Stroke. Introduction Stroke is a clinical syndrome of sudden focal or global cerebral dysfunction...

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Stroke Stroke

Transcript of Stroke. Introduction Stroke is a clinical syndrome of sudden focal or global cerebral dysfunction...

Page 1: Stroke. Introduction Stroke is a clinical syndrome of sudden focal or global cerebral dysfunction lasting more than 24 hours, of presumed vascular origin.

StrokeStroke

Page 2: Stroke. Introduction Stroke is a clinical syndrome of sudden focal or global cerebral dysfunction lasting more than 24 hours, of presumed vascular origin.

IntroductionIntroduction

• Stroke is a clinical syndrome of sudden Stroke is a clinical syndrome of sudden focal or global cerebral dysfunction focal or global cerebral dysfunction lasting more than 24 hours, of lasting more than 24 hours, of presumed vascular origin. It may occur presumed vascular origin. It may occur as a result of cerebral infarction as a result of cerebral infarction (ischaemic stroke), intracerebral (ischaemic stroke), intracerebral haemorrhage or subarachnoid haemorrhage or subarachnoid haemorrhage. Ischaemic stroke is the haemorrhage. Ischaemic stroke is the commonest type, accounting for about commonest type, accounting for about 85%. 85%.

Page 3: Stroke. Introduction Stroke is a clinical syndrome of sudden focal or global cerebral dysfunction lasting more than 24 hours, of presumed vascular origin.

Pathophysiology of Pathophysiology of ischaemic strokeischaemic stroke• Thrombo-embolic occlusion of blood flow triggers a Thrombo-embolic occlusion of blood flow triggers a

sequence of events, the ischaemic cascade. Failure of sequence of events, the ischaemic cascade. Failure of energy production leads to anaerobic glycolysis and energy production leads to anaerobic glycolysis and lactic acidosis, and failure of the ion pumps results in lactic acidosis, and failure of the ion pumps results in neuronal depolarisation and intracellular calcium neuronal depolarisation and intracellular calcium overload. These events lead to the release of neurotoxic overload. These events lead to the release of neurotoxic substances such as excitatory neurotransmitters substances such as excitatory neurotransmitters (chiefly glutamate), inflammatory mediators (eg. (chiefly glutamate), inflammatory mediators (eg. prostaglandins, leukotrienes), toxic free radicals (eg. prostaglandins, leukotrienes), toxic free radicals (eg. nitric oxide) and activated lytic enzymes (lipases, nitric oxide) and activated lytic enzymes (lipases, proteases), ultimately causing neuronal death (1). proteases), ultimately causing neuronal death (1).

• Ischaemic damage depends on the degree and the Ischaemic damage depends on the degree and the duration of ischaemia. Following complete occlusion of a duration of ischaemia. Following complete occlusion of a vessel, a central core of densely ischaemic tissue is vessel, a central core of densely ischaemic tissue is irreversibly damaged (infarction) within minutes.irreversibly damaged (infarction) within minutes.

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Around the infarction is an area of critical ischaemia Around the infarction is an area of critical ischaemia (ischaemic penumbra), which is inadequately (ischaemic penumbra), which is inadequately perfused.perfused.

• Neurones in the penumbra are energy deficient and Neurones in the penumbra are energy deficient and electrically quiescent, but have intact ion pumps electrically quiescent, but have intact ion pumps and are viable. Prolonged ischaemia will lead to and are viable. Prolonged ischaemia will lead to their death and extension of the infarct. If perfusion their death and extension of the infarct. If perfusion is restored within a certain period of time, neurones is restored within a certain period of time, neurones in the penumbra can be salvaged; this constitutes a in the penumbra can be salvaged; this constitutes a therapeutic window of opportunity. In humans, this therapeutic window of opportunity. In humans, this window period is believed to be 3 to 6 hours.window period is believed to be 3 to 6 hours.

• Early treatmentEarly treatment• Components of the early treatment of ischaemic Components of the early treatment of ischaemic

stroke are shown in Box 1. stroke are shown in Box 1.

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Box 1. Box 1. Early treatment of Early treatment of ischaemic strokeischaemic stroke

1. General care 1. General care 2. Specific treatment: thrombolysis, 2. Specific treatment: thrombolysis,

anticoagulants, antiplatelet agents and anticoagulants, antiplatelet agents and neuro-protective agents neuro-protective agents

3. Emergency approach 3. Emergency approach 4. Stroke unit care 4. Stroke unit care 5. Treatment of complications 5. Treatment of complications 6. Treatment of co-morbidity 6. Treatment of co-morbidity 7. Rehabilitation7. Rehabilitation

1. General care

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1. 1. General careGeneral care

General care of a stroke patient in the early stages aims at sustaining General care of a stroke patient in the early stages aims at sustaining life (eg. airway, breathing, circulation) and maintaining vital bodily life (eg. airway, breathing, circulation) and maintaining vital bodily functions (eg. fluid and electrolyte balance, blood glucose, nutrition, functions (eg. fluid and electrolyte balance, blood glucose, nutrition, swallowing, temperature, and bladder, bowel and skin care). swallowing, temperature, and bladder, bowel and skin care).

Autoregulation of regional cerebral blood flow is defective in the Autoregulation of regional cerebral blood flow is defective in the ischaemic penumbra, and blood flow is dependent on cerebral ischaemic penumbra, and blood flow is dependent on cerebral perfusion pressure. Volume depletion or a fall in blood pressure will perfusion pressure. Volume depletion or a fall in blood pressure will reduce perfusion pressure and lead to extension of the infarct (2,3). reduce perfusion pressure and lead to extension of the infarct (2,3). Attention to fluid and electrolyte balance is essential. Volume Attention to fluid and electrolyte balance is essential. Volume overload can lead to cerebral oedema, and volume depletion with overload can lead to cerebral oedema, and volume depletion with accompanying hypotension and electrolyte disturbances can accompanying hypotension and electrolyte disturbances can adversely affect outcome. Volume replacement should be by the oral adversely affect outcome. Volume replacement should be by the oral route, or a nasogastric tube when swallowing is impaired. Intravenous route, or a nasogastric tube when swallowing is impaired. Intravenous fluids when required should be given as isotonic saline. Aspiration is a fluids when required should be given as isotonic saline. Aspiration is a concern in the early stages, as swallowing difficulties are common. A concern in the early stages, as swallowing difficulties are common. A simple bedside test of swallowing is to give 1 or 2 teaspoonfuls of simple bedside test of swallowing is to give 1 or 2 teaspoonfuls of water with the patient seated; coughing or `developing a wet voice' water with the patient seated; coughing or `developing a wet voice' indicates impaired swallowing and oral feeding should not be indicates impaired swallowing and oral feeding should not be attempted.attempted.

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• Blood pressure management is critical after a stroke. Blood pressure management is critical after a stroke. A transient rise in blood pressure is seen in up to 80% A transient rise in blood pressure is seen in up to 80% of patients. This resolves spontaneously in most of patients. This resolves spontaneously in most cases by 7 to 10 days. Injudicious treatment of reflex cases by 7 to 10 days. Injudicious treatment of reflex elevation in blood pressure may lead to a fall in elevation in blood pressure may lead to a fall in perfusion pressure in the penumbra. Treatment perfusion pressure in the penumbra. Treatment should be started only when definite indications (Box should be started only when definite indications (Box 2) are present (2,3,4). In their absence blood pressure 2) are present (2,3,4). In their absence blood pressure should be monitored regularly but treatment withheld should be monitored regularly but treatment withheld for 10 days. Antihypertensive therapy is commenced for 10 days. Antihypertensive therapy is commenced if blood pressure remains persistently elevated after if blood pressure remains persistently elevated after 10 days. 10 days.

• Blood pressure reduction should be gradual, with a Blood pressure reduction should be gradual, with a targeted reduction of about 10 to 15% over 24 hours. targeted reduction of about 10 to 15% over 24 hours. Reducing blood pressure to below systolic <180, Reducing blood pressure to below systolic <180, diastolic <110 mmHg can be harmful (3,4). diastolic <110 mmHg can be harmful (3,4). Short Short acting oral agents (eg. captopril) are particularly acting oral agents (eg. captopril) are particularly useful. useful.

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  Box 2. Box 2. Indications for early Indications for early treatment of elevated blood treatment of elevated blood pressure in acute strokepressure in acute stroke• Evidence of pre-existing hypertension Evidence of pre-existing hypertension •   documented previous hypertension - clinic documented previous hypertension - clinic

records etc. evidence of hypertensive records etc. evidence of hypertensive target organ target organ

•   damage, hypertensive retinopathy, left damage, hypertensive retinopathy, left ventricular hypertrophy  on ECGventricular hypertrophy  on ECG

•   Evidence of a hypertensive emergency Evidence of a hypertensive emergency eg. hypertensive encephalopathy, left eg. hypertensive encephalopathy, left heart failure. heart failure.

•   Blood pressure is very high: systolic Blood pressure is very high: systolic >220-240, diastolic >120 mmHg >220-240, diastolic >120 mmHg

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• Blood glucose content is another critical determinant of Blood glucose content is another critical determinant of outcome after stroke. Both hypoglycaemia and outcome after stroke. Both hypoglycaemia and hyperglycaemia can be detrimental (4). Hypoglycaemia hyperglycaemia can be detrimental (4). Hypoglycaemia should be corrected with dextrose infusions. Hypergly-should be corrected with dextrose infusions. Hypergly-caemia is associated with aggravation of cerebral caemia is associated with aggravation of cerebral oedema and increased mortality, and needs treatment oedema and increased mortality, and needs treatment with insulin. Fever should be actively treated with with insulin. Fever should be actively treated with antipyretics, and the cause, usually an infection, sought antipyretics, and the cause, usually an infection, sought and treated. and treated.

• Bladder dysfunction is common after a stroke, and both Bladder dysfunction is common after a stroke, and both urinary retention and incontinence can occur. Urinary urinary retention and incontinence can occur. Urinary retention needs urethral catheterisation. In patients with retention needs urethral catheterisation. In patients with urinary incontinence, residual bladder volume after urinary incontinence, residual bladder volume after micturition should be assessed by bladder ultrasound micturition should be assessed by bladder ultrasound scan or by catherisation; an indwelling catheter is scan or by catherisation; an indwelling catheter is indicated where the residual volume is high, but others indicated where the residual volume is high, but others can be managed with external devices such as condom can be managed with external devices such as condom catheterscatheters

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2. 2. Specific therapySpecific therapya) Thrombolysisa) Thrombolysis • The success of thrombolytic therapy in acute myocardial The success of thrombolytic therapy in acute myocardial

infarction has rekindled interest in its use in stroke. infarction has rekindled interest in its use in stroke. Intravenous thrombolytic therapy has changed the Intravenous thrombolytic therapy has changed the treatment of acute ischaemic stroke. It appears that both treatment of acute ischaemic stroke. It appears that both the type of drug and the timing of administration are the type of drug and the timing of administration are important determinants of outcome. Initial studies that important determinants of outcome. Initial studies that used streptokinase did not show a definite benefit. used streptokinase did not show a definite benefit. However, the NINDS trial which used r-tPA within 3 hours However, the NINDS trial which used r-tPA within 3 hours of onset showed significant improvements in outcome of onset showed significant improvements in outcome (5). (5).

• The main complication of thrombolytic therapy is The main complication of thrombolytic therapy is bleeding, which may be intracranial or extracranial. bleeding, which may be intracranial or extracranial. Spontaneous haemorrhagic transformation, a recognised Spontaneous haemorrhagic transformation, a recognised complication of cerebral infarction, may be aggravated complication of cerebral infarction, may be aggravated by thrombolytic therapy. Thrombolysis increases the by thrombolytic therapy. Thrombolysis increases the severity of haemorrhage, rather than the incidence.severity of haemorrhage, rather than the incidence.

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• Early CT scans are useful not only to exclude Early CT scans are useful not only to exclude haemorrhage before thrombolysis, but also to identify haemorrhage before thrombolysis, but also to identify infarcts that may be at a higher risk of haemorrhagic infarcts that may be at a higher risk of haemorrhagic transformation. The dose of r-tPA is 0.9 mg/kg up to a transformation. The dose of r-tPA is 0.9 mg/kg up to a maximum of 90 mg, the first 10% as a bolus, and the maximum of 90 mg, the first 10% as a bolus, and the balance as an infusion over 60 min. There are many balance as an infusion over 60 min. There are many contraindications for r-tPA including seizure at onset, pre-contraindications for r-tPA including seizure at onset, pre-treatment BP systolic >185, diastolic>110 mm Hg, major treatment BP systolic >185, diastolic>110 mm Hg, major infarct on CT scan, previous intracranial haemmorhage, infarct on CT scan, previous intracranial haemmorhage, recent myocardial infarct, recent or intended surgery, use recent myocardial infarct, recent or intended surgery, use of anticoagulant recently etc. IV r-tPA is now standard of anticoagulant recently etc. IV r-tPA is now standard acute treatment in the USA, Australia and most European acute treatment in the USA, Australia and most European countries. Many concerns still remain largely owing to the countries. Many concerns still remain largely owing to the risk of bleeding and the difficulties in initiating treatment risk of bleeding and the difficulties in initiating treatment within 3 hours (5). Intra-arterial thrombolysis using r-tPA within 3 hours (5). Intra-arterial thrombolysis using r-tPA has been shown to be beneficial in posterior circulation has been shown to be beneficial in posterior circulation strokes due to basilar artery thrombosis. Its place in strokes due to basilar artery thrombosis. Its place in carotid territory strokes is under evaluation.carotid territory strokes is under evaluation.

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b) Anticoagulantsb) Anticoagulants • Anticoagulants are of two main types, and include Anticoagulants are of two main types, and include

parenteral heparin (unfractionated heparin and low parenteral heparin (unfractionated heparin and low molecular weight heparin _ LMWH) and oral molecular weight heparin _ LMWH) and oral warfarin. Oral warfarin is of proven benefit in warfarin. Oral warfarin is of proven benefit in prevention of stroke. Unfractionated heparin has prevention of stroke. Unfractionated heparin has been used in acute ischaemic stroke, especially in been used in acute ischaemic stroke, especially in stroke-in-evolution or cardio-embolic stroke, without stroke-in-evolution or cardio-embolic stroke, without much evidence of benefit. Many recent studies have much evidence of benefit. Many recent studies have failed to demonstrate an improvement in outcome failed to demonstrate an improvement in outcome (7), and unfractionated heparin has no place in the (7), and unfractionated heparin has no place in the management of acute ischaemic stroke. LMWH may management of acute ischaemic stroke. LMWH may be equally effective as unfractionated heparin, with be equally effective as unfractionated heparin, with a lower risk of bleeding. More large trials are a lower risk of bleeding. More large trials are necessary before they can be considered in routine necessary before they can be considered in routine clinical practice. clinical practice.

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c) Antiplatelet agentsc) Antiplatelet agents

• Aspirin and other antiplatelet agents are of proven Aspirin and other antiplatelet agents are of proven value in primary and secondary prevention of stroke. value in primary and secondary prevention of stroke. Two large trials, each randomising about 20 000 Two large trials, each randomising about 20 000 patients, addressed the value of early use of aspirin patients, addressed the value of early use of aspirin in acute ischaemic stroke. Data from both trials have in acute ischaemic stroke. Data from both trials have shown that early use of aspirin (160 to 300 mg within shown that early use of aspirin (160 to 300 mg within 48 hours) is beneficial in reducing deaths and 48 hours) is beneficial in reducing deaths and dependency (7,8). The benefits appear to be mainly dependency (7,8). The benefits appear to be mainly related to prevention of early recurrences. The place related to prevention of early recurrences. The place of other antiplatelet agents (such as dipyridamole, of other antiplatelet agents (such as dipyridamole, clopidogrel, ticlopidine and glycoprotein IIb/IIIa clopidogrel, ticlopidine and glycoprotein IIb/IIIa receptor antagonists) as acute treatment needs receptor antagonists) as acute treatment needs evaluationevaluation

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d) Neuro-protective agentsd) Neuro-protective agents

• Preserving the intergrity of the ischaemic neurones is Preserving the intergrity of the ischaemic neurones is important. Avoid factors that aggravate ischaemic important. Avoid factors that aggravate ischaemic damage; these include hypotension, hypoxia, damage; these include hypotension, hypoxia, hyperglycaemia and hyperpyrexia (1). Reducing the hyperglycaemia and hyperpyrexia (1). Reducing the energy requirements of ischaemic neurones by high energy requirements of ischaemic neurones by high dose barbiturate therapy and hypothermia have shown dose barbiturate therapy and hypothermia have shown promising results (1). Treatment with pharmacological promising results (1). Treatment with pharmacological agents that target specific events of the ischaemic agents that target specific events of the ischaemic cascade (neuro-protective agents) within the therapeutic cascade (neuro-protective agents) within the therapeutic window period is under evalution, and this may become window period is under evalution, and this may become first-line therapy in the future (4,9). Such agents include first-line therapy in the future (4,9). Such agents include calcium channel blockers (eg nimopidine), GABA calcium channel blockers (eg nimopidine), GABA antagonists (eg clomethiazole), glutamate antagonists antagonists (eg clomethiazole), glutamate antagonists (eg eliprodil), free radical scavengers (eg tirilazad) and (eg eliprodil), free radical scavengers (eg tirilazad) and sodium channel blockers (eg lubeluzole). sodium channel blockers (eg lubeluzole).

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3.3. Treating stroke as an emergencyTreating stroke as an emergency

• The main difficulty in using r-tPA and other potential The main difficulty in using r-tPA and other potential therapies is the need to initiate treatment within 3 therapies is the need to initiate treatment within 3 hours. Many countries have sucessfully overcome this hours. Many countries have sucessfully overcome this challenge by developing public educational campaigns, challenge by developing public educational campaigns, emergency pre-hospital medical care systems with emergency pre-hospital medical care systems with trained ambulance crews, rapid triage and 'fast-track' trained ambulance crews, rapid triage and 'fast-track' systems on admission to hospital, stroke units and systems on admission to hospital, stroke units and stroke teams. Stroke is now treated as an emergency.stroke teams. Stroke is now treated as an emergency.

• 4.4. Stroke units Stroke units • A stroke unit is a multidisciplinary team of health care A stroke unit is a multidisciplinary team of health care

professionals, providing organised inpatient stroke professionals, providing organised inpatient stroke care in a defined area. Compared with conventional care in a defined area. Compared with conventional care in a general medical ward setting, stroke unit care care in a general medical ward setting, stroke unit care produces significant improvements in short term and produces significant improvements in short term and long term outcome measures. Death, disability, long term outcome measures. Death, disability, dependency and hospital stay are reduced, and dependency and hospital stay are reduced, and functional capacity is improved (10). functional capacity is improved (10).

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5.5. Treatment of Treatment of complicationscomplications• Early detection and treatment of complications are Early detection and treatment of complications are

essential to improve outcome after a stroke. Cerebral essential to improve outcome after a stroke. Cerebral oedema, or brain swelling, is probably the most oedema, or brain swelling, is probably the most important early complication. Treatment of cerebral important early complication. Treatment of cerebral oedema should ideally be guided by intracranial oedema should ideally be guided by intracranial pressure monitoring. In the absence of such facilities, pressure monitoring. In the absence of such facilities, patients with alteration of consciousness, large infarcts, patients with alteration of consciousness, large infarcts, and evidence of mass effect (midline shift, compression and evidence of mass effect (midline shift, compression of ventricles) on CT scanning should be treated (Box 3). of ventricles) on CT scanning should be treated (Box 3). Other complications of stroke include haemorhagic Other complications of stroke include haemorhagic transformation, seizures, respiratory and urinary transformation, seizures, respiratory and urinary infection, deep vein thrombosis and pulmonary infection, deep vein thrombosis and pulmonary embolism, acute peptic ulcer, pressure sores, embolism, acute peptic ulcer, pressure sores, neuropsychiatric sequelae such as anxiety or depression neuropsychiatric sequelae such as anxiety or depression and musculo-skeletal sequelae such as contractures, and musculo-skeletal sequelae such as contractures, spasticity and adhesive capsulitis of the shoulder. spasticity and adhesive capsulitis of the shoulder.

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Box 3. Box 3. Management of raised Management of raised intracranial pressure after intracranial pressure after stroke stroke (3,4)(3,4) • Elevate head end by 30° Elevate head end by 30° • Avoid or correct aggravating factors _ Avoid or correct aggravating factors _

hypoxia, hyperglycaemia hypoxia, hyperglycaemia • Moderate fluid restriction Moderate fluid restriction • Avoid hypoosmolar fluids eg. dextrose Avoid hypoosmolar fluids eg. dextrose • Giving osmotic agents (eg iv. mannitol) as Giving osmotic agents (eg iv. mannitol) as

indicated indicated • Hyperventilation Hyperventilation • IV barbiturates IV barbiturates • NB. Steroids are of no valueNB. Steroids are of no value

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6. 6. Treatment of co-morbidityTreatment of co-morbidity• Patients with stroke are usually old and may have associated Patients with stroke are usually old and may have associated

co-morbid conditions. These may interfere with the co-morbid conditions. These may interfere with the rehabilitation process (eg. chronic lung disease), or the rehabilitation process (eg. chronic lung disease), or the treatment (eg. aspirin or warfarin in peptic ulcer disease), and treatment (eg. aspirin or warfarin in peptic ulcer disease), and need assessment and treatment in their own right.need assessment and treatment in their own right.

• 7.7. Rehabilitation Rehabilitation • Rehabilitation is the process by which patients after a stroke Rehabilitation is the process by which patients after a stroke

are restored to their previous functional, mental and social are restored to their previous functional, mental and social capacity. This is best carried out by a multidisciplinary stroke capacity. This is best carried out by a multidisciplinary stroke team with the active participation of patients and care givers. team with the active participation of patients and care givers.

• ConclusionConclusion• Stroke is an emergency, a 'brain attack'. Recent Stroke is an emergency, a 'brain attack'. Recent

developments in drug therapy and service organisation have developments in drug therapy and service organisation have led to an aggressive approach to treatment of ischaemic led to an aggressive approach to treatment of ischaemic stroke, replacing the widespread sense of therapeutic nihilism stroke, replacing the widespread sense of therapeutic nihilism in the past. Many new treatment modalities are being in the past. Many new treatment modalities are being increasingly used, more are being developed and evaluated, increasingly used, more are being developed and evaluated, and the future looks brighter for stroke patients.and the future looks brighter for stroke patients.

• The vascular diseases of cerebrum occupy one of the first The vascular diseases of cerebrum occupy one of the first places in the structure of organic pathology of the central places in the structure of organic pathology of the central nervous system (about 17%).nervous system (about 17%).

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• HAEMORRHAGIC STROKE HAEMORRHAGIC STROKE • Haemorrhagic stroke develops as a result of involuntary Haemorrhagic stroke develops as a result of involuntary

break of intracerebral vessel and is accompanied by break of intracerebral vessel and is accompanied by forming of haematoma. A intracerebral hemorrhage is forming of haematoma. A intracerebral hemorrhage is one of the heaviest forms of vascular defeat of one of the heaviest forms of vascular defeat of cerebrum. As a rule, a hemorrhage of brain develops as cerebrum. As a rule, a hemorrhage of brain develops as a result of hypertensive illness (50 — 60%), pathological a result of hypertensive illness (50 — 60%), pathological changes in the vessels of brain, more frequent — after changes in the vessels of brain, more frequent — after atherosclerosis. atherosclerosis.

• Physical examination, births, emotional stresses, Physical examination, births, emotional stresses, fluctuation in the temperature of body, alcoholic fluctuation in the temperature of body, alcoholic intoxication and others like that often predetermine the intoxication and others like that often predetermine the temporal increase of arterial pressure. A spontaneous temporal increase of arterial pressure. A spontaneous hemorrhage of brain mainly occurred in women. In hemorrhage of brain mainly occurred in women. In clinical practice hemorrhage is distinguished on lateral clinical practice hemorrhage is distinguished on lateral and medial simultaneously on both sides of internal and medial simultaneously on both sides of internal capsule. A medial hemorrhage is often accompanied capsule. A medial hemorrhage is often accompanied with penetration of haematoma in the cavity of lateral or with penetration of haematoma in the cavity of lateral or III ventricle.III ventricle.

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• ClinicClinic. Haemorrhagic stroke develops mainly sharply, often without . Haemorrhagic stroke develops mainly sharply, often without some forecasters. A clinic is characterized by a sudden fainting fit some forecasters. A clinic is characterized by a sudden fainting fit and local neurological symptoms. Sometimes there is vomits. The and local neurological symptoms. Sometimes there is vomits. The face of patient becomes crimson-red, pulse tense, slow, breathings face of patient becomes crimson-red, pulse tense, slow, breathings vowel, the temperature of body rises. A head and eyes is often vowel, the temperature of body rises. A head and eyes is often returned aside. Another local symptoms are paresis or paralysis of returned aside. Another local symptoms are paresis or paralysis of extremities on a side opposite to the cell of hemorrhage, which extremities on a side opposite to the cell of hemorrhage, which arise up as a result of compression of the haematoma on arise up as a result of compression of the haematoma on formations of internal capsule or vessels. If a hemorrhage is formations of internal capsule or vessels. If a hemorrhage is comparative small, motive violations are poorly expressed, while a comparative small, motive violations are poorly expressed, while a massive hemorrhage, squeezing an internal capsule, results in massive hemorrhage, squeezing an internal capsule, results in hemiplegia.hemiplegia.

• Exposure of other local symptoms, in particular violations of Exposure of other local symptoms, in particular violations of sensitiveness, hemianopsia, disorders of language, becomes sensitiveness, hemianopsia, disorders of language, becomes possible after the exit of patient from the comatose state and possible after the exit of patient from the comatose state and renewal of consiousness. During short time from the moment of renewal of consiousness. During short time from the moment of origin of stroke there are considerable vibrations of vegetative origin of stroke there are considerable vibrations of vegetative violations: a pallor of person changes by hyperemia or, opposite, violations: a pallor of person changes by hyperemia or, opposite, he covered by sweat, the distal departments of extremities are he covered by sweat, the distal departments of extremities are cold, often all these phenomena prevail on the side of paralysis. In cold, often all these phenomena prevail on the side of paralysis. In beginning of disease the increase of tone of muscles with beginning of disease the increase of tone of muscles with violation of motive function is characteristic. violation of motive function is characteristic.

• For diagnostics the most important method is computer For diagnostics the most important method is computer tomografy. If at the persons of middle and young ages young the tomografy. If at the persons of middle and young ages young the pressure of cerebrospinal liquid is frequently promoted, at the pressure of cerebrospinal liquid is frequently promoted, at the senile age people it can be normal or even reduced. The promoted senile age people it can be normal or even reduced. The promoted maintenance of albumen is often exposed. On maintenance of albumen is often exposed. On ЕЕЕЕG we can G we can observed the observed the М-еМ-еcho signal on opposite to hemorrhage sitecho signal on opposite to hemorrhage site

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• Very frequent is horizontal large amplitude tonic nistagm which Very frequent is horizontal large amplitude tonic nistagm which often unites with vertical, connected with asymmetrical position often unites with vertical, connected with asymmetrical position of eyes, «floating» eyeballs. Disorders of breathing appear in the of eyes, «floating» eyeballs. Disorders of breathing appear in the case of heavy defeat of trunk. case of heavy defeat of trunk.

• Treatment. As lethality as a result of brain hemorrhage treated Treatment. As lethality as a result of brain hemorrhage treated with conservative treatment is extraordinarily high, and in the with conservative treatment is extraordinarily high, and in the case of surgical treatment goes down, that is why the necessary case of surgical treatment goes down, that is why the necessary operation is a method of choice. operation is a method of choice.

• A lateral hemorrhage is an absolute testimony for surgical A lateral hemorrhage is an absolute testimony for surgical treatment. In the case of medial hemorrhage the prognosis for treatment. In the case of medial hemorrhage the prognosis for surgical treatment is worse.surgical treatment is worse.

• In the case of penetration of blood in the ventricles of brain the In the case of penetration of blood in the ventricles of brain the conservative treatment is uneffective conservative treatment is uneffective

• Two types of operations are applied: 1) dissection of brain and Two types of operations are applied: 1) dissection of brain and delete of haematoma; 2) urgent punction of haematoma through delete of haematoma; 2) urgent punction of haematoma through a brain with sucking of blood. The cavity of haematoma once or a brain with sucking of blood. The cavity of haematoma once or twice is washed by isotonic solution of sodium chloride. twice is washed by isotonic solution of sodium chloride.

• In the case of presence of blood clots in the cavity of ventricle In the case of presence of blood clots in the cavity of ventricle washing is ineffective. washing is ineffective.

• In the case of hemorrhage in a cerebellum haematoma is treated In the case of hemorrhage in a cerebellum haematoma is treated on the same principle, like the haematoma of large brain.on the same principle, like the haematoma of large brain.

• SHARP VIOLATION OF CEREBRAL CIRCULATION OF BLOODSHARP VIOLATION OF CEREBRAL CIRCULATION OF BLOOD• Sharp violation of cerebral circulation by the mechanism of Sharp violation of cerebral circulation by the mechanism of

development is related either to the hemorrhage in subdural development is related either to the hemorrhage in subdural space (haemorrhagic stroke) or with an ischemia of brain space (haemorrhagic stroke) or with an ischemia of brain (ischemic stroke). Sometimes there is transition of ischemic (ischemic stroke). Sometimes there is transition of ischemic stroke in haemorrhagic stroke.stroke in haemorrhagic stroke.

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