Stroke (cerebrovascular accidents)
Jan Fiksa
Stroke centre
Department of Neurology 1st Faculty of
Medicine and General Teaching Hospital
Stroke - epidemiology
Incidence: 300 per 100 000 inhabitants per year in
Czech Republic
age-associated disease
Mortality: 2nd-3rd place in total mortality
•Ischemic stroke 1/3 of patients die within
12 months
•ICH 2/3 of patients die within 6 months
•SAH 1/2 of patients die within 3 months
Work disability
Disrupted blood supply into a part of brain or whole brain
(ischemic strokes) - 80-85%
Hemorrhage to cerebral tissue (intracerebral hemorrhage –
ICH) or into subarachnoid space (subarachnoid hemorrhage SAH) - 15-20%
Ischemic strokes
Ischemic stroke - etiopathogenesis
Ischemic penumbra
Cerebral infarction
Ischemic stroke – classification by
disease of large arteries (macroangiopathy)
40-50% of ischemic strokes
disease of small arteries (microangiopathy)
20% of ischemic strokes
Small perforating arteries arising from
the Circle of Willis
lipohyalinosis, fibriniod necrosis, atherosclerosis
Ischemic strokes – classification by
cardioembolic strokes 20% of ischemic strokes
other defined types 5% of ischemic strokes
coagulopathies, migrainous infarction
other non-specified causes
5-15% ischemic strokes
Internal carotid artery
Oculo-cerebral syndrome
- one-sided vision disturbances, ipsilateral
- hemi-syndromes, contralateral
- neuropsychological deficit
Anterior cerebral artery
Always hemiparesis (paresis predominates on
lower limb)
1) left-sided lesion
+ apraxia of left-sided limbs
+ transcortical motor aphasia
+ apathy, abulia
+ urine incontinence
2) right-sided lesion
+ neglect on the left side
3) both-sided lesion
+ abulia or even akinetic mutism
Middle cerebral artery
Hemisensory syndromes
Homonymous contralateral hemianopia
Gaze palsies
aphasia, apraxia
disturbance of spatial perception
Posterior cerebral artery
Occlusion P 1
- sensory-motor hemiparesis
- hemianopia
Occlusion P 2
- hemianopia
- on the left Gerstmann syndrome, transc. sensory aphasia
- on the right neglect to the left, prosopagnosia
Bilateral occlusion (thrombosis of the rostral part of basilar artery)
- cortical blindness
- severe memory disturbance may be present as well (mediobasal
Clinical picture of
infratentorial lesion
Basilar artery
(vertigo, diplopia, transient atlernating right- and left-sided
hemisensory or hemiparetic symptoms)
- locked in syndrome
- coma with quadriplegia, oculomotor disturbances
Vertebral artery
Manifested as occlusion of posterior inferior cerebellar artery
Posterior inferior cerebellar artery
(Wallenberg´s sy)
- vertigo
- hemiataxia
- dysarthria
- Claude Bernard Horner´s sy homolateral
- contralateral hypesthesia for pain and temperature
- lesion of n. V., IV., X.,XI. (palatal myoclone)
Other brainstem vascular syndromes
III. + contralateral hemiparesis
III. + contralateral cerebellar ataxia + tremor
III. + contralat. cerebellar ataxia + hemiparesis
Millard Gubler
VII.+ sometimes VI. + contralateral hemiparesis
X. + contralateral hemihypesthesia
X. + XII. + contralateral hemihypesthesia
Specific clinical pictures
Carotid artery dissection
+ pain in neck, face, head
+ Claude Bernard Horner´s sy
…within hours to days …
+ retinal or cerebral ischemia
Vertebral artery dissection
Pain in occipital region
Claude Bernard Horner´s syndrome
Ischemia of brainstem
Subclavian steal syndrome
Often latent character
More frequently on the left
Different BP on the left and right arm
Symptoms :
pain or tactile disturbances in the arm region
transient vertigo, diplopia, uncertainty while walking
(may be provoked by work)
Vertebrobasilar insufficiency
transient or persistent disturbance of blood supply, duration
The base: arteriopathy in vertebrobasilar bloodstream
Difficulties are provoked by rotation or inclination of the head
Occipital headache, diplopia, vertigo,
Cortical disturbances of vision,
drop attacks (atonic falls)
Pseudobulbar paralysis
Based on multiple lacunes damaging corticobulbar pathways.
preceded by minimally 2 vascular accidents
eventually development without typical CV accident based on
status lacunaris
dysarthria, dysphagia, dysphonia, lesion of motor functions of
the tongue and muscles innervated by n. V. , VII., affective
Embolism to CNS
Sudden onset
headache may be present
epileptic seizure
(partial with secondary generalization)
always focal symptoms
(often TIA)
Venous sinus thrombosis
(pregnancy, postnatal, malign tumour, coagulopathy,
leads to intracranial hypertension
eventually with focal symptoms
(they are not typically localized according to arterial blood
Hypertensive encephalopathy
brain disorders induced by an acute critical rise of blood
Hypertensive encephalopathy
Nausea and vomit
Disturbed vision
Epileptic seizures
Focal neurological symptoms
Fundus of the eye – edema of the retina and optic disc,
MRI of brain - brain edema (also localized), petechial
hemorrhage and recent ischemic foci, PŘES (posterior
reversible encephalopathy syndrome)
Dementia after stroke
After stroke:
5x more frequent incidence of dementia/ 12 months
15-30% prevalence of dementia in the first 3 months
in 1/3: uncovered premorbid Alzheimer´s dementia
Ischemic stroke - diagnosis
1. Medical history
2. Clinical picture
differential diagnosis: tumours, abscesses, Todd´s paresis
after epileptic seizure, migraine with aura, episodes of
hypoglycemia, myasthenia gravis (brainstem lesions)
3. Urgent laboratory examination – biochemistry, blood cell
count, coagulation parameters
4. Imaging techniques
Ischemic stroke - diagnosis
Akutní stádium
Imaging techniques
computer tomography – (CT) –
method of the first choice
Po 24 hodinách
Ischemic stroke - diagnosis
CT angiography
Ischemic stroke - diagnosis
CT evaluation of brain
perfusion – perfusion CT
Ischemic stroke - diagnosis
MRI of brain
assessment of disruption of
perfusion and diffusion:
zone of malacia / zona
resonance angiography (MRA)
imaging of brain vessels without
necessity of contrast agent
Ischemic stroke - diagnosis
Digital subtraction angiography
Ischemic stroke - diagnosis
Sonographic examination
(extracranial supplying
arteries, intracranial brain
arteries – major branches)
Ischemic stroke - diagnosis
- therapy -
Stroke – organization of medical care
Europe-wide consensus from 1995
and recommendation
Europe Stroke Organization z r. 2008
National cerebrovascular program
(gazette of the Ministry of Health 2010)
Network of specialized centres:
Complex cerebrovascular centres
Stroke centres
Other work places
(subacute care centres and medical institutes of rehabilitation
and spa treatment)
Stroke – organization of med. care
„time is brain“
 brain - highly energetically demanding organ
- no energetic reserves
- necessity of adequate perfusion
 stroke – emergent condition
 therapy of stroke – struggle with time
Stroke – organization of care
Network of specialized centres
Reduces mortality (by 5%)
Shortens duration of hospitalization
Increases number of self-sufficient patients
Reduces an overall financial cost (by up to 30%)
Stage before hospitalization
 ABC protocol
 Rapid transport
 Not to treat elevated BP
„Time is brain“
Treatment benefit is time-dependent.
Every 10-minute delay in administration of thrombolytic
leads to deterioration of clinical condition by 1 point in
ESO 2009
Organization of hospital care
stroke centre
Rehabilitation department
Angio unit
Neurosurgical department
Treatment – basics
Emergent condition
1. Overall intensive early therapy
2. Recanalization
3. Treatment and prevention of secondary brain damage
4. Surgical procedures
5. Prevention
6. Rehabilitation and logopedic care
1. Overall intensive early therapy
Stabilization of vital functions
prevention of complications
Securing sufficient cerebral perfusion
Treatment of hyperpyrexia, hyperglycemia, reactive
together with the care of gastrointestinal tract
intensive rehabilitation
logopedic care
2. Recanalization
The goal – recovery of blood flow through the artery as
soon as possible
Tissue plasminogen activator (rtPA, alteplase, Actilyse)
intravenously, intraarterially, combined
Potentiation by exposure to ultrasound –
Medical history – Information on the time of onset
Neurological examination– NIHSS
Blood specimen
Brain CT
Normal finding/ early sings of ischaemia to the extent of 1/3 of the
medial cerebral artery territory
Carotid territory
< 4,5 hours
< 6 hours
< 12-24 hours
ECASS III (2009)
Perfusion CT of brain
CT angio
MR of brain
+ MR angio
Ultrasound of major arteries
/ event. within 24hours
Further assessment of NIHSS
Evaluation of blood results
Consideration of contraindications
Systemic thrombolysis (<4.5 hours)
alteplase-rtPA, 0,9mg/kg
(10% bolus, rest in 60 min infusion
+ event. transcranial sonothrombolysis
Local thrombolysis
Mechanic disobliteration <8hod
3. Surgical procedures
Early endarterectomy:
symptomatic stenoses ACI
Disobliteration to 6 hours after the onset
To 2 weeks after the onset: in very mild neurological
symptoms with minimal findings on CT
Other procedures postponed.
Neurosurgical intervention
Malignant infarction of MCA – decompressive craniectomy:
to 48 hs after the onset
to 60 years of age
when signs of ischaemia > 50% territory
Cerebellar infarction with expansive tendencies
is indication to ventriculostomy and
decompression (recommended even in patients in comatous
4. Treatment and prevention of
secondary damage of CNS
Slowdown of development and suppression of further
progression of ischemic brain damage – neuroprotective
therapy (studies)
Antiedematous treatment – drainage body position, sedation,
osmotherapy, decompressive craniectomy
5. Prevention
Primary prevention
set of measures to reduce risk of the stroke to minimal degree
A: elimination of risk factors that can be influenced
arterial hypertension
heart disease with high potential of embolism
diabetes mellitus
stenosing processes in accessory brain arteries
life-style regimen (cessation of smoking, moderate
consumption of alcohol, reduction of body weight, sufficient
physical activity)
Secondary prevention
set of measures aimed to reduce risk of the relapse
A: elimination of risk factors, suppression of development of
endothelial dysfunction, life-style measures
B: antiplatelet therapy – in all patients except from those with
severe risk of cardioembolism – acetylsalicylic a., combination
of acetylsalicylic acid with slowly released dipyridamol,
C: anticoagulation therapy – atrial fibrilation, conditions after
myocardial infarction with evidence for blood clots in left heart
compartments, artificial valves – warfarin
D: surgical and endovascular interventions
carotid endarterectomy (considered in stenosis more than 50%)
percutaneous transluminal angioplasty, stents
various reconstruction procedures
6. Rehabilitation a logopedic care
Multidisciplinary rehabilitation
The goal: to preserve maximum of
social functions.
Intracerebral hemorrhage (ICH)
ICH – pathogenesis
A. Anatomical abnormalities:
local lesion of vascular wall (atherosclerosis, lipohyalinosis,
fibrinoid necrosis) – small aneurysms
Deposition of amyloid into the vascular wall
Vascular anomalies (arteriovenous malformations, kavernous
angiomas, venous angiomas)
ischemic damage to vascular wall – hemorrhagic
transformation of infarction focus
ICH – pathogenesis
B. Hemodynamic abnormalities:
long-term or short-term elevation of blood pressure
C. Disorders of blood clotting (hemophilias) – rare
iatrogenic genesis – consequence of anticoagulation or
thrombolytic therapy, only rarely caused by antiplatelet therapy
ICH - classification
1. Typical hemorrhages:
deeply in the brain, cerebellum, brainstem, incidence
80%, hypertension
2. Atypical (lobar, globous) hemorrhages:
more superficially – subcortically, incid. 20%
rupture of vascular anomaly,
amyloid angiopathies in elders
ICH – clinical picture
Typical hemorrhages:
combined focal symptoms and symptoms of intracranial
bad prognosis, high mortality
Lobar hemorrhages:
focal symptomatology, initiated by focal epileptic seizure in 1/3
of patients, better prognosis
ICH – diagnosis
1. Medical history
2. Clinical picture
differential diagnosis: tumours, abscesses, Todd´s paresis
after epileptic seizure, migraine with aura, hypoglycemia,
myasthenia gravis (brainstem lesions)
3. Urgent laboratory examination – biochemistry, blood cell
count, coagulation parameters
4. Imaging techniques
ICH – diagnosis
Imaging techniques
CT of brain
CT angiography
MRI angiography
Determination of „age“ of the
it is possiblle to detect acute
hemorrhages and low-flow
anomalies - cavernomas
gradient echo
ICH – therapy
Emergent condition
Individualization of therapy
Stroke centre
Basics of therapy
 General intensive early therapy, including psychotherapy,
rehabilitation, logopedic care
 Suppression of progression of hemorrhage
 Treatment and prevention of secondary brain damage
ICH – general intensive treatment
stabilization of vital functions
Sufficient brain perfusion (CPP more than 60 mmHg)
Care of GIT and nutrition
Stability of homeostatis
Treatment of reactive depression
Prevention of venous thrombosis
and decubitus
Rehabilitation a logopedy
ICH – suppression of progression of
progression of bleeding ca. in 1/3 of patients
Treatment of hypertension
< BPmean 130 (BPs < 180) patients with intracranial
target BP 160/90
patients without IC hypertension
ICH – suppresion of progression of
Acceleration of formation of coagulum
Administration of plasmatic coagulation factors (frozen plasma)
Concentrated solution of plasmatic factors II, VII, IX, X
- vitamin K -
ICH – treatment of secondary brain
Surgical evacuation of hematoma
(cerebellar hemorrhages, lobar hemorrhages)
ICH – treatment of secondary brain
Antiedematous treatment
Monitoring ICP – SjO2 – inv. BP
1. Hyperventilation with target ETCO2 4,0-4,5 kPa
2. Liquor drainage, if possible
3. Osmotherapy – Manitol 0,25g/kg – 1 g/kg
(decrease of Hct and viscosity x increase of blood flow and
oxygen supply)
- NaCl 10% - target level Na 145-150mmol/l
ICH - prevention
Treatment of hypertension
Life-style regimen – cessation of smoking, using drugs of
abuse, moderate consumption of alcohol
Check-ups of anticoagulation therapy
ICH - prevention
prevalence 0,3-0,5%
Manifestation – seizures, focal symptoms (may be transient)
Incidence of hemorrhage: 2,5-5%/ 1 cavernoma
relapse of bleeding up to 66% !
Neurosurgical exstirpation
ICH - prevention
Arteriovenous malformations:
Presentation – hemorrhages (up to 80%), seizures (up to 50%),
cephalea (up to 50%), ischaemia or compression of
surrounding tissue (up to 40%)
Neurosurgery (inc navigation, fMRI,..) Endovascular procedures
(dural AVM, surgically inaccessible AVM); Combination of
neurosurgery and endovascular procedure
Radiotherapy (when size of AVM to 3cm)
Subarachnoidal hemorrhage (SAH)
SAH - definition
Penetration of the blood into leptomeningeal, ie. intermeningeal
space between pia mater and arachnoid mater.
Subarachnoidal hemorrhage (SAH) – 5% of all strokes
SAH - pathogenesis
rupture of aneurysm within arteries of Circle of Willis
bleeding from arteriovenous malformation
bleeding from dural malformation
traumatic SAH
SAH - aneurysms
aneurysms in the Circle of Willis and arising cerebral arteries 1-5% of population
Higher prevalence in patients with polycystic kidneys, Marfan´s
syndrome, Ehlers-Danlos´ syndrome, familiar cases
Yearly risk of the first rupture 1-2%
SAH - aneurysms
more frequently:
arteria communicans anterior
various shapes (saccate, fusiform,
SAH – clinical symptoms
Nausea, vomiting
Meningeal syndrome (may be absent)
SAH – clinical symptoms
Disturbances of consciousness
quantitative (from somnolence to coma)
qualitative (disorientation, agitation, aggression, confusion)
Acute death
5% of patients die before being admitted to the hospital
SAH - clinical symptoms
Scale according to Hunt and Hesse
Clinical picture
Aneurysma that has not bled yet
Mild headache, mild nuchal opposition, without focal symptoms
Moderate to severe headache, nuchal stiffness, paresis of cranial
nerve, without other focal symptom
Disturbed consciousness (somnolence, confusion), focal
neurological symptoms
Severe disturbance of consciousness (sopor, coma), hemiparesis
Coma, decerebration symptoms
SAH - diagnosis
Medical history and clinical picture
Imaging techniques and laboratory tests
CT of brain in the first 24 hours 95%-98% sensitivity
(MRI of brain – may show the age of hemorrhage)
Lumbal puncture and liquor examination
(spectrophotometry!) to exclude false negative finding
SAH - diagnosis
Imaging and laboratory tests
Angiography (DSA, MRA, CTA) to determine the cause
30% of SAHs – the source of bleeding not detected
Repeating angiography after 3-6 weeks = source detected in
other 10-20% of patients
SAH - complications
20-30% of patients in the first 30 days
mortality 60-70%
formation: 3rd-5th day, maximally 5th-14th day, disappear after
2-4 weeks
diagnosis: TCD, TCCS
therapy: 3H (hypertension, hypervolemia, hemodilution)
acute obstructive/low reabsorption
ventricular drainage
SAH - therapy
According to clinical condition (Hunt-Hess), imaging findings,
character of the source and its localization
1. Conservative treatment
2. Surgical and endovascular interventions
3. Treatment of complications
SAH - therapy
1. Conservative:
A: general intensive care (management of constipation,
coughing, stress – high fibre diet, laxatives, mucolytics,
analgesics, anxiolytics, hypnotics)
B: rest on the bed
SAH - therapy
2. Surgical and endovascular interventions
early - to 72 hs x postponed
opened (clipping) x endovascular (coiling)
SAH - therapy
3. Treatment of complications
A: nimodipine
B: ventricular drainage
Thanks for your

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