Chronic Ischemia of Brain

7/28/2019 Chronic Ischemia of Brain

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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)

Chronic Ischemia of Brain

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