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. Stroke definitions. Interruption of blood flow (ischaemic stroke)or Bleeding into or around the brain (haemorrhagic stroke). An injury to the brain caused by:. Transient ischaemic attack (TIA) . Brief episode in which neurological deficits sudde
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2. Stroke – definitions Interruption of blood flow (ischaemic stroke)
or
Bleeding into or around the brain (haemorrhagic stroke) Stroke is the generally preferred term for a group of cerebrovascular diseases that are of abrupt onset and cause neurological damage. An injury to the brain can be caused by
Sudden onset of inadequacies of blood flow to some or all of the brain (ischaemic stroke), or
Haemorrhage into brain tissue (parenchymatous haemorrhage) or spaces surronding the brain, most frequently the subarachnoid space (haemorrhagic stroke).
Stroke is the generally preferred term for a group of cerebrovascular diseases that are of abrupt onset and cause neurological damage. An injury to the brain can be caused by
Sudden onset of inadequacies of blood flow to some or all of the brain (ischaemic stroke), or
Haemorrhage into brain tissue (parenchymatous haemorrhage) or spaces surronding the brain, most frequently the subarachnoid space (haemorrhagic stroke).
3. Transient ischaemic attack (TIA) Brief episode in which neurological deficits suddenly occur, then disappear; can persist up to 24 hours
Temporary arterial blockage, with no resultant brain damage
If an ischaemic attack is brief with duration of less than 24 hours it is known as a transient ischaemic attack (TIA) rather than a stroke.
If an ischaemic attack is brief with duration of less than 24 hours it is known as a transient ischaemic attack (TIA) rather than a stroke.
4. Stroke - definitions There are two different types of stroke. One is called ischaemic stroke, and is caused by insufficient blood flow into part of the brain. Focal stroke conventionally is defined as a neurological deficit, lasting more than 24 hours caused by reduced blood flow in an artery supplying a part of the brain, and which ultimately results in infarction.
During an ischaemic stroke, blockage of an artery deprives part of the brain of blood flow and therefore oxygen and nutrients, leading to oxygen starvation (ischaemia) and tissue death.
If an ischaemic attack is brief with duration of less than 24 hours it is known as a transient ischaemic attack (TIA) rather than a stroke.
There are two different types of stroke. One is called ischaemic stroke, and is caused by insufficient blood flow into part of the brain. Focal stroke conventionally is defined as a neurological deficit, lasting more than 24 hours caused by reduced blood flow in an artery supplying a part of the brain, and which ultimately results in infarction.
During an ischaemic stroke, blockage of an artery deprives part of the brain of blood flow and therefore oxygen and nutrients, leading to oxygen starvation (ischaemia) and tissue death.
If an ischaemic attack is brief with duration of less than 24 hours it is known as a transient ischaemic attack (TIA) rather than a stroke.
5. Ischaemic strokes Areas of brain affected
Forebrain (frontal lobe and thalamus) > Brainstem > Cerebellum > Spinal cord
Lacunar stroke
Area of infarction has form of lacune or cavity (<15 mm). These are smaller strokes
6. Stroke – definitions There are two different types of stroke. One is called ischaemic stroke, and is caused by insufficient blood flow into part of the brain
The other is called haemorrhagic stroke and is the result of rupture of a blood vessel. During a haemorrhagic stroke, arterial rupture causes bleeding within the brain and its ventricles, which produces injury by distorting, compressing and tearing the surrounding brain tissue or by increasing intracranial pressure.
There are two different types of stroke. One is called ischaemic stroke, and is caused by insufficient blood flow into part of the brain
The other is called haemorrhagic stroke and is the result of rupture of a blood vessel. During a haemorrhagic stroke, arterial rupture causes bleeding within the brain and its ventricles, which produces injury by distorting, compressing and tearing the surrounding brain tissue or by increasing intracranial pressure.
7. Causes of haemorrhagic strokes Aneurysm rupture (often a subarachnoid haemorrhage occurs first)
AV malformation
8. Stroke – definitions Both ischaemic and haemorrhagic stroke lead to the death of brain cells, which disrupts the function that part of the brain controls. This can result in paralysis, speech and sensory problems, memory and reasoning deficits, coma, and possibly death.
Both ischaemic and haemorrhagic stroke lead to the death of brain cells, which disrupts the function that part of the brain controls. This can result in paralysis, speech and sensory problems, memory and reasoning deficits, coma, and possibly death.
9. Stroke – incidence and prevalence Stroke is the third commonest cause of death in the US after cardiovascular disease and cancer, and the leading cause of disability in adults. There are estimated to be 531.000 new cases of stroke and 200.000 recurrences of stroke each year in the US (Sorelle 2000).
In 22 European countries with a combined population of approximately 500 million, almost 1 million strokes are estimated to occur each year (Brainin et al 1999).
The incidence of stroke increases with age, thus the number of strokes is likely to increase in the future with the increase in life expectancy.
Mortality from stroke declined significantly from 1950 to 1990, most probably due to changes in lifestyle and advances in the control of severe hypertension, but since then has plateaued and even slightly increased in recent years (Wolf et al 1992).
References:
Sorelle R. Late-breaking trials at American Heart Association´s Scientific Sessions 2000. Circulation 2000;102:E9047-9.
Brainin M, Bornstein N, Boysen G, Demarin V. Acute neurological stroke care in Europe: results of the European Stroke Care Inventory. Eur J Neurol 1999;7:5-10.
Wolf PA, D´Agostino RB, O´Neal MA, Sytkowski P, Kase CS, Belanger AJ, et al. Secular trends in stroke incidence and mortality. The Framingham Study. Stroke 1992;23:1551-5.Stroke is the third commonest cause of death in the US after cardiovascular disease and cancer, and the leading cause of disability in adults. There are estimated to be 531.000 new cases of stroke and 200.000 recurrences of stroke each year in the US (Sorelle 2000).
In 22 European countries with a combined population of approximately 500 million, almost 1 million strokes are estimated to occur each year (Brainin et al 1999).
The incidence of stroke increases with age, thus the number of strokes is likely to increase in the future with the increase in life expectancy.
Mortality from stroke declined significantly from 1950 to 1990, most probably due to changes in lifestyle and advances in the control of severe hypertension, but since then has plateaued and even slightly increased in recent years (Wolf et al 1992).
References:
Sorelle R. Late-breaking trials at American Heart Association´s Scientific Sessions 2000. Circulation 2000;102:E9047-9.
Brainin M, Bornstein N, Boysen G, Demarin V. Acute neurological stroke care in Europe: results of the European Stroke Care Inventory. Eur J Neurol 1999;7:5-10.
Wolf PA, D´Agostino RB, O´Neal MA, Sytkowski P, Kase CS, Belanger AJ, et al. Secular trends in stroke incidence and mortality. The Framingham Study. Stroke 1992;23:1551-5.
10. Stroke – high rate of morbidity Leading cause of morbidity and long-term disability in most industrialised nations As well as a high mortality rate, stroke is one of the leading causes of morbidity and long-term disability in most industrialised nations (Hacke et al 2003). It is estimated that one third of the patients who suffer a stroke experience moderate to severe disabilities (Nazarko 2003).
In the Framingham Heart study, 31% of stroke survivors required help caring for themselves, 20% needed help with walking and 71% had impaired vocational capacity as assessed after an average of 7 years (American Heart Association 1996). Stroke can therefore cause considerable suffering and disruption to family life at home.
The data shown are from the Framingham Heart study, in which over 5000 patients aged 30–62 years were followed bi-annually over 22 years. The aim of the study was to analyse the epidemiological features of AF including risk factors and complications, such as stroke.
The graph illustrated in this slide shows the high percentage of patients who were left disabled and therefore requiring long-term care or unable to work after a stroke. Almost three quarters of the patients suffered significant impairment.
References:
Hacke W, Kaste M, Bogousslavsky J, Brainin M, Chamorro A, Lees K, et al. European Stroke Initiative Recommendations 2003. Ischeamic Stroke. 2003:www.eusi-stroke.com/recommendations-2003/eusi.2003.pdf
Nazarko L. Rehabilitation and continence promotion following a stroke. Nurs Times 2003;99:52-55.
American Heart Association. Heart and stroke facts: statistical supplement. Dallas, Texas, 1996.As well as a high mortality rate, stroke is one of the leading causes of morbidity and long-term disability in most industrialised nations (Hacke et al 2003). It is estimated that one third of the patients who suffer a stroke experience moderate to severe disabilities (Nazarko 2003).
In the Framingham Heart study, 31% of stroke survivors required help caring for themselves, 20% needed help with walking and 71% had impaired vocational capacity as assessed after an average of 7 years (American Heart Association 1996). Stroke can therefore cause considerable suffering and disruption to family life at home.
The data shown are from the Framingham Heart study, in which over 5000 patients aged 30–62 years were followed bi-annually over 22 years. The aim of the study was to analyse the epidemiological features of AF including risk factors and complications, such as stroke.
The graph illustrated in this slide shows the high percentage of patients who were left disabled and therefore requiring long-term care or unable to work after a stroke. Almost three quarters of the patients suffered significant impairment.
References:
Hacke W, Kaste M, Bogousslavsky J, Brainin M, Chamorro A, Lees K, et al. European Stroke Initiative Recommendations 2003. Ischeamic Stroke. 2003:www.eusi-stroke.com/recommendations-2003/eusi.2003.pdf
Nazarko L. Rehabilitation and continence promotion following a stroke. Nurs Times 2003;99:52-55.
American Heart Association. Heart and stroke facts: statistical supplement. Dallas, Texas, 1996.
11. Stroke – aetiology Approximately 85% of strokes are ischaemic strokes. Ischaemic stroke can be caused by cerebrovascular disease, most commonly the thickening of atherosclerotic plaques and/or local increases in blood pressure. Plaque rupture and subsequent thrombosis in the carotid artery can also cause ischaemic stroke, as emboli may form which then travel directly to the brain and become lodged in one of the small blood vessels.
The less common form of stroke, haemorrhagic stroke, which accounts for the remaining 15% of cases, is caused by rupture of a blood vessel and subsequent bleeding in the brain. The most frequent causes of the rupture of blood vessels include hypertension, aneurysms and arteriovenous malformations.
Reference:
Cerebral Embolism Task Force. Cardiogenic brain embolism. Arch Neurol 1986;43:71-84.Approximately 85% of strokes are ischaemic strokes. Ischaemic stroke can be caused by cerebrovascular disease, most commonly the thickening of atherosclerotic plaques and/or local increases in blood pressure. Plaque rupture and subsequent thrombosis in the carotid artery can also cause ischaemic stroke, as emboli may form which then travel directly to the brain and become lodged in one of the small blood vessels.
The less common form of stroke, haemorrhagic stroke, which accounts for the remaining 15% of cases, is caused by rupture of a blood vessel and subsequent bleeding in the brain. The most frequent causes of the rupture of blood vessels include hypertension, aneurysms and arteriovenous malformations.
Reference:
Cerebral Embolism Task Force. Cardiogenic brain embolism. Arch Neurol 1986;43:71-84.
12. Stroke – aetiology Approximately 20% of ischaemic strokes are a result of emboli arising from intracardiac thrombosis, a process known as cardiogenic embolism.
References:
Cerebral Embolism Task Force. Cardiogenic brain embolism. Arch Neurol 1986;43:71-84.Approximately 20% of ischaemic strokes are a result of emboli arising from intracardiac thrombosis, a process known as cardiogenic embolism.
References:
Cerebral Embolism Task Force. Cardiogenic brain embolism. Arch Neurol 1986;43:71-84.
13. Stroke – aetiology Sources of cardiogenic emboli include myocardial infarction, ventricular dysfunction, narrowing (stenosis) of the mitral atrioventricular orifice and prosthetic valves. The most common cause of cardiogenic embolism, however, accounting for more than 40% of cases, is nonvalvular AF.
AF often coexists with other cardiac pathologies, therefore more than half the strokes of cardiac origin occur in patients with AF.
Reference:
Cerebral Embolism Task Force. Cardiogenic brain embolism. Arch Neurol 1986;43:71-84.Sources of cardiogenic emboli include myocardial infarction, ventricular dysfunction, narrowing (stenosis) of the mitral atrioventricular orifice and prosthetic valves. The most common cause of cardiogenic embolism, however, accounting for more than 40% of cases, is nonvalvular AF.
AF often coexists with other cardiac pathologies, therefore more than half the strokes of cardiac origin occur in patients with AF.
Reference:
Cerebral Embolism Task Force. Cardiogenic brain embolism. Arch Neurol 1986;43:71-84.
14. Atrial fibrillation – key risk factor for stroke Approximately 20% of ischaemic strokes are a result of emboli arising from intracardiac thrombosis, a process known as cardiogenic embolism. The most common cause of cardiogenic embolism is non-valvular AF.
AF often coexists with other cardiac pathologies, therefore more than half the strokes of cardiac origin occur in patients with AF.
Reference:
Cerebral Embolism Task Force. Cardiogenic brain embolism. Arch Neurol 1986;43:71-84.Approximately 20% of ischaemic strokes are a result of emboli arising from intracardiac thrombosis, a process known as cardiogenic embolism. The most common cause of cardiogenic embolism is non-valvular AF.
AF often coexists with other cardiac pathologies, therefore more than half the strokes of cardiac origin occur in patients with AF.
Reference:
Cerebral Embolism Task Force. Cardiogenic brain embolism. Arch Neurol 1986;43:71-84.
15. Stroke – risk factors Important stroke risk factors include age over 55 years, with risk incidence doubling every decade after 55 years.
Men have a 30% greater risk than women.
Ethnicity, probably through a combination of genetic and cultural factors, also plays a role with African Americans, Hispanics and Chinese at greatest risk.
Not suprisingly, genetic factors also play a significant role, probably affecting multiple risk factors for heart disease, atherosclerosis and many others.
Because most strokes in the older population are attributable to atherosclerosis and cardiac disease, many risk factors can be modified by medication and life-style alteration. These factors include cardiac disease, hypertension, hyperlipidaemia, cigarette smoking, diabetes mellitus, physical inactivity and drug abuse.Important stroke risk factors include age over 55 years, with risk incidence doubling every decade after 55 years.
Men have a 30% greater risk than women.
Ethnicity, probably through a combination of genetic and cultural factors, also plays a role with African Americans, Hispanics and Chinese at greatest risk.
Not suprisingly, genetic factors also play a significant role, probably affecting multiple risk factors for heart disease, atherosclerosis and many others.
Because most strokes in the older population are attributable to atherosclerosis and cardiac disease, many risk factors can be modified by medication and life-style alteration. These factors include cardiac disease, hypertension, hyperlipidaemia, cigarette smoking, diabetes mellitus, physical inactivity and drug abuse.
16. Well documented modifiable risk factors for stroke Because most strokes in the older population are attributable to atherosclerosis and cardiac disease, many risk factors can be modified by medication and life-style alteration. These factors include cardiac disease, hypertension, hyperlipidaemia, cigarette smoking, diabetes mellitus, physical inactivity and drug abuse.
Reference:
Goldstein LB, Adams R, Becker K, Furberg CD, Gorelick PB, Hademenos G, et al. Primary prevention of ischemic stroke: A statement for healthcare professionals from the Stroke Council of the American Heart Association. Circulation 2001:103:163-82.
Because most strokes in the older population are attributable to atherosclerosis and cardiac disease, many risk factors can be modified by medication and life-style alteration. These factors include cardiac disease, hypertension, hyperlipidaemia, cigarette smoking, diabetes mellitus, physical inactivity and drug abuse.
Reference:
Goldstein LB, Adams R, Becker K, Furberg CD, Gorelick PB, Hademenos G, et al. Primary prevention of ischemic stroke: A statement for healthcare professionals from the Stroke Council of the American Heart Association. Circulation 2001:103:163-82.
17. Ischaemic stroke Stroke or Cerebrovascular Accident (CVA) produces neurological symptoms such as limb weakness or loss of sensation that persist for more than 24 hours. The most common cause of stroke is thrombus formation in association with atherosclerosis of a carotid or cerebral artery, resulting in a reduction in blood supply to part of the brain (stroke of arterial origin). However, strokes may also be due to emboli travelling to the cerebral circulation from a thrombus in the heart or blood vessels outside the brain (thromboembolic stroke), as seen with atrial fibrillation (AF).
Emboli from the internal carotid artery may block smaller cerebral vessels temporarily, leading to a transient ischaemic attack (TIA). TIAs are episodes of neurological symptoms such as limb weakness or difficulty with speech, that may last only a matter of minutes and by definition resolve in less than 24 hours.
Stroke or Cerebrovascular Accident (CVA) produces neurological symptoms such as limb weakness or loss of sensation that persist for more than 24 hours. The most common cause of stroke is thrombus formation in association with atherosclerosis of a carotid or cerebral artery, resulting in a reduction in blood supply to part of the brain (stroke of arterial origin). However, strokes may also be due to emboli travelling to the cerebral circulation from a thrombus in the heart or blood vessels outside the brain (thromboembolic stroke), as seen with atrial fibrillation (AF).
Emboli from the internal carotid artery may block smaller cerebral vessels temporarily, leading to a transient ischaemic attack (TIA). TIAs are episodes of neurological symptoms such as limb weakness or difficulty with speech, that may last only a matter of minutes and by definition resolve in less than 24 hours.
18. Cerebral ischaemia Inadequate delivery of oxygen or glucose to the brain initiates a cascade of events that ultimately results in infarction.
Inadequate delivery of oxygen or glucose to the brain initiates a cascade of events that ultimately results in infarction.
19. Cerebral ischaemia The severity of the insult, defined by the degree and duration of reduced blood flow, hypoxia or hypoglycaemia, determines whether the brain has only temporary dysfunction, such as a transient ischaemic attack (TIA), irreversible injury to only a few of the most vulnerable neurons (selective necrosis), or cerebral infarction, in which damage occurs to extensive areas involving all cell types (pan-necrosis).
The severity of the insult, defined by the degree and duration of reduced blood flow, hypoxia or hypoglycaemia, determines whether the brain has only temporary dysfunction, such as a transient ischaemic attack (TIA), irreversible injury to only a few of the most vulnerable neurons (selective necrosis), or cerebral infarction, in which damage occurs to extensive areas involving all cell types (pan-necrosis).
20. Cerebral ischaemia Cerebral ischaemia sufficient to cause clinical signs or symptoms, if severe, can produce irreversible injury to highly vulnerable neurons in 5 minutes.
Cerebral ischaemia sufficient to cause clinical signs or symptoms, if severe, can produce irreversible injury to highly vulnerable neurons in 5 minutes.
21. Cerebral ischaemia Cerebral ischaemia sufficient to cause clinical signs or symptoms, if severe, can produce irreversible injury to highly vulnerable neurons in 5 minutes.
Cerebral ischaemia sufficient to cause clinical signs or symptoms, if severe, can produce irreversible injury to highly vulnerable neurons in 5 minutes.
22. Cerebral ischaemia Cerebral ischaemia sufficient to cause clinical signs or symptoms, if severe, can produce irreversible injury to highly vulnerable neurons in 5 minutes.
Progressively longer duration of ischaemia increases the probability of permanent damage. If cerebral ischaemia persists for more than about 6 hours, infarction of part or all of the involved vascular territory is completed and the only strategies for treatment entail rehabilitation.
Cerebral ischaemia sufficient to cause clinical signs or symptoms, if severe, can produce irreversible injury to highly vulnerable neurons in 5 minutes.
Progressively longer duration of ischaemia increases the probability of permanent damage. If cerebral ischaemia persists for more than about 6 hours, infarction of part or all of the involved vascular territory is completed and the only strategies for treatment entail rehabilitation.
23. Cerebral ischaemia Cerebral ischaemia sufficient to cause clinical signs or symptoms, if severe, can produce irreversible injury to highly vulnerable neurons in 5 minutes.
Progressively longer duration of ischaemia increases the probability of permanent damage. If cerebral ischaemia persists for more than about 6 hours, infarction of part or all of the involved vascular territory is completed and the only strategies for treatment entail rehabilitation.
Whether clinical evidence of permanent brain injury from ischaemia is detectable depends on the location of the brain tissue involved
Cerebral ischaemia sufficient to cause clinical signs or symptoms, if severe, can produce irreversible injury to highly vulnerable neurons in 5 minutes.
Progressively longer duration of ischaemia increases the probability of permanent damage. If cerebral ischaemia persists for more than about 6 hours, infarction of part or all of the involved vascular territory is completed and the only strategies for treatment entail rehabilitation.
Whether clinical evidence of permanent brain injury from ischaemia is detectable depends on the location of the brain tissue involved
24. Degree of neurologic injury Degree of neurologic injury as a function of the duration of ischaemia. Neuropathologic data from a primate model of cerebral ischaemia were used to generate this figure. Neurologic damage is the percentage of monkeys exhibiting infarcts of any size. CR = the maximum duration of ischaemia compatible with complete recovery; ET50 = the duration of ischaemia that results in half-maximal damage; NR = the minimum time for no recovery.
Reference:
Zivin JA: Factors determining the therapeutic window for stroke. Neurology 1998;50:599–603.
Degree of neurologic injury as a function of the duration of ischaemia. Neuropathologic data from a primate model of cerebral ischaemia were used to generate this figure. Neurologic damage is the percentage of monkeys exhibiting infarcts of any size. CR = the maximum duration of ischaemia compatible with complete recovery; ET50 = the duration of ischaemia that results in half-maximal damage; NR = the minimum time for no recovery.
Reference:
Zivin JA: Factors determining the therapeutic window for stroke. Neurology 1998;50:599–603.
25. Intracranial haemorrhage Bleeding into the subarachnoid space from a ruptured aneurysm or other vascular malformation produces a chemical (sterile) meningitis and can induce vasospasm, particularly in the vessels constituting of the circle of Willis. If the vasospasm is sufficiently severe it can result in cerebral infarction and death.
Intraparenchymal haemorrhage may be relatively benign. Bleeding into the region of previous infarction causes no additional functional loss.
Primary parenchymatous haemorrhage damages tissue in several ways, however. If a large vesssel ruptures, the amount of bleeding into the brain can be severe. The portion of the vascular distribution distal to the site of rupture is no longer supplied with blood, resulting in infarction. At the site of rupture, bleeding into the brain may cause traumatic injury to the exposed brain tissue, and blood or its breakdown products in the parenchyma damages brain tissues. Also the extravascular blood in the brain parenchyma increases total brain volume, and the oedema that rapidly forms in and around the site of bleeding increases the intracranial contents. Because the cranial capacity is fixed, intracranial pressure rapidly increases and cerebral herniation may occur. Bleeding into the subarachnoid space from a ruptured aneurysm or other vascular malformation produces a chemical (sterile) meningitis and can induce vasospasm, particularly in the vessels constituting of the circle of Willis. If the vasospasm is sufficiently severe it can result in cerebral infarction and death.
Intraparenchymal haemorrhage may be relatively benign. Bleeding into the region of previous infarction causes no additional functional loss.
Primary parenchymatous haemorrhage damages tissue in several ways, however. If a large vesssel ruptures, the amount of bleeding into the brain can be severe. The portion of the vascular distribution distal to the site of rupture is no longer supplied with blood, resulting in infarction. At the site of rupture, bleeding into the brain may cause traumatic injury to the exposed brain tissue, and blood or its breakdown products in the parenchyma damages brain tissues. Also the extravascular blood in the brain parenchyma increases total brain volume, and the oedema that rapidly forms in and around the site of bleeding increases the intracranial contents. Because the cranial capacity is fixed, intracranial pressure rapidly increases and cerebral herniation may occur.
26. Intracranial haemorrhage Bleeding into the subarachnoid space from a ruptured aneurysm or other vascular malformation produces a chemical (sterile) meningitis and can induce vasospasm, particularly in the vessels constituting of the circle of Willis. If the vasospasm is sufficiently severe it can result in cerebral infarction and death
Intraparenchymal haemorrhage may be relatively benign. Bleeding into the region of previous infarction causes no additional functional loss.
Primary parenchymatous haemorrhage damages tissue in several ways, however. If a large vesssel ruptures, the amount of bleeding into the brain can be severe. The portion of the vascular distribution distal to the site of rupture is no longer supplied with blood, resulting in infarction. At the site of rupture, bleeding into the brain may cause traumatic injury to the exposed brain tissue, and blood or its breakdown products in the parenchyma damages brain tissues. Also the extravascular blood in the brain parenchyma increases total brain volume, and the oedema that rapidly forms in and around the site of bleeding increases the intracranial contents. Because the cranial capacity is fixed, intracranial pressure rapidly increases and cerebral herniation may occur.
Bleeding into the subarachnoid space from a ruptured aneurysm or other vascular malformation produces a chemical (sterile) meningitis and can induce vasospasm, particularly in the vessels constituting of the circle of Willis. If the vasospasm is sufficiently severe it can result in cerebral infarction and death
Intraparenchymal haemorrhage may be relatively benign. Bleeding into the region of previous infarction causes no additional functional loss.
Primary parenchymatous haemorrhage damages tissue in several ways, however. If a large vesssel ruptures, the amount of bleeding into the brain can be severe. The portion of the vascular distribution distal to the site of rupture is no longer supplied with blood, resulting in infarction. At the site of rupture, bleeding into the brain may cause traumatic injury to the exposed brain tissue, and blood or its breakdown products in the parenchyma damages brain tissues. Also the extravascular blood in the brain parenchyma increases total brain volume, and the oedema that rapidly forms in and around the site of bleeding increases the intracranial contents. Because the cranial capacity is fixed, intracranial pressure rapidly increases and cerebral herniation may occur.
27. Intracranial haemorrhage Bleeding into the subarachnoid space from a ruptured aneurysm or other vascular malformation produces a chemical (sterile) meningitis and can induce vasospasm, particularly in the vessels constituting of the circle of Willis. If the vasospasm is sufficiently severe it can result in cerebral infarction and death
Intraparenchymal haemorrhage may be relatively benign. Bleeding into the region of previous infarction causes no additional functional loss.
Primary parenchymatous haemorrhage damages tissue in several ways, however. If a large vesssel ruptures, the amount of bleeding into the brain can be severe. The portion of the vascular distribution distal to the site of rupture is no longer supplied with blood, resulting in infarction. At the site of rupture, bleeding into the brain may cause traumatic injury to the exposed brain tissue, and blood or its breakdown products in the parenchyma damages brain tissues. Also the extravascular blood in the brain parenchyma increases total brain volume, and the oedema that rapidly forms in and around the site of bleeding increases the intracranial contents. Because the cranial capacity is fixed, intracranial pressure rapidly increases and cerebral herniation may occur.
Bleeding into the subarachnoid space from a ruptured aneurysm or other vascular malformation produces a chemical (sterile) meningitis and can induce vasospasm, particularly in the vessels constituting of the circle of Willis. If the vasospasm is sufficiently severe it can result in cerebral infarction and death
Intraparenchymal haemorrhage may be relatively benign. Bleeding into the region of previous infarction causes no additional functional loss.
Primary parenchymatous haemorrhage damages tissue in several ways, however. If a large vesssel ruptures, the amount of bleeding into the brain can be severe. The portion of the vascular distribution distal to the site of rupture is no longer supplied with blood, resulting in infarction. At the site of rupture, bleeding into the brain may cause traumatic injury to the exposed brain tissue, and blood or its breakdown products in the parenchyma damages brain tissues. Also the extravascular blood in the brain parenchyma increases total brain volume, and the oedema that rapidly forms in and around the site of bleeding increases the intracranial contents. Because the cranial capacity is fixed, intracranial pressure rapidly increases and cerebral herniation may occur.
28. Intracranial haemorrhage Bleeding into the subarachnoid space from a ruptured aneurysm or other vascular malformation produces a chemical (sterile) meningitis and can induce vasospasm, particularly in the vessels constituting of the circle of Willis. If the vasospasm is sufficiently severe it can result in cerebral infarction and death
Intraparenchymal haemorrhage may be relatively benign. Bleeding into the region of previous infarction causes no additional functional loss.
Primary parenchymatous haemorrhage damages tissue in several ways, however. If a large vesssel ruptures, the amount of bleeding into the brain can be severe. The portion of the vascular distribution distal to the site of rupture is no longer supplied with blood, resulting in infarction. At the site of rupture, bleeding into the brain may cause traumatic injury to the exposed brain tissue, and blood or its breakdown products in the parenchyma damages brain tissues. Also the extravascular blood in the brain parenchyma increases total brain volume, and the oedema that rapidly forms in and around the site of bleeding increases the intracranial contents. Because the cranial capacity is fixed, intracranial pressure rapidly increases and cerebral herniation may occur.
Bleeding into the subarachnoid space from a ruptured aneurysm or other vascular malformation produces a chemical (sterile) meningitis and can induce vasospasm, particularly in the vessels constituting of the circle of Willis. If the vasospasm is sufficiently severe it can result in cerebral infarction and death
Intraparenchymal haemorrhage may be relatively benign. Bleeding into the region of previous infarction causes no additional functional loss.
Primary parenchymatous haemorrhage damages tissue in several ways, however. If a large vesssel ruptures, the amount of bleeding into the brain can be severe. The portion of the vascular distribution distal to the site of rupture is no longer supplied with blood, resulting in infarction. At the site of rupture, bleeding into the brain may cause traumatic injury to the exposed brain tissue, and blood or its breakdown products in the parenchyma damages brain tissues. Also the extravascular blood in the brain parenchyma increases total brain volume, and the oedema that rapidly forms in and around the site of bleeding increases the intracranial contents. Because the cranial capacity is fixed, intracranial pressure rapidly increases and cerebral herniation may occur.
29. Intracranial haemorrhage Bleeding into the subarachnoid space from a ruptured aneurysm or other vascular malformation produces a chemical (sterile) meningitis and can induce vasospasm, particularly in the vessels constituting of the circle of Willis. If the vasospasm is sufficiently severe it can result in cerebral infarction and death
Intraparenchymal haemorrhage may be relatively benign. Bleeding into the region of previous infarction causes no additional functional loss.
Primary parenchymatous haemorrhage damages tissue in several ways, however. If a large vesssel ruptures, the amount of bleeding into the brain can be severe. The portion of the vascular distribution distal to the site of rupture is no longer supplied with blood, resulting in infarction. At the site of rupture, bleeding into the brain may cause traumatic injury to the exposed brain tissue, and blood or its breakdown products in the parenchyma damages brain tissues. Also the extravascular blood in the brain parenchyma increases total brain volume, and the oedema that rapidly forms in and around the site of bleeding increases the intracranial contents. Because the cranial capacity is fixed, intracranial pressure rapidly increases and cerebral herniation may occur.
Bleeding into the subarachnoid space from a ruptured aneurysm or other vascular malformation produces a chemical (sterile) meningitis and can induce vasospasm, particularly in the vessels constituting of the circle of Willis. If the vasospasm is sufficiently severe it can result in cerebral infarction and death
Intraparenchymal haemorrhage may be relatively benign. Bleeding into the region of previous infarction causes no additional functional loss.
Primary parenchymatous haemorrhage damages tissue in several ways, however. If a large vesssel ruptures, the amount of bleeding into the brain can be severe. The portion of the vascular distribution distal to the site of rupture is no longer supplied with blood, resulting in infarction. At the site of rupture, bleeding into the brain may cause traumatic injury to the exposed brain tissue, and blood or its breakdown products in the parenchyma damages brain tissues. Also the extravascular blood in the brain parenchyma increases total brain volume, and the oedema that rapidly forms in and around the site of bleeding increases the intracranial contents. Because the cranial capacity is fixed, intracranial pressure rapidly increases and cerebral herniation may occur.
30. Intracranial haemorrhage Bleeding into the subarachnoid space from a ruptured aneurysm or other vascular malformation produces a chemical (sterile) meningitis and can induce vasospasm, particularly in the vessels constituting of the circle of Willis. If the vasospasm is sufficiently severe it can result in cerebral infarction and death
Intraparenchymal haemorrhage may be relatively benign. Bleeding into the region of previous infarction causes no additional functional loss.
Primary parenchymatous haemorrhage damages tissue in several ways, however. If a large vesssel ruptures, the amount of bleeding into the brain can be severe. The portion of the vascular distribution distal to the site of rupture is no longer supplied with blood, resulting in infarction. At the site of rupture, bleeding into the brain may cause traumatic injury to the exposed brain tissue, and blood or its breakdown products in the parenchyma damages brain tissues. Also the extravascular blood in the brain parenchyma increases total brain volume, and the oedema that rapidly forms in and around the site of bleeding increases the intracranial contents. Because the cranial capacity is fixed, intracranial pressure rapidly increases and cerebral herniation may occur.
Bleeding into the subarachnoid space from a ruptured aneurysm or other vascular malformation produces a chemical (sterile) meningitis and can induce vasospasm, particularly in the vessels constituting of the circle of Willis. If the vasospasm is sufficiently severe it can result in cerebral infarction and death
Intraparenchymal haemorrhage may be relatively benign. Bleeding into the region of previous infarction causes no additional functional loss.
Primary parenchymatous haemorrhage damages tissue in several ways, however. If a large vesssel ruptures, the amount of bleeding into the brain can be severe. The portion of the vascular distribution distal to the site of rupture is no longer supplied with blood, resulting in infarction. At the site of rupture, bleeding into the brain may cause traumatic injury to the exposed brain tissue, and blood or its breakdown products in the parenchyma damages brain tissues. Also the extravascular blood in the brain parenchyma increases total brain volume, and the oedema that rapidly forms in and around the site of bleeding increases the intracranial contents. Because the cranial capacity is fixed, intracranial pressure rapidly increases and cerebral herniation may occur.
31. Intracranial haemorrhage Bleeding into the subarachnoid space from a ruptured aneurysm or other vascular malformation produces a chemical (sterile) meningitis and can induce vasospasm, particularly in the vessels constituting of the circle of Willis. If the vasospasm is sufficiently severe it can result in cerebral infarction and death
Intraparenchymal haemorrhage may be relatively benign. Bleeding into the region of previous infarction causes no additional functional loss.
Primary parenchymatous haemorrhage damages tissue in several ways, however. If a large vesssel ruptures, the amount of bleeding into the brain can be severe. The portion of the vascular distribution distal to the site of rupture is no longer supplied with blood, resulting in infarction. At the site of rupture, bleeding into the brain may cause traumatic injury to the exposed brain tissue, and blood or its breakdown products in the parenchyma damages brain tissues. Also the extravascular blood in the brain parenchyma increases total brain volume, and the oedema that rapidly forms in and around the site of bleeding increases the intracranial contents. Because the cranial capacity is fixed, intracranial pressure rapidly increases and cerebral herniation may occur.
Bleeding into the subarachnoid space from a ruptured aneurysm or other vascular malformation produces a chemical (sterile) meningitis and can induce vasospasm, particularly in the vessels constituting of the circle of Willis. If the vasospasm is sufficiently severe it can result in cerebral infarction and death
Intraparenchymal haemorrhage may be relatively benign. Bleeding into the region of previous infarction causes no additional functional loss.
Primary parenchymatous haemorrhage damages tissue in several ways, however. If a large vesssel ruptures, the amount of bleeding into the brain can be severe. The portion of the vascular distribution distal to the site of rupture is no longer supplied with blood, resulting in infarction. At the site of rupture, bleeding into the brain may cause traumatic injury to the exposed brain tissue, and blood or its breakdown products in the parenchyma damages brain tissues. Also the extravascular blood in the brain parenchyma increases total brain volume, and the oedema that rapidly forms in and around the site of bleeding increases the intracranial contents. Because the cranial capacity is fixed, intracranial pressure rapidly increases and cerebral herniation may occur.
32. Stroke – cerebrovascular accident (CVA) Stroke, or cerebrovascular accident (CVA), produces neurological symptoms such as limb weakness or loss of sensation that persist for more than 24 hours.
The principal consequence of stroke is the death of brain cells and therefore impaired function in one area of the brain.
In severe cases stroke leads to permanent disability or death.
Additional consequences of stroke, wich increase the risk of death and delay rehabilitation, include falls, pressure sores, urinary tract infections, chest infections, epileptic seizures and venous thromboembolism (VTE).
Stroke, or cerebrovascular accident (CVA), produces neurological symptoms such as limb weakness or loss of sensation that persist for more than 24 hours.
The principal consequence of stroke is the death of brain cells and therefore impaired function in one area of the brain.
In severe cases stroke leads to permanent disability or death.
Additional consequences of stroke, wich increase the risk of death and delay rehabilitation, include falls, pressure sores, urinary tract infections, chest infections, epileptic seizures and venous thromboembolism (VTE).
33. Functional impact of stroke Of strokes occurring in patients with AF, nearly three quarters are either fatal or leave patients with significant impairment.
This pie chart does not illustrate or account for silent stroke that may take a toll on cognitive function (eg, multi-infarct dementia) in elderly patients with AF.
NB. The numbers in the pie chart do not add up to 100% because one case was lost to follow-up.
Reference:
Fisher CM. Reducing risks of cerebral embolism. Geriatrics 1979;34:59-61.Of strokes occurring in patients with AF, nearly three quarters are either fatal or leave patients with significant impairment.
This pie chart does not illustrate or account for silent stroke that may take a toll on cognitive function (eg, multi-infarct dementia) in elderly patients with AF.
NB. The numbers in the pie chart do not add up to 100% because one case was lost to follow-up.
Reference:
Fisher CM. Reducing risks of cerebral embolism. Geriatrics 1979;34:59-61.
34. AF-related stroke In patients with AF, there is a greater risk of stroke being fatal or leaving the patient with a long-term disability compared with patients without AF, resulting in:
increased duration of hospital stay and need for long-term institutional care
greater family, social and financial burden of stroke As illustrated previously, AF-related stroke is associated with a greater rate of mortality, morbidity and long-term disability than stroke in patients without AF.
Higher rates of morbidity and long-term disability result in an increase in demands for costly, long-term care.
AF-related stroke therefore imposes a significantly greater family, social and economic burden compared with stroke in patients without AF. Thus, the need for effective prophylactic therapy is particularly high in patients with AF.As illustrated previously, AF-related stroke is associated with a greater rate of mortality, morbidity and long-term disability than stroke in patients without AF.
Higher rates of morbidity and long-term disability result in an increase in demands for costly, long-term care.
AF-related stroke therefore imposes a significantly greater family, social and economic burden compared with stroke in patients without AF. Thus, the need for effective prophylactic therapy is particularly high in patients with AF.
35. Permanent neurological deficits of stroke Weakness or paralysis
Loss of sensation
Problems with vision
Difficulty in speech comprehension / talking
Difficulty with organization or perception
Clumsiness or lack of balance
36. What stroke can mean for patients Sudden numbness or weakness of the face, arm or leg, especially on one side of the body
Sudden confusion, trouble speaking or understanding speech
Sudden trouble seeing, on one or both eyes
Sudden trouble walking, dizziness, loss of balance or co-ordination
Sudden severe headache with no known cause
37. What stroke can mean for family and carers
Recovery from stroke is seldom complete and it is estimated that 40% of patients living at home after stroke need help in daily living.
Four out of five patients survive a stroke, ten years later the patient has only a 50% chance of still being alive.
38. Stroke – diagnosis Symptoms of stroke vary with the area of the brain affected. Common symptoms include weakness and sensory loss down one side of the body, disturbances of consciousness and confusion, and impairment of speech, vision and co-ordination of movement.
Symptoms of stroke vary with the area of the brain affected. Common symptoms include weakness and sensory loss down one side of the body, disturbances of consciousness and confusion, and impairment of speech, vision and co-ordination of movement.
39. Computed tomography (CT) and magnetic resonance imaging (MRI) Numerous tests, are available that allow the generation of images of the brain and measurements of the electrical activity and blood flow within the brain. Computerised axial tomographic (CT) scanning and magnetic resonance imaging (MRI) are the most widely used techniques, as they are well established and non-invasive.
Numerous tests, are available that allow the generation of images of the brain and measurements of the electrical activity and blood flow within the brain. Computerised axial tomographic (CT) scanning and magnetic resonance imaging (MRI) are the most widely used techniques, as they are well established and non-invasive.
40. Computed tomography (CT) and magnetic resonance imaging (MRI) In both CT and MRI, patients lie on a narrow table that slides into a tunnel where images are taken in two-dimensional slices, which are sometimes reconstructed into three-dimensional images of the brain or cerebral blood vessels.
In both CT and MRI, patients lie on a narrow table that slides into a tunnel where images are taken in two-dimensional slices, which are sometimes reconstructed into three-dimensional images of the brain or cerebral blood vessels.
41. Computed tomography (CT) CT technology relies on the differential absorption of x-ray beams by different tissues. CT scans take less time, are less expensive, and are more readily available in emergency rooms. However, if done too early in the stroke, most CT scans will not detect signs of ischaemia.
The photons that pass through the patient are registered for imaging. Brain tissue tends to appear relatively dark on CT scans, with the white matter brighter than the grey matter. Blood products are easily detected on CT scans. In fact, a CT scan can identify almost all brain haemorrhages larger than 1 cm in diameter. CT scans can also demonstrate hydrocephalus and provide evidence of brain oedema and herniation.
CT technology relies on the differential absorption of x-ray beams by different tissues. CT scans take less time, are less expensive, and are more readily available in emergency rooms. However, if done too early in the stroke, most CT scans will not detect signs of ischaemia.
The photons that pass through the patient are registered for imaging. Brain tissue tends to appear relatively dark on CT scans, with the white matter brighter than the grey matter. Blood products are easily detected on CT scans. In fact, a CT scan can identify almost all brain haemorrhages larger than 1 cm in diameter. CT scans can also demonstrate hydrocephalus and provide evidence of brain oedema and herniation.
42. Magnetic resonance imaging (MRI) Magnetic resonance imaging (MRI) is a high-resolution neural imaging technique. MRI is possible due to the microscopic magnetic fields of the water molecules in the human body. The protons in the water molecules can be magnetised and then returned to the equilibrium states in two relaxation times, T1 and T2. Different parts of the brain (e.g. grey matter, white matter, cerebral spinal fluid, blood vessels) have different signal intensities on T1- or T2-weighted images.
Magnetic resonance imaging (MRI) is a high-resolution neural imaging technique. MRI is possible due to the microscopic magnetic fields of the water molecules in the human body. The protons in the water molecules can be magnetised and then returned to the equilibrium states in two relaxation times, T1 and T2. Different parts of the brain (e.g. grey matter, white matter, cerebral spinal fluid, blood vessels) have different signal intensities on T1- or T2-weighted images.
43. Diffusion-weighted imaging (DWI) MRI Diffusion-weighted imaging (DWI) MRI is the best way to image acute stroke. It uses a rapid pulse sequence with an average total imaging time of less than 2 minutes. Ischaemia may be visualised on the DWI MRI scans as early as within 30 minutes of stroke. DWI MRI can also distinguish between new and old strokes.
Diffusion-weighted imaging (DWI) MRI is the best way to image acute stroke. It uses a rapid pulse sequence with an average total imaging time of less than 2 minutes. Ischaemia may be visualised on the DWI MRI scans as early as within 30 minutes of stroke. DWI MRI can also distinguish between new and old strokes.
44. Diffusion-weighted imaging (DWI) MRI Diffusion-weighted imaging (DWI) MRI is the best way to image acute stroke. It uses a rapid pulse sequence with an average total imaging time of less than 2 minutes. Ischaemia may be visualised on the DWI MRI scans as early as within 30 minutes of stroke. DWI MRI can also distinguish between new and old strokes.
DWI MRI relies on a reduction in the random diffusion or Brownian motion of water after acute stroke. In the ischaemic region, the cells are swollen (cytotoxic oedema) due to the failure of the sodium-potassium pump. The swollen cells and the reduced extracellular space lead to a decrease in the diffusion of water molecules in the extracellular space, or a reduced diffusion coefficient.
Diffusion-weighted imaging (DWI) MRI is the best way to image acute stroke. It uses a rapid pulse sequence with an average total imaging time of less than 2 minutes. Ischaemia may be visualised on the DWI MRI scans as early as within 30 minutes of stroke. DWI MRI can also distinguish between new and old strokes.
DWI MRI relies on a reduction in the random diffusion or Brownian motion of water after acute stroke. In the ischaemic region, the cells are swollen (cytotoxic oedema) due to the failure of the sodium-potassium pump. The swollen cells and the reduced extracellular space lead to a decrease in the diffusion of water molecules in the extracellular space, or a reduced diffusion coefficient.
45. Computed tomography (CT) scan A: Computed tomography (CT) scan of a patient with a left hemisphere infarction 6 to 24 hours after symptom onset shows hypodensity in the basal ganglia region and compression of the frontal horn of the lateral ventricle.
B: CT scan shows the chronic infarction 1 year later; atrophy and loss of tissue volume are visible.
A: Computed tomography (CT) scan of a patient with a left hemisphere infarction 6 to 24 hours after symptom onset shows hypodensity in the basal ganglia region and compression of the frontal horn of the lateral ventricle.
B: CT scan shows the chronic infarction 1 year later; atrophy and loss of tissue volume are visible.
46. Computed tomography (CT) scan A CT-scan (computed tomography) of the head can confirm:
whether or not a stroke has occurred,
the nature of the stroke (ischaemic or haemorrhagic), and
the extent of damage to the brain.
A CT-scan (computed tomography) of the head can confirm:
whether or not a stroke has occurred,
the nature of the stroke (ischaemic or haemorrhagic), and
the extent of damage to the brain.
47. Magnetic resonance imaging (MRI) Magnetic resonance imaging (MRI) shows early ischaemic changes obtained 6 hours after the onset of right-sided weakness in a patient with an occluded left internal carotid artery.
Magnetic resonance imaging (MRI) shows early ischaemic changes obtained 6 hours after the onset of right-sided weakness in a patient with an occluded left internal carotid artery.
48. Diffusion-weighted imaging (DWI) MRI Magnetic resonance imaging (MRI) scans showing possible advantages of diffusion-weighted imaging (DWI) MRI relative to conventional MRI at early times after vascular occlusion.
Top: conventional T2-weighted MRI 4 hours after symptom onset that appears normal.
Middle: at the same time, a DWI scan shows abnormalities in the left hemisphere.
Bottom: repeat T2-weighted MRI 1 month later showed an infarction in the same location as the initial DWI scan.
Magnetic resonance imaging (MRI) scans showing possible advantages of diffusion-weighted imaging (DWI) MRI relative to conventional MRI at early times after vascular occlusion.
Top: conventional T2-weighted MRI 4 hours after symptom onset that appears normal.
Middle: at the same time, a DWI scan shows abnormalities in the left hemisphere.
Bottom: repeat T2-weighted MRI 1 month later showed an infarction in the same location as the initial DWI scan.
49. Ischaemic damage Ischaemic damage depends on the duration and degree of cerebral blood flow impairment, or hypoperfusion. Timely diagnosis and treatment are absolutely critical. Ideally, treatment would begin in the ambulance as the patient is transported to the hospital.
The first goal of acute ischaemic stroke treatment is to restore blood flow by dissolving the clot. In ischaemic strokes, the clot can be dissolved by interfering with different steps of the coagulation pathway.
Cerebral infarction evolves rapidly over the first few hours of ischaemic insult, and to be effective therapies must be delivered within the logistically restrictive window in order to optimise the prospects for favourable outcomes. Ischaemic damage depends on the duration and degree of cerebral blood flow impairment, or hypoperfusion. Timely diagnosis and treatment are absolutely critical. Ideally, treatment would begin in the ambulance as the patient is transported to the hospital.
The first goal of acute ischaemic stroke treatment is to restore blood flow by dissolving the clot. In ischaemic strokes, the clot can be dissolved by interfering with different steps of the coagulation pathway.
Cerebral infarction evolves rapidly over the first few hours of ischaemic insult, and to be effective therapies must be delivered within the logistically restrictive window in order to optimise the prospects for favourable outcomes.
50. Ischaemic stroke – prevention and treatment The first goal is to restore blood flow (thrombolysis)
Prophylaxis of subsequent ischaemic strokes with antiplatelets such as acetylsalicylic acid
51. Thrombolytics (t-PA) Drugs that dissolve the fibrin clots, called thrombolytics or fibrinolytics are the indicated acute therapy for stroke.
When given intravenously within three hours of the start of stroke symptoms, recombinant tissue plasminogen activator (t-PA) is clearly effective as it reduces progression of the ischaemic lesion and thus improves the functional outcome. Thrombolytic therapy with t-PA should not be initiated more than 3 hours after onset of symptoms of stroke because effectiveness diminishes after that time. Thrombolytic therapy is associated with a significant risk of bleeding, particularly after more than three hours after onset of ischaemic stroke, when conversion to haemorrhagic infarction (that is bleeding into an infarct) is feared. Drugs that dissolve the fibrin clots, called thrombolytics or fibrinolytics are the indicated acute therapy for stroke.
When given intravenously within three hours of the start of stroke symptoms, recombinant tissue plasminogen activator (t-PA) is clearly effective as it reduces progression of the ischaemic lesion and thus improves the functional outcome. Thrombolytic therapy with t-PA should not be initiated more than 3 hours after onset of symptoms of stroke because effectiveness diminishes after that time. Thrombolytic therapy is associated with a significant risk of bleeding, particularly after more than three hours after onset of ischaemic stroke, when conversion to haemorrhagic infarction (that is bleeding into an infarct) is feared.
52. Antiplatelets Because of the increased bleeding risk in patients treated with early thrombolysis, prophylaxis of subsequent ischaemic strokes with antiplatelets such as acetylsalicylic acid (ASA), also called secondary prevention, should be started not earlier than 24 hours after thrombolysis.
In patients who do not merit or qualify for aggressive acute thrombolytic treatment, antiplatelet therapy with ASA is warranted. ASA reduces the risk of new thrombosis and infarction by acting on platelets to reduce their activation, adhesion and aggregation at sites of vascular injury. ASA should be started within 48 hours of stroke onset, and may be used safely in combination with low doses of subcutaneous heparin for DVT prophylaxis.
For patients who have experienced their first stroke, the appropriate antiplatelet agent for secondary prevention is ASA. Starting ASA within 48 hours of ischaemic stroke onset has a small benefit without increasing the risk for intracerebral haemorrhage. In patients with a contraindication for ASA, dypiridamole or clopidogrel can be used. Also in patients who have recurrent stroke while taking ASA, clopidogrel or a dipyridamole/ASA combination can be considered.
Because of the increased bleeding risk in patients treated with early thrombolysis, prophylaxis of subsequent ischaemic strokes with antiplatelets such as acetylsalicylic acid (ASA), also called secondary prevention, should be started not earlier than 24 hours after thrombolysis.
In patients who do not merit or qualify for aggressive acute thrombolytic treatment, antiplatelet therapy with ASA is warranted. ASA reduces the risk of new thrombosis and infarction by acting on platelets to reduce their activation, adhesion and aggregation at sites of vascular injury. ASA should be started within 48 hours of stroke onset, and may be used safely in combination with low doses of subcutaneous heparin for DVT prophylaxis.
For patients who have experienced their first stroke, the appropriate antiplatelet agent for secondary prevention is ASA. Starting ASA within 48 hours of ischaemic stroke onset has a small benefit without increasing the risk for intracerebral haemorrhage. In patients with a contraindication for ASA, dypiridamole or clopidogrel can be used. Also in patients who have recurrent stroke while taking ASA, clopidogrel or a dipyridamole/ASA combination can be considered.
53. Neuroprotective therapy Neuroprotective therapies are currently under development to save the penumbra (the area surrounding the core of the primary ischaemia) from the damage caused by reduced blood flow to this region. Neuroprotective therapies are currently under development to save the penumbra (the area surrounding the core of the primary ischaemia) from the damage caused by reduced blood flow to this region.
