (TGA)

– diplopia

Risk after TIA1707 TIA’s patients, 90 daysfollow up

• 428 (25.1 %) hospital readmission (for several reasons)

• 216 recurrent TIA – (12.7 %).• 44 cardiovascularis events (2.6 %)

• 45 death (2.6 %),

Clinical groups - TIA

• 10% of all cerebrovasc. disorders• 10% of all stroke patients have a

history of prior TIA

• 1/3 of persons who had TIA will develop stroke within 5 years

EPIDEMIOLOGY of STROKE

Stroke

• A leading cause of serious, long-term disability (25-50% of stroke victims remains handicapped)

• 730.000 new or recurrent strokes occur per year in the US

• 40.000-50 000 /year hospital admission due to stroke in Hungary (a new stroke inevery 13th minute…!)

• Third leading cause of death after cardiovascular diseases and cancer

Józan Péter: Agyérbetegségek, 1998. 4: 2-6, KSH 2001

0% 20% 40% 60% 80% 100%

2000

1990

1980

1970

Stroke hearth+periph.art. other

Distribution of mortality in Hungary

0

50

100

150

200

250

300

1970197

2197

419

7619

78198

019

82198

4198

619

88199

019

92199

4199

6Russia

BULGaRIA

PORTUGAL

Hungary.

Sveden

France

Stroke mortality (1970-1997)

Józan Péter: Agyérbetegségek, 1998. 4: 2-6

Epidemiology

• Season differences: more frequent in winter and in spring

• Daily differences: most frequent at daybreak

• Sexual differences: Men> 2x> Women (stroke rates rise rapidly in menopausa)

Autoregulation of the brain circulation

0102030405060708090

100

0 50 75 100 125 150 175 200 225 250

NormalHypertension

Tension (Hgmm)

CBF

�In 90% of the cases occlusion of the intra/extracranialarteries can be detected

�Without reperfusion the majority of the ischemic damage is irreversible

�80-85%-of all strokes are ischemic

Thrombolysis in acute ischemic stroke

PenumbraInfarktus

CORE

PENUMBRA

H:min

0:00

0:35

2:15

2:45

3:15

3:45

4:15

5:00

5:35

6:00 hours

Intravenous (or intra-arterial)administration of thrombolytic agents

can achieve recanalization and improve outcome in carefully

selected patients with acute ischemic stroke

Thrombolysis

• Iv. rt-PA (0.9mg/kg) with 10% of the dose in iv. bolus, followed by infusion lasting 60 min –within 3 hours of onset of ischemic stroke

• Iv. administration of streptokinase is dangerous• Intra-arterial treatment of acute MCA occlusion

in 6 hour time window is rec. (using pro-urokinase) – not registered

• Acut basilar occlusion may be treated with intra-arterial therapy – not registered

Beforethrombolysis

CT, no contrast

Before thrombolysis

CT, no contrast

Beforethrombolysis

MRI T2

Beforethrombolysis: diffusionMRI

Before thrombolysisMRI angiography

After 6 hours of thrombolysis: recanalisation

After 6 hoursof thrombolysis

MRI T2

After 2 days ofthrombolysis

CT, no contrast

How to decreaseconsequences of stroke

Primary prevention

Acut stroke treatment

Secundary prevention Rehabilitation

RiskRisk factorsfactorsAge

0 - 14 1 / 30 00015 - 24 1 / 10 00025 - 34 1 / 900035 - 44 1 / 500045 - 54 1 / 100055 - 64 1 / 30065 - 74 1 / 10075 - 84 1 / 5085 + 1 / 30

�strong association with the age

Stroke risk/year

Age groups

Risk factors of strokeRisk factors of strokeNon Non -- modificablemodificable

Age, Gender, Race, HeredityAge, Gender, Race, Heredity

ModificableModificable

Medical ConditionsMedical Conditions BehaviorsBehaviorsHypertensionHypertension Cigarette smokingCigarette smoking

Cardiac diseaseCardiac disease Alcohol abuseAlcohol abuse

AtrialAtrial fibrillationfibrillation Physical inactivityPhysical inactivity

HyperlipidemiaHyperlipidemia

Diabetes mellitusDiabetes mellitus

Carotid Carotid stenosisstenosis

Hypertension is the most important Hypertension is the most important risk factor of strokerisk factor of stroke!!

��MetaanalysisMetaanalysis of 14 large randomized of 14 large randomized controlled trial controlled trial showed, that showed, that decrease of decrease of diastolicdiastolic blood pressure by 5blood pressure by 5--6 6

HgmmHgmm decreases the relative risk of decreases the relative risk of stroke by stroke by 42%42%

��DoDo notnot decreasedecrease thethe bloodblood pressurepressure ininacuteacute strokestroke! (200/100, 150/100 ! (200/100, 150/100 ininhemorrhagehemorrhage))

HypertoniaHypertonia megelmegelıızzéésese

�� 40 40 éév alatt kv alatt kééttéévente vvente véérnyomrnyomáásmsméérrééss

�� 40 40 éév felett v felett éévente, 50 felett fvente, 50 felett féélléévente vente vvéérnyomrnyomáásmsméérrééss

�� HypertoniaHypertonia esetesetéén 140/85 n 140/85 HgmmHgmm alaláá kell a kell a vvéérnyomrnyomáást best beáállllíítani az tani az ééletmletmóód d mmóódosdosííttáássáával ill. gyval ill. gyóógyszerrel (I. szintgyszerrel (I. szintőőevidencia)evidencia)

PrimaryPrimary preventionprevention

Red wine from Red wine from VillVilláányny ……??

Primary preventionPrimary prevention

Primary preventionPrimary prevention

Primary preventionPrimary prevention

Aspirin in primary stroke Aspirin in primary stroke preventionprevention

Recurrence of stroke

Ischemic stroke (%)First year 6-12

in 5 years 30-40Myocardial infarction 15

Vascular death 15

AspirinAspirin: 300: 300--100 mg/100 mg/dayday

ClopidogrelClopidogrel

DipiridamolDipiridamol plusz plusz AspirinAspirin

Oral anticoagulationOral anticoagulation

relative risk reduction forstroke of 60-65 %, with a target internationalnormalisedratio of 2.0-3.0

BMJ 2002;324:656

Cholesterol lowering therapy in Cholesterol lowering therapy in secondary prevention of strokesecondary prevention of stroke

secondary prevention of strokesecondary prevention of stroke

CarotidCarotid endarterectomyendarterectomy ((oror stentstent?)?)

Clinical manifestations of atherothrombosis

Adapted from: Drouet L. Cerebrovasc Dis2002; 13(suppl 1): 1–6.

TransienTransientt ischaemiischaemiccattackattack

Angina:• Stabil• Instable

IschaemiIschaemiccstrokestroke

Myocardial infarction

Peripherial vessel diseases

Small artery occlusive stroke

• 15-20% of thrombotic stroke

• Lipohyalinosis, local arteriosclerosis of smallpenetrating arteries

• Etiology: long standing hypertension or diabetes• Typical localisation:basal ganglia, thalamus,

pons, internal capsule• Infarction are smaller than 1,5 cm in diameter• Gradual progression

Lacunar infarction

Symptoms

• Pure motor paresis (internal capsule, pons)

• Pure sensory deficit (thalamus, corona radiata

• Dysarthria-clumsy hand (pons, internal capsule)

• Ataxic hemiparesis (internal capsule)• Multiple infarction are associated with

vascular dementia

Cerebral embolism

• 20% of ischemic stroke• Younger patients• Acute onset, maximal severe deficit,

quickly improvement• Recurrent stroke (more than one vascular

territory)• Cortical infarction• Cardiac diseases in the anamnesis

Cerebral embolismIntracardialthrombus

Vegetation on theaortic valve

Etiology

• Atrial fibrillation (most important risk factor of stroke in elderly women

• AMI –stroke complicates 2-4%, usually in the first 4-5 weeks (mural thrombus)

• ventricular aneurysm• Valve disorders• Prosthetic valve• Infective endocarditis• Intracardial tumors• Cardiac procedures (angiography, bypass,

PTCA)

Hemodynamic stroke

• Global reduction of the CBF• Cardiac dysfunction, hypotension,

hypoxia, hypoglycemia, severe carotid artery stenosis

• Multifocal ischemic lesions (cortex, anterior-posterior watershed infarction

Intracerebral hemorrhage

• 10-14% of all strokes, typical age 50-70 years

• Overall mortality vary between 25-60%• Etiology: history of hypertension:72-81%• The chronic hypertension is associated

with fibrinoid degeneration of small arteries of the brain (Charcot-Bouchard microaneurysm)

Etiology

• Vascular malformations (aneurysm, AVM, cavernous angioma)– Leading cause of stroke in younger age group

(female predominance)– Typical lobar hemorrhage (temporal-frontal)– Cavernous angiomas are often located in the

sub cortical white matter and in the pons– Clinical presentation: seizures (30-70%), ICH

(10-30%), progressive neurological deficit (35%)

Etiology of ICH

• Intracranial tumors– Less than 10% of ICH (glioblastoma, metastases)

• Bleedind disorders: hemophylia, ITP, leukemia)• Anticoagulant (10%) and fibrinolytic treatment

– Slowly progressive course is typical, large volumehematomas, high mortality

• Cerebral amyloid angiopathy (selectivedeposition of amyloid in cerebral vessels (cortex-leptomeninges)– Elderly, nonhypertensive patients, reccurent lober ICH

or SAV– Association with histopathological features of

Alzheimer’s disease, progressive dementia

Etiology of ICH

• Granulomatosus angitis (vasculitis)– Monocular inflamation in the wall of intracranial

arteries

• Hemorrhagic transformatio of cerebral infarction(cerebral embolism)

• Trauma: hematoma occurs in surface of brain, often multiple

• Sympathomimetic agents (amphetamines, cocain)– Subcortical white matter localisation

Clinical manifestation

• Sudden onset, followed by progression• Symptomes of elevetad ICP (haedache,

womiting, depressed level of consciousness• Focal neurological deficit, rarely seizures• Size of hematoma:

– small:<1cm- good prognosis– Medial:1-3 cm- prognosis is related on localisation– Large: 3-5 cm – poor prognosis– Extralarge: >5cm - fatal

Anatomical forms of ICH

• Putaminal: 35% , mortality: 37%• Caudate: 5%, mortality: 10%• Thalamic: 10-15%, mortality: 30%• Lobar: 25% mortality: 30%• Cerebellar: 5-10% , mortality: 20%• Pontin: 5%, paramedian:mortality: 80%• Mesencephalic: rare• Medullary: rare, mortality: 100%• Intraventricular: secondary form (caudate, thalamic,

putaminal, lobar), primary form: sunependymalmalformation

Subarachnoid haemorrhage

• Incidence: 15/100.000/year• 6-10% of all strokes• Etiology: a)intracranial aneurysm (75%), b)

arteriovenosus malformation (5%) c)other• Pathogenesis:

– Classification of aneurysm: morfological: 1. saccular, 2. fusiform, 3. dissecting

– Size: <3mm, 3-6 mm, 7-10 mm, 11-25 mm, >25 mm (giant)

– Origin: congenital (90%)-arise from defects in themuscular layer of cerebral arteries?, degenerativechanges? Both ?

– Other origin: arteriosclerotic, septic-mycotic, traumatic, neoplastic

– Location_ arterial bifurcation of the circle of Willis

Clinical symptoms of SAV

• A: unruptured aneurysm: – Anterior comm. artery- visual field defects– Posterior comm. artery- oclulomotor nerv palsy– Middle cerebral artery- aphasia, hemiparesis, seizures

• B: ruptured aneurysm: – Sudden oncet headache, often extremly severe, womiting– Meningeal sign– Neurological deficit– Depressed level of consciousness

Hunt –Hess clinical score

• Grade 0: unruptured aneurysm• Grade I: asymptomatic or mild headache• Grade II: moderate or severe headache,

nuchal rigidity, cranial nerve palsy• Grade III: drowsiness, mild deficit• Grade IV: stupor, moderat to severe

hemiparesis, vegetative disturbances• Grade V: deep coma, decerebrate rigidity,

moribund state

Potential complications ofSAV

• Rebleeding (10-30%) (prevention of rebleeding: endovascular occlusion of the aneurysm, as soon as possible)

• Delayed ischaemia related to vasospasm 3-14 days

• Cerebral oedema• Acut obstructive hydrocephalus• Delayed communicating hydrocephalus• Intracerebral, subdural haematoma