Cerebrovascular diseases are the third leading cause of death and a primary cause of disability. 30% of stroke patients die within the first month, and 45-48% die by the end of the year. Strokes can be classified as acute (transient or permanent) or chronic. Transient ischemic attacks are temporary episodes caused by temporary blockages, while permanent strokes include cerebral infarction (85%) and hemorrhages. Diagnosis involves imaging tests and analysis of risk factors. Treatment depends on the type of stroke but generally focuses on stabilization, blood pressure control, and prevention of complications.

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VASCULAR DISORDERS

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Сerebrovascular diseases
- 3 place on death rate
- leading cause of disability
- 30% of stroke sufferers die in
the course of the first month from
the moment of stroke
- 45-48% of patients die by the
end of the year

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Cerebrovascular diseases
Clinical classification
I. Acute
1.Transient strokes
- Transient ischemic attack (TIA)
- Cerebral hypertensive crises
- Acute hypertensive encephalopathy
2. Permanent strokes
- Cerebral infarction (85%)
- Subarachnoid haemorrhage (1-5%)
- Intracerebral haemorrhage (10-12%) II.
Chronic diseases

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Cerebrovascular diseases
Classification (ICD-10):
I60 Subarachnoid haemorrhage
I61 Intracerebral haemorrhage
I62 Other nontraumatic intracranial
haemorrhage
I63 Cerebral infarction
I64 Stroke, not specified as
haemorrhage or infarction G45
Transient cerebral ischemic
attacks and related syndromes

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Transient strokes
Transient ischemic attack (TIA) ―
is an acute episode of temporary
neurologic dysfunction resulting from
focal cerebral ischemia not associated
with permanent cerebral infarction
and lasting less than 24h.
• TIA is caused by a temporary
blockage of one of the arteries that
supply the brain.

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Symptoms of TIA in carotid
arteries
• hemiparesis
• hemihypesthesia
• aphasia and apraxia (in damage of
the dominant hemisphere)
• anosognosia
• blindness or decreased vision in one
eye
• central paresis of the facial nerve

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Symptoms of TIA in in vertebral
and basilar arteries
- dizziness
- nausea and vomiting
- double vision
- dysarthria and dysphagia
- ataxia
- amnesia
- cortical blindness
- tetraparesis
- hearing loss
- peripheral paresis of the facial nerve

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Cerebral hypertensive crises
are associated with hypertensive
diseases and accompanied by
symptoms of increased intracranial
pressure.
Symptoms: occipital headache and
visual disorders (photopsy);
hyperhydrosis; hyperemia of face;
a sharp headache; a nausea;
vomiting; nonsystemic vertigo;
epileptic
attacks.

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Acute hypertensive
encephalopathy is typically associated with
hypertensive renal disease
Symptoms:
-elevated blood pressure,
-psychomotor agitation,
-nausea, vomiting,
-visual and sensitive disorders,
-impairment of consciousness,
-symptoms of increased intracranial
pressure,
-meningeal symptoms,

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-local symptoms and epileptic attacks are
probable.
Permanent strokes
Ischemic Stroke is a syndrome
characterized by a sudden loss of
brain function caused by the
interruption of cerebral blood flow
and lasting more than 24 hours.
Etiology / risk factors
1. Atherosclerosis
2. Arterial hypertension

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4. Heart diseases (atrial fibrillation,
myocardial infarction, left ventricular
aneurysm,artificial heart valve, rheumatic
disease of the heart valves,
myocardiopathy, bacterial endocarditis)).
5. Vasculitis
6. Diabetes
Etiology / risk factors
6. Hematological diseases (erythremia, sickle
cell anemia, thrombocytosis, leukemia)
7. Immunological disorders (antiphospholipid
syndrome)

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8. Venous thrombosis
9. Dissection of the precerebral or cerebral
arteries
10. Migraine
11. In women - taking oral contraceptives
12. Smoking
Pathogenesis of the Ischemic Stroke
- thrombosis
- Embolism
- decreased perfusion
Pathogenetic types:
- aterotrombotic (15-20%)

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- cardioembolic (15-20%)
- hemodynamic (5-10%)
- lacunar (infarct size ≤1.5 cm) (15-20%)
- hemorheologic
- cryptogenic (20-30%)

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Pathogenesis of the Ischemic Stroke

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Metabolic changes in reply to the acute
focal ischemia of the brain:
1.Decrease of cerebral blood flow below
55 ml (100 g/min) causes
deceleration of proteins’ synthesis in
neurons.
2. Decrease of the cerebral blood flow
below 35 ml (100 g/min) stimulates
anaerobic glycolysis.
3. Decrease of the cerebral blood flow
below 20 ml leads to redundant

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release of the excitatory
neurotransmitters and to the energy
metabolism disorders.
4. Anoxic cell membrane depolarization
― apoptosis (death of neuron cells)
occurs due to reduction of the
cerebral blood flow below 10 ml.
Сentral zone of the Cerebral infarction
(«nucleus») is formed in 6-8 minutes after
acute focal ischemia development. In the
course of several hours cerebral infarction

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«nucleus» is surrounded by a zone of
«ischemic penumbra».
Penumbra is an area of dynamic
metabolic changes, in which brain
bloodflow is reduced to 20-40 ml (100
g/min) and only functional changes take
place.
Duration of penumbra existence defines
time period called «a therapeutic
window»

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― the period when medical actions
are most perspective and can limit
cerebral infarction area.
The great mass of cerebral infarction
is formed in 3-6 h after the first
clinical symptoms occurrence, and its
formation comes to the end in 48-56
h.
Periods of the stroke:
• up to 6 hours;
• acute (from 1 day to 1 month);

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• early rehabilitation period (up to 3
months);
• late rehabilitation period (from 3
months to 1 year);
• sequelas of stroke (from a year and
more).
Symptoms of Cerebral infarction
in MCA:
• contralateral hemiparesis,
hemihypesthesia, homonymous
hemianopsia

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• paresis of gaze
• motor and/or sensory aphasia
• autotopagnosia, anosognosia
(neglect)

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• MCA Superior Division Infarction

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• MCA Inferior Division Infarction

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• Bilateral MCA proximal main stem terriotry
infarct.

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• MCA cortical branch Infarction

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Symptoms of Cerebral infarction
in ACA:
• contralateral paresis of the legs, less
significant paresis of the arm
• contralateral hemianesthesia, mainly in the
leg
• urinary incontinence
• contralateral grasping reflex, sucking reflex
• abulic-akinetic syndrome, akinetic mutism
• apraxia of walking; apraxia in the
extremities
• emotional lability, euphoria

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• Anterior Cerebral Artery Infarction

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Symptoms of Cerebral infarction
in PCA:
• contralateral homonymous hemianopsia;
bilateral lesions can lead to cortical blindness
• Occlusion of the PCA in the dominant
hemisphere can cause amnestic aphasia,
alexia, agraphia, or amnesia
• Blockage of the thalamoperforating arteries
can cause depression of consciousness,
paresis of the gaze up; contralateral
hemianesthesia, ataxia, transient
hemiparesis, choreoathetosis, pain and
paresthesia.

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• Posterior Cerebral Artery Infarction

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Symptoms of Cerebral infarction
in vertebral, basilar arteries:
• bilateral hemiparesis, hemihypesthesia
• cerebellar ataxia and nystagmus
• classical alternating syndromes
• impaired consciousness and vital functions
• cortical blindness, oculomotor disorders,
hyperkinesis, sleep disorders, hallucinations,
amnesia
• Bulbar syndrome

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• Obstruction of the artery of the labyrinth
may manifest as dizziness and sudden
unilateral deafness.
• Multiple Lacunar State
Lateral Medullary Infarction

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Inferior Cerebellar Infarction

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Diagnostics of CI
- emergency examination of the patient with a
diagnosis within 45 min from the time of
delivery

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-assessment of neurological deficit according to
NIHSS
- general analysis of blood and urine; blood
chemistry (+lipid profile); coagulogram
- blood pressure monitoring
• ECG; chest x-ray
• CT or MRI of the brain (+with angioprogram)
Diagnostics of CI
• Ultrasound of the heart
• Ultrasound of the precebral arteries
• lumbar puncture in the absence of
contraindications

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• EEG, consultation of a cardiologist,
angiosurgeon according to indications
• Occluded middle cerebral artery on CT
angiography

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Occluded middle cerebral artery on CT angiography
Carotid ultrasound

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Carotid ultrasound

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Treatment of CI
• treatment in intensive care unit
• ALV, installation of a nasogastric tube,
urinary catheter according to indications
• raising the head end of the bed by 30⁰
• blood pressure correction is performed on
the first day if systolic blood pressure is
˃220 mm Hg, diastolic blood pressure is
˃120 mm Hg
• If necessary, blood pressure is reduced by no
more than 15% from the initial level within

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24 hours (urapidil iv, ACE inhibitors,
angiotensin receptor antagonists)
Treatment
• maintaining normovolemia
• neuroprotective therapy: glycine, magnesium
sulfate
• parasympathomimetic drugs: ipidacrine,
choline alfoscerate
• In presence of cerebral edema: osmotic
diuretics + furosemide
• In big cerebellar infarction- consultation of a
neurosurgeon

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• Antiplatelet agents (acetylsalicylic acid) and
anticoagulants if indicated
• In hyperlipidemia: atorvastatin, rosuvastatin
Treatment of CI
• in vomiting: domperidone, metoclopramide
• in epileptic syndrome: phenytoin,
carbomazepine, valproic acid
• in spastic syndrome: baclofen, tolperisone
• in dizziness: betahistine
• in extrapyramidal syndrome: amantadine
• in psychomotor agitation: tofisopam,
diazepam, chlorprotixen

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• Early rehabilitation of patients in a stable
state, physiotherapy, exercise therapy,
speech therapist
Systemic thrombolysis
ALTEPLAZA 0.9 mg / kg (maximum dose 90
mg) -10% of the entire dose i/v in a bolus
for 1 min, the remaining dose is
administered in i/v infusion for 1 hour
Conditions:
1. absence of hemorrhagic changes on brain
CT
2. BP less than 180/105 mm Hg

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3. age 18-80 years
4. the onset of symptoms less than 4.5
hours before treatment
Systemic thrombolysis
Contraindications:
- Hemorrhage on CT or signs of cerebral infarction with
size more than 1/3 of the cerebral hemisphere;
- minimal symptoms of CI
- suspicion of SAH
- internal bleeding in the last 3 weeks
- hemorrhagic diseases
- intracranial surgery or head injury last 3 months
- major surgical interventions last 14 days

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- lumbar puncture last 7 days
- intracranial hemorrhage, aneurysm, AVM in anamnesis
- CI + epileptic seizures
- myocardial infarction last 3 months
Emergency endovascular procedures
• Intra-arterial thrombolysis: medications
delivered directly to the brain.
• Removing the clot with a stent retriever

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(thrombectomy, thrombaspiration) Carotid
endarterectomy Angioplasty and stents

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Intracerebral hemorrhage
is a clinical form of stroke,

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caused by blood vessel rupture
causing blood penetration into
cerebral parenchyma.
Сauses
- arterial hypertension and rupture of
microaneurysms
- vascular malformations
- saccular cerebral aneurysms
- coagulopathies (hemorrhagic diathesis)
- use of anticoagulants
- vasculitis
-brain tumors

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-amyloid angiopathy
-alcohol, cocaine usage
Symptoms of intracranial
hemorrhage :
• abrupt onset during physical or emotional
stress;
• sharp headache, nausea, vomiting
• epileptic seizures are possible
• impaired consciousness (from stunning to
coma)
• autonomic disorders: the skin is
hyperemic, hyperhidrosis, tense pulse,
increased blood pressure, hyperthermia

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• meningeal symptoms;
• retinal edema and hemorrhages on the
eye-ground;
• Severe focal neurological signs.

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Intracerebral hemorrhage

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The subarachnoid hemorrhage
in most cases (to 80%) occurs
owing to:
• ruptured cerebral aneurysm;
• arteriovenous malformation;
• systemic connective tissue
disorders;
• blood disorders;
• hypertensive diseases and
cerebral atherosclerosis.

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Symptoms:
• sudden sharp headache, nausea,
vomiting
• epileptic seizures are possible
• impaired consciousness (from stunning
to coma)
• psychomotor agitation
• main syndrome is meningeal
• autonomic disorders: hyperemia of the
skin, change in heart rate, increased
blood pressure, hyperthermia, changes
in the ECG

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• focal neurological symptoms are usually
absent, but possible

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Diagnostics of SAH
- general analysis of blood and urine; blood
chemistry; coagulogram
• ECG; chest x-ray X-ray of the skull (if head
injury is suspected)
• CT or MRI of the brain with angioprogram
• digital subtraction angiography
• transcranial dopplerography
• lumbar puncture in the absence of
contraindications
• neurosurgeon consultation

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• consultation of an ophthalmologist and
therapist
subarachnoid hemorrhage

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A: Digital subtraction angiography of the cerebral vessels,
demonstrating an aneurysm (black arrow) at the junction of the A1

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and A2 segments of the right
ACA. B: Complete
embolization of the aneurysm
sac after coiling.
Magnetic
Resonance
Angiography
(MRA)
Treatment of
ICH and SAH
• treatment in
intensive care unit

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• ALV, installation of a nasogastric tube,
urinary catheter according to indications
• raising the head end of the bed by 30⁰
• maintaining blood pressure not more than
150 mm Hg (to reduce BP - urapidil)
• For the prevention and treatment of
vasospasm: nimodipine orally or i/v
• maintaining normovolemia
• analgesia and sedation during all
manipulations

59. Treatment
• neuroprotective therapy: emoxipin, mexibel,
magnesium sulfate
• in hypertensive hemorrhages by the type of
hemorrhagic impregnation: vitamin K, and
etamzilat
• In presence of cerebral edema: osmotic
diuretics + furosemide
• in psychomotor agitation: tofisopam,
diazepam, chlorprotixen

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• in pain and hyperthermia: analgin,
paracetamol, diclofenac, ketoprofen,
ketorolac, meloxicam, ibuprofen, tramadol59
Treatment
• in vomiting: domperidone, metoclopramide
• in epileptic syndrome: phenytoin,
carbomazepine, valproic acid
• in spastic syndrome: baclofen, tolperisone
• in dizziness: betahistine
• in extrapyramidal syndrome: amantadine

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• IN ICH early rehabilitation of patients in a
stable state, physiotherapy, exercise therapy
• Surgical treatment according to
indications
Indications for Surgical treatment in ICH
1.Increase of intracranial pressure in patients
with putamenny and subcortical hematomas
with a volume of more than 40 cm³ and
cerebellar hematomas more than 15 cm³

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2.Hemispheric hematoma with a volume of 30-
40 cm³ and the absence of the effect of
treatment for 3-5 days
3.Thalamus hemorrhage + ventricular
tamponade and / or occlusive hydrocephalus
Contraindications for Surgical treatment
in ICH
Relative contraindication: age older than 70
years; somatic pathology in the stage of
subcompensation or decompensation;
hemorrhage in brainstem and thalamus

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Absolute contraindications: coma (GCS ≤7).
In acute occlusive hydrocephalus -
installation of external ventricular drainage
Chronic cerebral ischemia ―
discirculatory encephalopathy
3 stages:
First stage.
Subjective patient complains of
headaches, weakness, fatigability,
emotional lability, memory and

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attention decrease, dizziness,
instability at walking, sleep
disturbance.
Second stage.
Patient’ s complaints are similar
to the first stage, but they
degrade.
The focal signs progress:

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- coordination and oculomotor
disorders;
- pyramidal insufficiency;
- amyostatic syndrome; -
- memory and emotional disorders.
Third stage.
The quantity of complaints
decreases.

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Neurological symptoms :
coordination disorders, pyramidal,
bulbar, pseudobulbar, amyostatic,
psychoorganic syndromes.
Patients are invalid; social and
communal maladjustment is
observed.