Cerebrovascular diseases. Dynamic cerebral blood circulation disturbances. - презентация

1 Cerebrovascular diseases. Dynamic cerebral blood circulation disturbances.

2 The main reasons Atherosclerosis of cerebral vessels and general atherosclerosis. In 75 % of all cases it is the main reason of all acute cerebral blood - circulation disturbances. Atherosclerosis of cerebral vessels and general atherosclerosis. In 75 % of all cases it is the main reason of all acute cerebral blood - circulation disturbances. Hypertension – the frequency of hypertension in case of stroke is about 72 %. Hypertension – the frequency of hypertension in case of stroke is about 72 %. Combination of atherosclerosis and hypertension. Combination of atherosclerosis and hypertension. Besides these main reasons there are some others which can cause cerebral blood - circulation disturbances. Symptomatic arterial hypertension (for example caused by kidney diseases) Symptomatic arterial hypertension (for example caused by kidney diseases) Heart diseases such as inborn and acquired cardiac abnormalities, arrhythmias, IHD, atherosclerosis, cardiosclerosis, angina pectoris, myocardial infarction. Heart diseases such as inborn and acquired cardiac abnormalities, arrhythmias, IHD, atherosclerosis, cardiosclerosis, angina pectoris, myocardial infarction. Infectious and infectious – allergic vasculitis (at rheumatism, connective tissue diseases, lues) Infectious and infectious – allergic vasculitis (at rheumatism, connective tissue diseases, lues) Arterial hypotension. Arterial hypotension. Vasomotor dystonia. Vasomotor dystonia.

3 The main reasons Blood diseases (polycythemia, leucosis, haemophilia) Blood diseases (polycythemia, leucosis, haemophilia) Kidney diseases. Kidney diseases. Endocrine diseases (diseases of thyroid gland, pancreas, suprarenal glands) Endocrine diseases (diseases of thyroid gland, pancreas, suprarenal glands) Diabetes mellitus. Diabetes mellitus. Toxic lesion of vessels at endogenous and exogenous intoxication ( at acute and chronic kidney or liver failure, alcoholic intoxication ) Toxic lesion of vessels at endogenous and exogenous intoxication ( at acute and chronic kidney or liver failure, alcoholic intoxication ) Traumatic lesion of vessels (at hemorrhage - subdural, epidural, ventricular, parenchymatous). Traumatic lesion of vessels (at hemorrhage - subdural, epidural, ventricular, parenchymatous). Artery and vein compression (especially in cervical part of spinal cord – for example at osteochondrosis) Artery and vein compression (especially in cervical part of spinal cord – for example at osteochondrosis) Inborn and acquired Willis circle abnormalities - occlusion, stenosis of MAH and neck, aneurism, constriction of vessels. Inborn and acquired Willis circle abnormalities - occlusion, stenosis of MAH and neck, aneurism, constriction of vessels. Brain tumors. Brain tumors.

4 The risk – factors Age (the elder person is, the highest risk of cerebrovascular disease is) Age (the elder person is, the highest risk of cerebrovascular disease is) Sex (at the age of up to 55 – 60 years fatality from cerebrovascular disease is higher in men, after 55 – 60 years – it is higher in women) Sex (at the age of up to 55 – 60 years fatality from cerebrovascular disease is higher in men, after 55 – 60 years – it is higher in women) Heredity (in particular to heart and cerebrovascular diseases) Heredity (in particular to heart and cerebrovascular diseases) Alcohol abuse and Cigarette smoking Alcohol abuse and Cigarette smoking Hyperlipidemia and hyperglycemia Hyperlipidemia and hyperglycemia Arterial hypertension Arterial hypertension Hypodynamia Hypodynamia Meteorological dependence ( especially people with labile autonomic nervous system ) Meteorological dependence ( especially people with labile autonomic nervous system ) Personal type (picnotic type), stress, high carbohydrate diet. Personal type (picnotic type), stress, high carbohydrate diet. Combination of three and more factors increases risk of development of acute neurological deficit. Combination of three and more factors increases risk of development of acute neurological deficit.

5 Classification Premonitary and initial symptoms of brain blood supply insufficiency Acute cerebral blood circulation disturbances 1. Dynamic cerebral blood circulation disturbances Transient ischemic attack Transient ischemic attack Hypertonic crisis Hypertonic crisis Acute hypertonic encephalopathy Acute hypertonic encephalopathy 2. Strokes Hemorrhage of membrane Hemorrhage of membrane – subdural - epidural - subarachnoid

6 Classification Intracerebral hemorrhage - parenchimatous - parenchimatous-subarachnoid - ventricular infarction (nonembolic) infarction (nonembolic) Brain infarction (embolic) Brain infarction (embolic) Dyscirculative encephalopathy (chronic cerebral blood circulation insufficiency or slowly progressive insufficiency of cerebral blood circulation) Dyscirculative encephalopathy (chronic cerebral blood circulation insufficiency or slowly progressive insufficiency of cerebral blood circulation) - I stage - II stage - III stage

7 Dynamic cerebral blood circulation disturbances (DCBCD) are acute brain dyscirculation events which usually are developed against the main diseases. They are associated with temporary general and focal brain symptoms. They have tendency to involution during 24 hours are acute brain dyscirculation events which usually are developed against the main diseases. They are associated with temporary general and focal brain symptoms. They have tendency to involution during 24 hours

8 DCBCD Transient ischemic attacks ( TIA ) – they take about 1/3 of all DCBCD Transient ischemic attacks ( TIA ) – they take about 1/3 of all DCBCD Hypertonic crisis - it takes about 2/3 of all DCBCD Hypertonic crisis - it takes about 2/3 of all DCBCD

9 Etiology Atherosclerosis Atherosclerosis Stenosis of MAH Stenosis of MAH Heart diseases (abnormalities, myocardial infarction) Heart diseases (abnormalities, myocardial infarction) Sometimes vasculitis, systemic vascular diseases Sometimes vasculitis, systemic vascular diseases

10 Pathogenesis Thromboembolic Microembols are divided into arteriogenic and cardiogenic Microembols are divided into arteriogenic and cardiogenic Arteriogenic microembols are small units that originate from clots and are the result of destroyed atherosclerotic plaques Arteriogenic microembols are small units that originate from clots and are the result of destroyed atherosclerotic plaques Thrombocytic embols are crumbling. That is the main reason of rapid involution of neurological deficit Thrombocytic embols are crumbling. That is the main reason of rapid involution of neurological deficit Cardiogenic microembols can cause TIA in patients with arrhythmias, heart abnormalities, after myocardial infarction, in patients with rheumatic endocarditis Cardiogenic microembols can cause TIA in patients with arrhythmias, heart abnormalities, after myocardial infarction, in patients with rheumatic endocarditis

11 Pathogenesis Haemodynamic mechanisms Atherosclerotic stenosis of cerebral vessels or MAH, especially in association with hypotension, arrhythmias and myocardial infarction. Atherosclerotic stenosis of cerebral vessels or MAH, especially in association with hypotension, arrhythmias and myocardial infarction. Thrombosis of neck magistral artery. Thrombosis of neck magistral artery. In the subclavian steal syndrome the patient has a narrowed subclavian artery and the arm steals blood from the basilar artery via the vertebral artery. There may be a cervical bruit and a difference in blood pressure between the arms. At times of arm exercise the patient may experience vertebrobasilar insufficiency. In the subclavian steal syndrome the patient has a narrowed subclavian artery and the arm steals blood from the basilar artery via the vertebral artery. There may be a cervical bruit and a difference in blood pressure between the arms. At times of arm exercise the patient may experience vertebrobasilar insufficiency. Spasm of cerebral vessels and as a result perivascular edema and hypoxia of brain tissue. Spasm of cerebral vessels and as a result perivascular edema and hypoxia of brain tissue. Inborn stenosis, abnormalities of MAH Inborn stenosis, abnormalities of MAH Compression of vertebral artery by osteophytes at cervical osteochondrosis. Compression of vertebral artery by osteophytes at cervical osteochondrosis. Vessels insufficiency (contradiction between real and demandable blood supply). This can occur at heart failure, hypotension, internal bleeding. Vessels insufficiency (contradiction between real and demandable blood supply). This can occur at heart failure, hypotension, internal bleeding.

12 Blood supplying of the brain cortex А - convecsital, Б – medial surface, В – frontal section (red – anterior cerebral artery region, blue - medial, yellow – posterior cerebral arteries) А Б В

13 Anterior cerebral artery region

14 Medial cerebral artery region

15 Vertebral artery region

16 Clinical picture of TIA TIA is usually characterized by focal neurological symptoms. The last usually dominate over general brain symptoms. Thus TIA is regional DCBCD. They are usually acute and develop suddenly. TIA is usually characterized by focal neurological symptoms. The last usually dominate over general brain symptoms. Thus TIA is regional DCBCD. They are usually acute and develop suddenly. There are 2 main groups of TIAs symptoms: General - usually manifest as headache, dizziness, short loss of consciousness General - usually manifest as headache, dizziness, short loss of consciousness Focal symptoms depend on the vessel territory Focal symptoms depend on the vessel territory

17 TIAs in carotid distribution They take 30 % of all TIAs They take 30 % of all TIAs Carotid distribution – is a territory of internal carotid arteries and their branches – ophthalmic artery, anterior cerebral artery, and middle cerebral artery. Via anterior cerebral artery carotid distribution supplies anterior part of frontal lobe, internal surface of hemisphere to sulcus parietooccipitalis, via middle cerebral artery – the cortex of frontal, parietal, temporal lobe, internal capsula and nucleus. Carotid distribution – is a territory of internal carotid arteries and their branches – ophthalmic artery, anterior cerebral artery, and middle cerebral artery. Via anterior cerebral artery carotid distribution supplies anterior part of frontal lobe, internal surface of hemisphere to sulcus parietooccipitalis, via middle cerebral artery – the cortex of frontal, parietal, temporal lobe, internal capsula and nucleus.

18 TIAs in carotid distribution The most common symptoms are subjective sensory disorders, such as numbness, tingling in face and extremities; and objective sensory disorders such as hyperesthesia of superficial sensation in face and extremities, sometimes deep sensation in fingers and toes The most common symptoms are subjective sensory disorders, such as numbness, tingling in face and extremities; and objective sensory disorders such as hyperesthesia of superficial sensation in face and extremities, sometimes deep sensation in fingers and toes Very often motor disorders together with sensory ones are observed. They are central paresis of extremity or fingers with hyperreflexia, pathologic signs of Babinski, Rossolimo. Hemiparesis or hemiplegia is observed only in severe cases. Very often motor disorders together with sensory ones are observed. They are central paresis of extremity or fingers with hyperreflexia, pathologic signs of Babinski, Rossolimo. Hemiparesis or hemiplegia is observed only in severe cases. Sometimes distorting language (transient aphasia) is observed. Sometimes distorting language (transient aphasia) is observed. When TIA occurs in the internal carotid artery territory ophthalmic – piramidal syndrome is developed. It usually manifests as blindness or reduction of vision on the same side and hemiparesis on the opposite side. It is known as Lasko – Radowich syndrome. When TIA occurs in the internal carotid artery territory ophthalmic – piramidal syndrome is developed. It usually manifests as blindness or reduction of vision on the same side and hemiparesis on the opposite side. It is known as Lasko – Radowich syndrome. Focal Jackson motor or sensory epileptic attacks are observed in patients with MAH pathology. Focal Jackson motor or sensory epileptic attacks are observed in patients with MAH pathology.

19 TIAs in vertebrobasilar distribution They take about 70 % of all TIAs They take about 70 % of all TIAs This territory provides blood supply of brainstem, cerebellum, occipital lobe cortex, mediobasal structures of temporal lobes. This territory provides blood supply of brainstem, cerebellum, occipital lobe cortex, mediobasal structures of temporal lobes. Vestibular syndrome. It manifests as systemic dizziness, occipital headache, nystagmus, equilibrium disorders. Vestibular syndrome. It manifests as systemic dizziness, occipital headache, nystagmus, equilibrium disorders. Brainstem – cerebellum syndrome. It manifests as equilibrium, coordination and synergy of action disorders. Brainstem – cerebellum syndrome. It manifests as equilibrium, coordination and synergy of action disorders. Paresis of oculomotor muscles with convergence disorders, diplopia, cross – eye. Paresis of oculomotor muscles with convergence disorders, diplopia, cross – eye. Bulbar syndrome with swallowing, voice and speech disorders. Bulbar syndrome with swallowing, voice and speech disorders. Alternation syndromes are quite rare. Alternation syndromes are quite rare. Vision disorders of cortex character such as photopsias, hemianopsia, quadric hemianopsia and optic phenomena. Vision disorders of cortex character such as photopsias, hemianopsia, quadric hemianopsia and optic phenomena. Atonic – adynamic syndrome. It is observed at acute ischemia of reticular formation and lower olives in medulla oblongata in Atonic – adynamic syndrome. It is observed at acute ischemia of reticular formation and lower olives in medulla oblongata in

20 TIAs in vertebrobasilar distribution case of drop – attacks – the attacks of sudden loss of muscle tone that cause patients falling down without loss of consciousness (cervical spinal cord disorders in case of sudden turning out or head retroversion. Sometimes symptom of Sistine chapel can occur when loss of muscle tone is associated with loss of consciousness) case of drop – attacks – the attacks of sudden loss of muscle tone that cause patients falling down without loss of consciousness (cervical spinal cord disorders in case of sudden turning out or head retroversion. Sometimes symptom of Sistine chapel can occur when loss of muscle tone is associated with loss of consciousness) At ischemia of mediobasal structures of temporal lobe one can Korsakov syndrome observe – the attacks of temporary memory disorders on current events associated with confabulator component and disorientation. At ischemia of mediobasal structures of temporal lobe one can Korsakov syndrome observe – the attacks of temporary memory disorders on current events associated with confabulator component and disorientation. Paroxysmal hypersomnic and katalepsic syndromes with autonomic – vascular crisis (ischemia of hypothalamic structures) Paroxysmal hypersomnic and katalepsic syndromes with autonomic – vascular crisis (ischemia of hypothalamic structures) Syndrome of temporal epilepsy. Syndrome of temporal epilepsy. Subclavian steal syndrome the patient has a narrowed subclavian artery and the arm steals blood from the basilar artery via the vertebral artery. There may be a cervical bruit and a difference in blood pressure between the arms. At times of arm exercise the patient may experience vertebrobasilar insufficiency. Subclavian steal syndrome the patient has a narrowed subclavian artery and the arm steals blood from the basilar artery via the vertebral artery. There may be a cervical bruit and a difference in blood pressure between the arms. At times of arm exercise the patient may experience vertebrobasilar insufficiency.

21 Associated dynamic cerebral blood circulation disturbances Coronary – cerebral crisis Coronary – cerebral crisis Aorto - cerebral crisis Aorto - cerebral crisis Liver- cerebral crisis Liver- cerebral crisis Cholecysto – cerebral crisis Cholecysto – cerebral crisis TIA with neurological symptoms that clinically disappear within 24 hours but leave changes at CT such as low density zones are regarded as minor ischemic strokes. TIA with neurological symptoms that clinically disappear within 24 hours but leave changes at CT such as low density zones are regarded as minor ischemic strokes. It is important to mention that the duration of TIAs is from several minutes up to 24 hours. But usually it is 10 – 15 minutes. It is important to mention that the duration of TIAs is from several minutes up to 24 hours. But usually it is 10 – 15 minutes. One of TIAs characteristic features is relapse, when attacks are observed 3 – 5 times per year. There is one more peculiarity, which is necessary to remember – the attacks in vertebrobasilar territory are more common and are frequently repeated in spite of TIA in carotid territory. One of TIAs characteristic features is relapse, when attacks are observed 3 – 5 times per year. There is one more peculiarity, which is necessary to remember – the attacks in vertebrobasilar territory are more common and are frequently repeated in spite of TIA in carotid territory. But TIA in carotid territory prognosis is much more serious. Usually in one or two years after first attack stroke is developed. But TIA in carotid territory prognosis is much more serious. Usually in one or two years after first attack stroke is developed. Another peculiarity is that if TIA is observed several times per 24 hours it means there is pathology of MA. Transient in word TIA concerns only neurological clinical picture, but has nothing to do with hemodynamic cerebral disturbances, as they are observed during the next 3 weeks. Another peculiarity is that if TIA is observed several times per 24 hours it means there is pathology of MA. Transient in word TIA concerns only neurological clinical picture, but has nothing to do with hemodynamic cerebral disturbances, as they are observed during the next 3 weeks.

22 Types of crisises Hyperkinetic type usually is accompanied by increasing of heart outflow with increased heart index more than 4.5 l per min in m² and normal general peripheral resistance. Hyperkinetic type usually is accompanied by increasing of heart outflow with increased heart index more than 4.5 l per min in m² and normal general peripheral resistance. Hypokinetic type is accompanied by decreasing of heart outflow with decreased heart index to 2.8 l per min in m² and high general peripheral resistance. Hypokinetic type is accompanied by decreasing of heart outflow with decreased heart index to 2.8 l per min in m² and high general peripheral resistance. Eukinetic type is accompanied by normal heart outflow and slightly increased general peripheral resistance. Eukinetic type is accompanied by normal heart outflow and slightly increased general peripheral resistance.

23 Hyperkinetic crisis There is a rapid development of crisis without portents. There is a rapid development of crisis without portents. Mainly systolic blood pressure is increased (More than mm) Mainly systolic blood pressure is increased (More than mm) General cerebral symptoms are well - expressed. That means psychomotor agitation, severe headache with nausea and vomiting. General cerebral symptoms are well - expressed. That means psychomotor agitation, severe headache with nausea and vomiting. There are well – expressed autonomic disorders, such as shortness of breath, red or pale skin, polyuria. There are well – expressed autonomic disorders, such as shortness of breath, red or pale skin, polyuria. The duration of crisis is up to several hours. The duration of crisis is up to several hours.

24 Hypokinetic crisis There is gradual development against long lasting hypertension background. There is gradual development against long lasting hypertension background. Mainly diastolic blood pressure is increased. Mainly diastolic blood pressure is increased. There are well – expressed EKG – changes: slow intra - ventricular conductivity, decreasing of ST – segment. There are well – expressed EKG – changes: slow intra - ventricular conductivity, decreasing of ST – segment. In this case the risk of ischemic stroke is too high. In this case the risk of ischemic stroke is too high.

25 Eukinetic crisis A rapid development. A rapid development. Both systolic and diastolic blood pressures are increased. Both systolic and diastolic blood pressures are increased. The symptoms of acute left - ventricular insufficiency and lung edema can be observed. The symptoms of acute left - ventricular insufficiency and lung edema can be observed.

26 Duration of hypertensive crisises Mild, which last up to 1 hour Mild, which last up to 1 hour Mediate (they last several hours) Mediate (they last several hours) Severe (they last from 5 –6 hours up to 24 hours) Severe (they last from 5 –6 hours up to 24 hours) The frequency: Mild hypertensive crisis are: Frequent – means they are observed more than 4 times per month; Frequent – means they are observed more than 4 times per month; Moderate frequent - means they are observed 3 – 4 times per month; Moderate frequent - means they are observed 3 – 4 times per month; Rare - means they are observed times per month; Rare - means they are observed times per month; Mediate and severe hypertensive crisis are: Frequent – means they are observed more than 5 times per year; Frequent – means they are observed more than 5 times per year; Moderate frequent - means they are observed 3 – 5 times per year; Moderate frequent - means they are observed 3 – 5 times per year; Rare - means they are observed times per year. Rare - means they are observed times per year.

27 Additional methods

28 Additional methods of medical examination Ultrasonic doplerography - finds out the absence or presence of stenosis and occlusions of magistral arteries of head and neck. Ultrasonic doplerography - finds out the absence or presence of stenosis and occlusions of magistral arteries of head and neck. Rheoencephalography – finds out asymmetry of blood circulation, the state of vessel tonus and elasticity of vessels. Rheoencephalography – finds out asymmetry of blood circulation, the state of vessel tonus and elasticity of vessels. EEG – finds out diffuse and local changes of brain bioelectric potentials. EEG – finds out diffuse and local changes of brain bioelectric potentials. X –ray examination of cervical part of spinal cord – finds out osteochondrosis, spinal abnormalities. X –ray examination of cervical part of spinal cord – finds out osteochondrosis, spinal abnormalities. EKG – finds out the state of coronal vessels, rhythm disorders, and coronary insufficiency. EKG – finds out the state of coronal vessels, rhythm disorders, and coronary insufficiency. Otoneurological examination is recommended in case of expressed vestibular syndrome in order to exclude labyrinth pathology. Otoneurological examination is recommended in case of expressed vestibular syndrome in order to exclude labyrinth pathology. Ophthalmic examination – finds out sclerotic or hypertensive changes on eye fundus. Ophthalmic examination – finds out sclerotic or hypertensive changes on eye fundus. Blood analysis. Blood analysis. Coagulation test - finds out increased aggregation of thrombocytes, erythrocytes, hematocrit. Coagulation test - finds out increased aggregation of thrombocytes, erythrocytes, hematocrit. Biochemical blood analysis - finds out proteinemia, increased cholesterin, - lipoprotein, pre- - lipoprotein. Biochemical blood analysis - finds out proteinemia, increased cholesterin, - lipoprotein, pre- - lipoprotein.

29 Differential diagnosis Dynamic blood circulation disturbances are usually differentiated with: Migraine crisis Migraine crisis Partial epileptic attacks Partial epileptic attacks Vestibular crisis Vestibular crisis Multiple sclerosis Multiple sclerosis Brain tumor Brain tumor Hypoglycemia Hypoglycemia Faint Faint

30 Treatment of dynamic blood circulation disturbances Hospitalization is necessary for the patients with: Severe cerebral – vascular crisis that can result in stroke Severe cerebral – vascular crisis that can result in stroke Repeated attacks with well – expressed focal symptoms Repeated attacks with well – expressed focal symptoms Severe hypertensive crisis with high blood pressure Severe hypertensive crisis with high blood pressure Coronary – cerebral attack, suspected myocardial infarction or angina pectoris. Coronary – cerebral attack, suspected myocardial infarction or angina pectoris.

31 The main principals of treatment To normalize blood pressure To normalize blood pressure To improve brain hemodynamic To improve brain hemodynamic To improve microcirculation and rheologic properties of blood, to prevent aggregation of blood cells To improve microcirculation and rheologic properties of blood, to prevent aggregation of blood cells To decrease vessels penetrance To decrease vessels penetrance To prevent brain edema, to decrease intracranial hypertension To prevent brain edema, to decrease intracranial hypertension To improve heart activity To improve heart activity To improve brain metabolism To improve brain metabolism To overcome autonomic syndrome To overcome autonomic syndrome

32 Treatment of hypertonic crisis All kinds of crisis : Clofelin 1ml 0.01 % i/v in 20 ml of physiologic solution Clofelin 1ml 0.01 % i/v in 20 ml of physiologic solution Dibasol 0.5% 2 – 4 ml i/m or i/v Dibasol 0.5% 2 – 4 ml i/m or i/v Euphyllini 2.4% 10.0 i/v in physiologic solution Euphyllini 2.4% 10.0 i/v in physiologic solution Antagonists of Calcium (finoptini 0.5% 2 ml i/v in 10 ml of physiologic solution) Antagonists of Calcium (finoptini 0.5% 2 ml i/v in 10 ml of physiologic solution) Cardioselective -adrenoblockers (athenolol 25 – 50 mg per day) Cardioselective -adrenoblockers (athenolol 25 – 50 mg per day) Nifidipine mg Nifidipine mg Inhibitors of ACE – Enalapril 5 – 10 mg Inhibitors of ACE – Enalapril 5 – 10 mg In case of too high blood pressure with left ventricule insufficiency and lung edema ganglioblockers are used – benzohexonium 2.5 % 0.5 – 1 ml i/m or s/c in glucose solution by drops. In case of too high blood pressure with left ventricule insufficiency and lung edema ganglioblockers are used – benzohexonium 2.5 % 0.5 – 1 ml i/m or s/c in glucose solution by drops.

33 Hypertonic hypokinetic crisis Dibasol 0.5% 4 – 6 ml Dibasol 0.5% 4 – 6 ml -adrenoblockers – Anaprilini 0.1% 5 ml i/v -adrenoblockers – Anaprilini 0.1% 5 ml i/v But the last are contraindicated at bradycardia, disoders of atrioventricular conduction. But the last are contraindicated at bradycardia, disoders of atrioventricular conduction. Hypokinetic crisis : Apresin – 2% 1 ml i/v by drops; Apresin – 2% 1 ml i/v by drops; Diazoxid 1.5% 20 ml 3 – 4 times per day. Diazoxid 1.5% 20 ml 3 – 4 times per day. Eukinetic crisis: Clofelini Clofelini antagonists of calcium antagonists of calcium spasmolytics spasmolytics

34 All kinds of hypertonic crisis with psychoemotional and autonomic reaction Aminazini 2.5% 1 ml in 200 ml of physiologic solution Aminazini 2.5% 1 ml in 200 ml of physiologic solution Sibazoni 0.5% 2 ml Sibazoni 0.5% 2 ml Pipolfeni 2.5% 2 ml Pipolfeni 2.5% 2 ml In order to prevent brain edema we use euphillini 2.4 % solution 10 ml with 2 ml lazix In order to prevent brain edema we use euphillini 2.4 % solution 10 ml with 2 ml lazix To decrease brain hypoxia we use Na oxybutiras 20% 10 ml i/v in glucose solution. To decrease brain hypoxia we use Na oxybutiras 20% 10 ml i/v in glucose solution.

35 Treatment of TIA 1. Blood pressure normalization At heart failure and systolic blood pressure less than 120 mm glycosides are used: At heart failure and systolic blood pressure less than 120 mm glycosides are used: Corglyconi 0.06 % strophantini 0.05 % 1.0 in 20 ml of 40 % glucose i/v Corglyconi 0.06 % strophantini 0.05 % 1.0 in 20 ml of 40 % glucose i/v Cordiamini 1 ml s/c Cordiamini 1 ml s/c Sulfocamfocaini 10 % 2ml i/m Sulfocamfocaini 10 % 2ml i/m Cofeini 10 % 1ml s/c Cofeini 10 % 1ml s/c Mesatoni % 1 ml s/c or i/m at low BP Mesatoni % 1 ml s/c or i/m at low BP Prednisoloni 60 – 120 mg i/v by drops with 200 ml 5 % glucose Prednisoloni 60 – 120 mg i/v by drops with 200 ml 5 % glucose At hypertension hypotensive therapy and spasmolytics are used in usual doses. At hypertension hypotensive therapy and spasmolytics are used in usual doses.

36 Treatment of TIA 2. To improve brain hemodynamic vasoactive medications are used: Euphilini 2.4 % 10 ml Euphilini 2.4 % 10 ml Cavintoni 10 – 20 mg i/v with 20 ml 0.9 % NaCl Cavintoni 10 – 20 mg i/v with 20 ml 0.9 % NaCl Sermioni 4 –8 mg i/v by drops Sermioni 4 –8 mg i/v by drops Ksantinoli nicotinas 15 % 2 ml i/m Ksantinoli nicotinas 15 % 2 ml i/m

37 Treatment of TIA 3. To improve microcirculation and rheologic properties of blood, to prevent aggregation of blood cells (It is especially important in case of well expressed focal neurological symptoms in order to prevent stroke). Direct anticoagulants: Direct anticoagulants: - Heparini 5 – U. s/c 3 –4 times per day during 3 –5 days, than U. 4 times per day during 3 – 4 days - Heparini 5 – U. s/c 3 –4 times per day during 3 –5 days, than U. 4 times per day during 3 – 4 days - Fraxiparini 0.3 x 2 - Fraxiparini 0.3 x 2 Indirect anticoagulants: Indirect anticoagulants: Pelentani 0.1 – 0.3 Pelentani 0.1 – 0.3 Fenilini – 0.03 Fenilini – 0.03 Syncumar times per day during 2-3 weeks Syncumar times per day during 2-3 weeks

38 Treatment of TIA 4. Antiagregants: Aspirini 70 –80 mg once a day Aspirini 70 –80 mg once a day Ticlidi times per day during 2- 3 months Ticlidi times per day during 2- 3 months Trentali 2% 5 ml i/v by drops (it is contraindicated at myocardial infarction, do not use it with heparin or on an empty stomach) Trentali 2% 5 ml i/v by drops (it is contraindicated at myocardial infarction, do not use it with heparin or on an empty stomach) Agapurini 1 pill 3 times per day Agapurini 1 pill 3 times per day Reopoliglucini 200 –400 ml i/v by drops Reopoliglucini 200 –400 ml i/v by drops Solcoserili 10 –20 ml i/v by drops during 5 –7 days Solcoserili 10 –20 ml i/v by drops during 5 –7 days Ksantinoli nicotinas 15 % 1 –2 ml i/m Ksantinoli nicotinas 15 % 1 –2 ml i/m Kurantili times per day (it is contraindicated at low BP, heart failure) Kurantili times per day (it is contraindicated at low BP, heart failure) Plavix 75 mg per day Plavix 75 mg per day Parmidini times per day Parmidini times per day

39 Treatment of TIA 5. To prevent brain edema, to decrease intracranial hypertension: Furosemidi 40 –80 mg per day Furosemidi 40 –80 mg per day Lasix 1% 2ml i/v or i/m Lasix 1% 2ml i/v or i/m Manitoli 10 –20 % 200 ml i/v Manitoli 10 –20 % 200 ml i/v Dexoni 4-6 mg i/v or i/m Dexoni 4-6 mg i/v or i/m Albumini 5 % 100 ml Albumini 5 % 100 ml Vit E 5% 2 ml i/m, Aevit 1 ml i/m, Unitioli 5 ml Vit E 5% 2 ml i/m, Aevit 1 ml i/m, Unitioli 5 ml

40 Treatment of TIA 6. To improve brain metabolism: Nootropil 20 % ml Nootropil 20 % ml Instenoni 2 ml i/m or i/v by drops Instenoni 2 ml i/m or i/v by drops Solcoserili 10 –20 ml i/v by drops Solcoserili 10 –20 ml i/v by drops Actovegini 2 ml i/m or i/v (it is contraindicated at cardiovascular failure, oliguria, lung edema) Actovegini 2 ml i/m or i/v (it is contraindicated at cardiovascular failure, oliguria, lung edema) Cerebrolisini 15 % 1.0 ml i/m Cerebrolisini 15 % 1.0 ml i/m

41 Treatment of TIA 7. Antioxydants: Vit E 1 ml i /m Vit E 1 ml i /m Tiatriasolini 1 ml i /m Tiatriasolini 1 ml i /m Emoxipini 2.0 i/m Emoxipini 2.0 i/m 8. Symptomatic treatment: At vomiting and hiccup – cerukal, aminasini, galoperidol, validol At vomiting and hiccup – cerukal, aminasini, galoperidol, validol At headache – tramadol, analgini At headache – tramadol, analgini At agitation – sedatives and anxyolytics At agitation – sedatives and anxyolytics 9. Surgical treatment – is used at stenosis of general or internal carotid artery (when stenosis is more than 70 % according to ultrasonographic data). Thrombinectomy is used.

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