Cerebrovascular disorders

Prof. Daiva Rastenytė

Department of Neurology

2017/2018
• Generals
• Symdromes
• Ischemic stroke
• Hemorrhagic stroke
 Post. Cerebellar a.
Post. Communicating a.
Sup. Cerebellar a. Middle cerebral a.
Basilar a. Anterior cerebral a.
AICA a. ophtalmica
sinus cavernosus
Internal carotid a.
Externsl carotid a.

PICA
Vertebral a.

Common carotid a.
Subclavian a.
Brachiocephalic trunk
Aorta
Arterial circle of Willis
Ant. Communicating a.
ACI
ACA
Middle cerebral a.

Post. Communicating a.

a. cerebellaris sup. ACP

a. basilaris
AICA

a. vertebralis

PICA
Carotid (anterior circulation)
and vertebrobasilar (posterior
circulation) distribution
Major cerebral vessels that branch from the ICA
The branches and distribution of the
Middle cerebral artery and principal regions
of cerebral localisation
The branches and distribution of the
Anterior cerebral artery and principal regions
of cerebral localisation
The branches and distribution of the
Posterior cerebral artery and principal anatomic
structures
 Th

PCA

Basilar

PICA

Vertebral
 Stroke Epidemiology

• Stroke is the third most common cause of death in developed countries,

exceeded only by coronary heart disease and cancer
• 795,000 new or recurrent strokes occur per year in the US, accounting for
approximately 1 in 18 deaths
• The prevalence of stroke in the US is about 7 million (3.0%) at an
estimated cost in 2010 of 73.7 billion US-$
• In Europe, the incidence of stroke varies from 101.1 to 239.3 per 100,000
in men and 63.0 to 158.7 per 100,000 in women
• The estimated cost of stroke in Europe in 2010 was approx. € 64.1 billion
• In China, the prevalence of stroke ranges between 1.8% (rural areas)
and 9.4% (urban areas)
• Worldwide, China has one of the highest rates of mortality (19.9% of all
deaths in China), along with Africa and parts of South America

Gustavsson et al. Eur Neurpsychopharmacol 2011;21:718-779.

AHA and Stroke Statistics Writing Group. Circulation 2010;123:e1-e192.
EROS Investigators. Stroke 2009;40:1557-1563.
Sousa et al. Lancet 2009;374:1821-1830. The Atlas of heart disease and stroke, WHO 2004.
Epidemiology

Lithuania:
• > 11 thousand stroke victims every year
• nearly 5000 deaths from CVD every year
• IV-III cause of death
• III cause of handicap

Lietuvos sveikatos informacijos centras

 Stroke Types and Incidence
12%
Haemorrhagic
Other
5%
Atherosclerotic
Cryptogenic cerebrovascular
30% disease
20%

Small vessel
Cardiac disease
embolism “lacunes”
20% 25%

Ischaemic stroke
88%
Albers et al. Chest 2004;126 (3 Suppl):438S-512S.
Thom et al. American Heart Association. Circulation 2006;113:e85-e151.
Focal neurological symptoms
• Weakness (monoparesis, hemiparesis, paraparesis, hemiplegia)

• Sensory loss (hemihypoesthesia, hypoesthesia)

• Incoordination (ataxia)

• Hemianopia

• Aphasia, dysphasia

• Apraxia, hemi-inattention, anosognosia, graphesthesia,

stereognosis, etc.
The internal carotid artery (ICA) syndrome
(the anterior circulation syndrome)

• Contralateral hemiparesis and/or hemihypesthesia

• Contralateral homonymous hemianopia
• Cortical dysfunction (graphesthesia, stereognosis, aphasia,
apraxia, hemi-inattention, anosognosia (unawareness of illness),
etc.)

• A forced deviation of eyes and head towards the side of

the infarct (away from the paretic side, in case of large MCA
infarcts)
The posterior circulation syndrome
• Brainstem symptoms
– Diplopia
– Dizziness
– Dysarthria
– Dysphagia
– Dysmetria-dyssynergia (with involvement of cerebellar pathways)
• Contralateral to the brainstem deficits hemiparesis/
hemihypesthesia
• Hemianopia with sparing of central vision

• A forced deviation of eyes and head away from the side of

the infarct (towards the paretic side, in case of pons infarcts)
• A red flag for BA syndromes is impairment of the level of
consciousness, which can include coma
 Lateral medullary syndrome (Walenberg,
PICA, a.vertebralis)
– Vertigo, nausea and vomiting (VIII)
– Dysphagia, dysarthria (IX, X n. ambiguus)
– Dissociated sensory loss (pain, t°C):
• Face – ipsilateraly (n.tr.spinalis n. trigeminus)
• Trunk & extremities – contralateraly (tr. spinothalamicus lateralis)
– Ipsilateral cerebellar signs and symptoms
• Asynergia (pedunculus cerebellaris inferior)
• Muscle hypotonia, ataxia (tr. spinocerebellaris anterior)
– Ipsilateral Horner’s s. (tr. sympaticus centralis)

The motor system, tongue movements, and vibration & position

sense are typically spared
 Medial medullary syndrome (a.vertebralis,
a.spinalis anterior)

• Ipsilateral flaccid paresis, atrophy, and fibrillation of the tongue

(XII). The protruted tongue deviates toward the lesion (away from
hemiplegia)
• Non-spastic contralateral hemiplegia (pyramids)
• Contralateral loss of position and vibratory sensation (lemniscus
medialis)
• Vertical nystagmus (FLM)
• Pain and temperature sensation are spared
Small vessel syndromes -
lead to smaller infarcts called lacunes
• Pure motor s. (CI, pons)
– Contralateral hemiparesis
• Pure sensory s. (Th)
– Contralateral hemihypestesia
• Ataxic hemiparesis (Pons)
– Kontralateralinė hemiparezė (koja > ranka)
– Kontralateralinė ataksija
• Sensorimotor (Th)
– Contralateral hemiparesis and hemihypestesia
• Dysarthria-clumsy hand s. (anterior limb of CI)
• Dystonia and hemiballismus/hemichorea (head of caudate
n., thalamus, subthalamus)
 Definitions (1)

• Stroke is a clinical syndrome defined by acute

neurological deficits (symptoms) in the setting of
focal disruption of cerebral circulation
 Definitions (2)

• Three main types of stroke:

– Ischemic stroke due to blockage of a brain artery by
an embolus or by thrombosis.
• If the neurological deficit lasts for more than 24 hours
it is a completed stroke
• If the neurological deficit lasts for less than 24 hours it
is a transient ischemic attack (TIA)
 Definitions (3)

• Three main types of stroke:

– Ischemic stroke

– Intracerebral hematoma (hemorrhagic stroke) due to

bursting of a brain blood vessel into cerebral parenchyma

– Subarachnoid hemorrhage due to rupture of a blood

vessel aneurysm into the cerebrospinal fluid within the
subarachnoid space
Risk factors
Potentially modifiable RF Nonmodifiable RF

• Hypertension Age
• Cigarette smoking Sex
• Diabetes
Race
• Heart disease (AF, MI, CHF)
Genetic prediposition
• TIA
• Elevated cholesterol
• Hyperhomocysteinemia
• Narcotics
• Contraceptives
• Obesity
• Inactivity
• Elevated fibrinogen
Ischemic stroke (cerebral infarction)
Onset
• Relatively slow (over minutes, hours) progression of
focal neurological symptoms and signs; onset during
night sleep is common

Symptoms
• Symptoms seen in individual acute ischemic stroke
patient reflect the brain region affected by the ischemic
injury
Clinical findings
• Abnormal findings on the neurological exam, like the
symptoms, reflect the brain region affected by the
ischemic event
Laboratory tests

• Blood count, glucose, electrolits, ECG

• CT, CTA, CT perfusion
• MRI
• Angiography
• Carotid and transcranial ultrasound
• EchoCG, ECG, Holter ECG monitoring
L
L
L
CT

L
CT MRI
 Oxford Community Stroke Project
classification of stroke

• Total anterior circulation infarction, TACI

– Unilateral motor and sensory deficit, hemianopia, disturbance of
higher cerebral function
• Partial anterior circulation infarction, PACI
– Any two of above
– Isolated disturbance of higher cerebral function
• Posterior circulation infarction, POCI
– Signs of brainstem dysfunction
– Isolated hemianopia
• Lacunar infarction, LACI

Bamford et al., 1991

Differential diagnosis

– Tumor, subdural hematoma, acute hydrocephalia

– Migraine
• Slow progression of positive symptoms (flashing lights
(photopsia), tingling) together with headache
– Seizures
• Positive symptoms predominate (twitches), impairment of
consciousness
• Seizures are not common to arterial ischemic stroke (5% of
cases); think about venous stroke or other causes
– Hypotension
– Hypoglycaemia
– Hyponatremia
Differential diagnosis

• Negative symptoms are typical for stroke (hypestesia, hemiparesis

(weakness), aphasia), not positive (tingling, twitching flashing lights)

• Impairment of consciousness is not typical for TIA and usually is

observed in case of severe stroke in MCA territory or SAH. If
impairment of consciousness is present, think about direct (brainstem
stroke) or indirect (edema or transtentorial herniation) dysfunction of
brainstem or thalamus.
 Stroke Chain of Survival

 Rapid patient recognition and reaction to stroke warning signs

 Rapid emergency medical services (EMS) dispatch

 Rapid EMS system transport and hospital pre-notification

 Delivery direct to imaging

 Rapid in-hospital diagnosis and treatment

 Effective EMS systems can minimise delays in pre-hospital

dispatch, assessment, and transport, and ultimately increase
the number of stroke patients reaching the hospital and being
prepared for thrombolytic therapy within the approved time
window
AHA. Circulation 2005;112:111-120.
Wojner-Alexandrov. Stroke 2005;36:1512-1518.
Deng et al. Neurology 2006;66:306-312.
The mainstays of acute treatment

• Treatment and stabilisation of general conditions (AH,

t0C, glucose level)
• Specific therapy (either recanalisation of a vessel occlusion or
prevention of mechanisms leading to neuronal death in the ischemic
brain (neuroprotection))
• Prophylaxis and treatment of complications (secondary
hemorrhage, space-occupying edema or seizures, aspiration,
infection, decubital ulcers, deep venous thrombosis, pulmonary
embolism)
• Early secondary prevention
• Early rehabilitation

ESO, 2008
 General treatment

 Intermittently monitor neurological status, pulse, BP, t0C, O2 saturat.

 O2 - if O2 saturation falls <95%
 Regularily monitor fluid balance and electrolytes in pts with severe
stroke or swallowing problems
 Normal saline (0.9%) during first 24 hrs after stroke
 Cautious BP lowering (BP >220/120 mmHg) or with severe CF, aortic
dissection, HE
 Serum glucose levels >10 mmol/l - insulin
 Severe hypoglicemia (<2.8 mmol/l) – I.V. 10-20% glucose
 Search for concurrent infection in case of pyrexia (t0C >37.5C)
 t0C >37.5C – paracetamol and fanning
Acute stroke care – specific treatment

• Acute anti-thrombotic therapy

– Thrombolysis/thrombectomy (Class IA)
– Anticoagulation
– ASA
• Treatment of elevated ICP and brain edema
– Medical treatment
– Surgical treatment
 ESO Guidelines for the Management of Ischaemic Stroke
and Transient Ischaemic Attack

• I.V. rt-PA (0.9 mg/kg body weight, max. 90 mg), with 10%
of the dose given as a bolus followed by a 60-minute
infusion, is recommended within 4.5 hours of onset of
ischaemic stroke (Class I, Level A)

ESO Guidelines 2009 Update. www.eso-stroke.org

 Inclusion and exclusion criteria for the
NINDS t-PA stroke study
• Inclusion Criteria • Exclusion criteria
1. Ischemic stroke with: 1. Stroke or serious head
a. Clearly defined onset trauma within the previous
time 3 months
b. Measurable deficit on 2. Major surgery within
the NIH Stroke Scale 14 days
2. CT scan without evidence 3. History of intracranial
of intracranial hemorrhage hemorrhage
3. Patient older than 18yrs 4. BP of >185/110 or
aggressive means to lower
the BP below this goal
 Inclusion and exclusion criteria for the NINDS t-
PA stroke study (cont)
• Inclusion Criteria • Exclusion criteria
1. Ischemic stroke with: 5. Rapidly improving or minor
a. Clearly defined onset symptoms
time 6. Symptoms suggestive of
b. Measurable deficit on subarachnoid hemorrhage
the NIH Stroke Scale 7. Gastrointestinal or
2. CT scan without evidence genitourinary hemorrhage
of intracranial hemorrhage within the previous 21 days
3. Patient older than 18yrs 8. Arterial puncture at a
noncompressible site within
7 days
 Inclusion and exclusion criteria for the NINDS t-PA
stroke study (cont)
• Inclusion Criteria • Exclusion criteria
1. Ischemic stroke with: 9. Seizure at onset of the
a. Clearly defined onset stroke
time 10. Laboratory data:
b. Measurable deficit on a. Glucose >10 or <2.8 mmol/l
the NIH Stroke Scale b. Prothrombin time >15 sec.
2. CT scan without evidence or INR >1.7
of intracranial hemorrhage c. Platelet count <100,000 cm3
3. Patient older than 18yrs d. Elevated partial-
thromboplastin time in the
setting of receiving heparin
within 48 hours.
 Updated Pooled Analysis:
Favourable Outcome (mRS 0-1) vs. Time
5
Odds ratio (OR)
4
Odds ratio and 95% CI

OR OR OR OR
2.55 1.6 1.3 1.2
3 4 4 2

0
60 90 120 150 180 210 240 270 300 330 360
OTT (min)
NNT NN NN NN
4-5 T9 T T
NNT, Number needed to treat 14 21
OTT, Time from stroke onset to start of treatment
mRS, modified Rankin Scale
Lees et al. Lancet 2010;375:1695-1703.
 Mechanical thrombectomy for acute
ischemic stroke
Five recently published RCTs (MR CLEAN, EXTEND-IA, SWIFT
PRIME, REVASCAT, and ESCAPE) employing MT with modern
stent retriever devices clearly demon- strated the
superiority of endovascular treatment, which is now
considered standard first-line therapy (class 1a
recommendation) for selected patients with acute ischemic
stroke exhibiting large cerebral artery occlusion in the
anterior circulation
• Time window – 6 hrs

N Engl J Med 2015;372:11-20; 1009-1018; 1019-1030; 2296-2306.

Int J Stroke 2015;10:439-448.
 Įtariamas ūminis galvos smegenų
kraujotakos sutrikimas

BKT, EKG, gliukozė kr.,

krešėjimo tyrimai

Neurochirurgo konsultacija; Jei randama aneurizma, jos

Neurologo apžiūra SAK angiografinis tyrimas išjungimas

TAIP AKS korekcija, osmoziniai

KT: kraujosruva? ISK Neurochirurgo konsultacija
diuretikai, bazinis gydymas

NE

Ūminė smegenų išemija

Bazinis gydymas

<4,5 val. Indikacijos IVT IVT Antitrombozinis gydymas;

etiologijos įvertinimas;
ankstyva reabilitacija;
komplikacijų prevencija;
<6,0 val. Indikacijos TE TE antrinė profilaktika
 Specific treatment: ASA
• Aspirin (160-325 loading dose) – within 48 hrs after
ischemic stroke (I,A)
• If thrombolytic therapy is planned or given, aspirin or
other antiplatelet therapy should not be initiated within
24 hrs (IV, GCP)
• Heparin is not recommended routinely (just in selected
pts with cardiac sources of embolism with high risk of re-
embolis, arterial dissection or high-grade stenosis prior to
surgery)

• N.B.: The use of clopidogrel, dipyridamole, or

combinations of oral antiplatelet agents in acute ischemic
stroke has not been evaluated ESO, 2008
 Specific treatment: increased ICP and brain
edema

• Surgical decompressive therapy within 48 hrs – in pts up

to 60 yrs with evolving malignant MCA infarcts (I,A)

• Head elevation (up to 300) & Osmotherapy (10% glycerol

250 ml x 4; mannitol 25-50 g every 3-6 hrs) (III, C)

• Ventriculostomy or surgical decompression – in case of

large cerebellar infarctions that compress the brainstem
Secondary prevention and treatment of
complications
• Infections – appropriate antibiotics
• Venous tromboembolism – early rehidratation and
graded compression stockings, early mobilisation
• Seizures – anticonvulsants
• High risk of DVT or pulmonary embolism – low dose s.c.
Heparin
• High risk of falls – Calcium Vit D supplements
• Impaired swallowing – early nasogastric feeding (within
48 hrs)
• PEG should be considered after the first 2 weeks

ESO, 2008
Early secondary prevention

• Optimal management of vascular risk factors

• Antithrombotic therapy
– Aspirin, triflusal, clopidogrel, aspirin and dipyridamol
– Oral anticoagulation (INR 2.0-3.0) after II associated with AF
• CAE – for pts with 70-99% stenosis within the first 2
weeks
• Carotid percutaneous transluminal angioplasty and/or
stenting (CAS) is only recommended in selected pts with
severe symptomatic CA stenosis: those with
contraindications to CEA, stenosis at a surgically
inaccessible site, restenosis after earlier CEA, and post-
radiation stenosis

ESO, 2008
Early rehabilitation

• Should be started within the first few days (mobilisation)

• Should be multidisciplinary
• Should be continued within the first year

ESO, 2008
Spontaneous intracerebral hemorrhage
• Onset
– Usually sudden, during physical activity

• Symptoms depends on
– Location
– Size
– Cause
– Intensity of bleeding
and reflect the brain region affected by the hematoma
Headache, deterioriation of consciousness, nausea & vomiting
because of increased ICP is more common compared with
ischemic strokes
• Abnormal findings on the neurological exam, like the
symptoms, reflect the brain region affected by the
hematoma
• Etiology
– Rupture of small cerebral vessels, affected by AH or
amyloidosis – 80 %

– Brain tumors, aneurysms, arteriovenous

malformations, coagulation disorders (hemophilia),
anticoagulants, vasculitis, drug abuse, et. – up to 20
%
• Typical locations
– Hypertension-related ICH
• Basal ganglia
• Thalamus
• Cerebellum
• Pons
– Amyloid angiopathy related IVH
• Lobar, can be multofocal
Laboratory tests

• CT
L
L
L
The mainstays of acute treatment

• Respiratory function and O2 sats >95%

• Close BP control
• Osmotherapy (mannitol 25-50 g every 3-6 hrs)
• Seizures – anticonvulsants
• Fluid balance and electrolites
• Early nasogastric feeding (within 48 hrs)
• Prevention of obstipation and deep vein thrombosis
• Surgical treatment is contraversial except for larger
cerebellar hematomas
Subarachnoid hemorrhage
Onset
• Severe headache of the instantaneous onset (“blow to
the head”)
Symptoms
• Headache
• Transient or prolonged loss of consciousness
• Epileptic seizures
• Nausea and vomiting
Clinical findings
• Signs of meningeal irritation: neck stiffness, Kernig’s,
Brudzinski’s signs
• Focal neurological signs may be present
Subarachnoid hemorrhage

Ethiology
• Intracranial aneurysms – 85 %
• Perimesencephalic (interpeduncular r.) SAH – 10 %
• A-V malformations – 5 %
• 80 % aneurysms – anterior circulation teritory
• 25 % - multiplex
 Subarachnoid hemorrhage

• Risk factors
– Cigarette smoking x 10
– AH
– Alcohol (binge drinking)
– Family history
• Up to 2 % of pts. have first line relatives with SAH
• Risk of first lines relatives of the patient, especially of
siblings  4x
Diagnostic tests

• CT
• Lumbar puncture
• Angiography
Subarachnoid hemorrhage
Subarachnoid hemorrhage
The mainstays of acute treatment

• Three “H” therapy

– Hypertensive therapy, hypervolemia, hemodilution
• Prevention of cerebral ischemia due to arterial
spasm
– Calcium antagonists (Nimodipine)
• surgery
Good luck!
 Potential to Reverse Neurologic Impairment With
Thrombolytic Reperfusion

Ischaemic core
(brain tissue
destined to die)
Penumbra
(salvageable
brain area)

An untreated patient loses

Reperfusion offers the
approximately 1.9 million
potential to reduce the
neurons every minute in
extent of ischaemic injury
the ischaemic area

Saver. Stroke 2006;37:263-266.

González. Am J Neuroradiol 2006;27:728-735.
Donnan. Lancet Neurol 2002;1:417-425.