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Chronic Cerebral Ischemia
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Definition
Vascular cerebral pathology caused by
slowly progressive, diffuse circulatory
disturbance of brain with incremental
various defects of its functioning.
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Overview of cerebral circulation
Anterior
Cerebralartery
Middle
Cerebral
artery
Posterior
Cerebral
artery
Internal
Carotid
artery
(70% of CBF)
Vertebral
artery
Basilarartery
30%
of
CBF
Arterial supply
A little Anatomy
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Overview of cerebral circulation
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Focal ischemia
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Focal ischemia
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Focal ischemia
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MRI NormalMRI Chronic cerebralischemia
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Risk factors
Separated into 2 groups:
Correctable
Non-Correctable
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Correctable Risk factors
Hypertension
Chronic hypertension
Hypertensive crisis
Atherosclerosis
Diabetes
Smoking
Lack of exercise
Malnutrition
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Non Correctable Risk Factors
Old Age
Gender
Genetic predisposition
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Etiology
Occlusive atherosclerotic stenosis
Thrombosis
Embolism
Traumatic separation of cerebral arteries Extravasal compression due to pathology inspine or neck muscles
Deformation of arteries
Changes in blood Increse of hematocrit Incressed viscosity
Fibrinogen and platelet aggregation and adhesion
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Pathophysiology
Pathogenesis: cerebrovascular
insufficiency in a stable form or intermittent
episodes of dyscirculation.
Pathological changes to vascular walls:
developing hypertension, atherosclerosis,
vasculitis, etc.
Ischemia
Ischemic cascade
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Ischmic cascade
1. Reduction in cerebral blood flow.
2. Increase in glutamate excitotoxicity.
3. Ca accumulation and lactic acidosis.
4. Activation of intracellular enzymes.
5. Activation of local and systemic proteolysis.
6. Appearance and progression of oxidative stress.
7. Gene expression of early response to the developmentof plastic depression of protein and lower energy
processes.8. Long term effects of iscemia (local inflamamtory
response, microcirculatory disorders, damage to BBB)
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Oxidative Stress
Excessive intracellular accumulation of
free radicals, activation of lipid
peroxidation, excessive accumulation of
lipid peroxidate products.
At excytotoxicity NDMA-receptors (N-
methyl-D-aspartete) are hyperstimulated,
causinf massive inflow of calcium into cellsactivating proteases.
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Pathology
Ischemic changes of neurons
Development of gliosis
Development of small lacuane and homes
Lacunar state Fibrinoid necrosis of vessel walls
Plasmatic impregnation
Miliary aneurysm
Stenosis Cerebral ischemia subsortical and cortical
Atrophy of cortex
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Clinical Picture
Common syptoms: Headache
Diziness
Noise in my head
Memory loss
Reduced mental capacity
Clinical stages
Stage 1 Stage 2
Stage 3
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Stage 1
Subjective disorders
Headache
Fatigue
Diziness
Emotional lability
Memory and attention loss
Sleep disorder
Anisoreflexia
Dyscoordinatory phenomena
Occulomotor deficiency
Oral automatism
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Stage 2
More marked memory impairement
Increased cognitive and intellectualdisorders.
Disiness
Unsteady when walking
Central damage of facial and hypoglossal
nerves Coordination and occulomotor
disturbances.
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Stage 3
Objective neurological disorders
Dyscoordination
Pyramidal syndrome
Pseudobulbar syndrome
Amyostatic syndrome
Psychoorgnic syndrome
Vertigo, Syncope
Decompensation in form of small strokes
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Diagnosis
Anamnesis with causative factors
Clinical investigation: Presence of neurological dysfunction
Neuropsychological
Psychiatric
Instrumental ECG
Doppler
MRI CT
Biochemical blood tests
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Treatment
Pthogenetic Therapy: Treat hypertension
Atherosclerosis
Statins
Diet, lifestyle Symptomatic treatment
Antioxidants
Antiplatelets
Drugs: Mexidol (antioxidant)
Mildronate (gamma butyroinhydroxiase inhibitor-fatty acid inhib.)
Actovegin (antioxidant)