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
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
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
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)
Recurrence of stroke
Ischemic stroke (%)First year 6-12
in 5 years 30-40Myocardial infarction 15
Vascular death 15
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
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
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
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