Stroke: Wikis
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A stroke (sometimes called a cerebrovascular accident (CVA)) is the rapidly developing loss of
function(s) due to disturbance in the
to the brain, caused by a blocked or burst blood vessel. This can be due to
(lack of glucose and oxygen supply) caused by
or due to a . As a result, the affected area of the brain is unable to function, leading to , inability to
speech, or inability to .
A stroke is a
and can cause permanent
damage, complications, and death. It is the leading cause of adult disability in the United States and Europe. It is the number two cause of death worldwide and may soon become the leading cause of death worldwide.
for stroke include ,
(high blood pressure), previous stroke or
(TIA), , ,
and . High blood pressure is the most important modifiable
of stroke.
A stroke is occasionally treated with
("clot buster"), but usually with supportive care (,
and ) in a "stroke unit" and secondary prevention with
drugs ( and often ), blood pressure control, , and in selected patients with
The traditional definition of stroke, devised by the
in the 1970s, is a "neurological deficit of cerebrovascular cause that persists beyond 24 hours or is interrupted by death within 24 hours". This definition was supposed to reflect the reversibility of tissue damage and was devised for the purpose, with the time frame of 24 hours being chosen arbitrarily. The 24-hour limit divides stroke from , which is a related syndrome of stroke symptoms that resolve completely within 24 hours. With the availability of treatments that, when given early, can reduce stroke severity, many now prefer alternative concepts, such as brain attack and acute ischemic cerebrovascular syndrome (modeled after
respectively), that reflect the urgency of stroke symptoms and the need to act swiftly.
A slice of brain from the autopsy of a person who suffered an acute
Strokes can be classified into two major categories: ischemic and hemorrhagic. Ischemic strokes are those that are due to interruption of the blood supply, while hemorrhagic strokes are the ones which are due to rupture of a
or an abnormal vascular structure. 80% of strokes the remainder are due to hemorrhage. Some hemorrhages develop inside areas of ischemia ("hemorrhagic transformation"). It is unknown how many hemorrhages actually start off as ischemic stroke.
Main articles:
In an ischemic stroke, blood supply to part of the brain is decreased, leading to dysfunction of the brain tissue in that area. There are four reasons why this might happen:
1. Thrombosis (obstruction of a blood vessel by a blood clot forming locally)
2. Embolism (obstruction due to an embolus from elsewhere in the body, see below),
3. Systemic hypoperfusion (general decrease in blood supply, e.g. in )
Stroke without an obvious explanation is termed "cryptogenic" (of unknown origin); this constitutes 30-40% of all ischemic strokes.
There are various classification systems for acute ischemic stroke. The Oxford Community Stroke Project classification (OCSP, also known as the Bamford or Oxford classification) relies primarily on
based on the extent of the symptoms, the stroke episode is classified as
(POCI). These four entities predict the extent of the stroke, the area of the brain affected, the underlying cause, and the prognosis. The TOAST (Trial of
in Acute Stroke Treatment) classification is based on clinical symptoms as well as results of fu on this basis, a stroke is classified as being due to (1) thrombosis or embolism due to
of a large artery, (2) embolism of
origin, (3) occlusion of a small blood vessel, (4) other determined cause, (5) undetermined cause (two possible causes, no cause identified, or incomplete investigation).
Main articles:
CT scan showing an intracerebral hemorrhage with associated intraventricular hemorrhage.
Intracranial hemorrhage is the accumulation of blood anywhere within the skull vault. A distinction is made between
(blood inside the brain) and
(blood inside the skull but outside the brain). Intra-axial hemorrhage is due to
(blood in the ventricular system). The main types of extra-axial hemorrhage are
(bleeding between the
and the skull),
(in the ) and
(between the
and ). Most of the hemorrhagic stroke syndromes have specific symptoms (e.g. , previous ).
(ICH) is bleeding directly into the brain tissue, forming a gradually enlarging
(pooling of blood).[citation needed]
Stroke symptoms typically start suddenly, over seconds to minutes, and in most cases do not progress further. The symptoms depend on the area of the brain affected. The more extensive the area of brain affected, the more functions that are likely to be lost. Some forms of stroke can cause additional symptoms: in intracranial hemorrhage, the affected area may compress other structures. Most forms of stroke are not associated with , apart from subarachnoid hemorrhage and cerebral venous thrombosis and occasionally intracerebral hemorrhage.
Various systems have been proposed to increase recognition of stroke by patients, relatives and emergency first responders. A , updating a previous systematic review from 1994, looked at a number of trials to evaluate how well different
findings are able to predict the presence or absence of stroke. It was found that sudden-onset face weakness, arm drift (e.g. if a person, when asked to raise both arms, involuntarily lets one arm drift downward) and abnormal speech are the findings most likely to lead to the correct identification of a case of stroke (+
of 5.5 when at least one of these is present). Similarly, when all three of these are absent, the likelihood of stroke is significantly decreased (–
of 0.39). While these findings are not perfect for diagnosing stroke, the fact that they can be evaluated relatively rapidly and easily make them very valuable in the acute setting.
Proposed systems include FAST (face, arm, speech, and time), as advocated by the
and , the Los Angeles Prehospital Stroke Screen (LAPSS) and the
(CPSS). Use of these scales is recommended by professional guidelines.
For people referred to the , early recognition of stroke is deemed important as this can expedite diagnostic tests and treatments. A scoring system called ROSIER (recognition of stroke in the emergency room) is recommen it is based on features from the medical history and physical examination.
If the area of the brain affected contains one of the three prominent —the , , and
(), symptoms may include:
reduction in sensory or vibratory sensation
In most cases, the symptoms affect only one side of the body (). The defect in the brain is usually on the opposite side of the body (depending on which part of the brain is affected). However, the presence of any one of these symptoms does not necessarily suggest a stroke, since these pathways also travel in the
and any lesion there can also produce these symptoms.
In addition to the above CNS pathways, the
also consists of the 12 . A stroke affecting the brain stem therefore can produce symptoms relating to deficits in these cranial nerves:
altered smell, taste, hearing, or vision (total or partial)
drooping of eyelid () and weakness of
decreased reflexes: gag, swallow, pupil reactivity to light
decreased sensation and muscle weakness of the face
altered breathing and heart rate
weakness in
with inability to turn head to one side
weakness in tongue (inability to protrude and/or move from side to side)
is involved, the CNS pathways can again be affected, but also can produce the following symptoms:
(inability to speak or understand language from involvement of
(altered voluntary movements)
memory deficits (involvement of )
(involvement of )
disorganized thinking, confusion,
gestures (with involvement of frontal lobe)
anosognosia (persistent denial of the existence of a, usually stroke-related, deficit)
is involved, the patient may have the following:
trouble walking
altered movement coordination
and or disequilibrium
, headache, and vomiting usually occurs more often in hemorrhagic stroke than in thrombosis because of the increased intracranial pressure from the leaking blood compressing on the brain.
If symptoms are maximal at onset, the cause is more likely to be a subarachnoid hemorrhage or an embolic stroke.
Thrombotic stroke
In thrombotic stroke a thrombus (blood clot) usually forms around
plaques. Since blockage of the artery is gradual, onset of symptomatic thrombotic strokes is slower. A thrombus itself (even if non-occluding) can lead to an embolic stroke (see below) if the thrombus breaks off, at which point it is called an "embolus." Two types of thrombosis can cause stroke:
Large vessel disease involves the common and , , and the . Diseases that may form thrombi in the large vessels include (in descending incidence): atherosclerosis,
(tightening of the artery), ,
or , various inflammatory diseases of the blood vessel wall (, , ), noninflammatory vasculopathy,
Small vessel disease involves the smaller arteries inside the brain: branches of the , middle cerebral artery, stem, and arteries arising from the distal vertebral and . Diseases that may form thrombi in the small vessels include (in descending incidence):
(build-up of fatty hyaline matter in the blood vessel as a result of high blood pressure and aging) and fibrinoid degeneration (stroke involving these vessels are known as ) and microatheroma (small atherosclerotic plaques).
, which can cause
to clump up and block blood vessels, can also lead to stroke. A stroke is the second leading killer of people under 20 who suffer from sickle-cell anemia.
Embolic stroke
An embolic stroke refers to the blockage of an artery by an , a travelling particle or debris in the arterial bloodstream originating from elsewhere. An embolus is most frequently a thrombus, but it can also be a number of other substances including
(e.g. from
in a ), air,
cells or clumps of
(usually from infectious ).
Because an embolus arises from elsewhere, local therapy only solves the problem temporarily. Thus, the source of the embolus must be identified. Because the embolic blockage is sudden in onset, symptoms usually are maximal at start. Also, symptoms may be transient as the embolus is partially resorbed and moves to a different location or dissipates altogether.
Emboli most commonly arise from the
(especially in ) but may originate from elsewhere in the arterial tree. In , a
embolises through an
in the heart into the brain.
Cardiac causes can be distinguished between high and low-risk:
High risk: atrial fibrillation and ,
disease, , known cardiac thrombus of the atrium or vertricle, , sustained , recent myocardial infarction, chronic myocardial infarction together with
&28 percent, symptomatic
with ejection fraction &30 percent, , , , , ,
(CABG) surgery
Low risk/potential: calcification of the annulus (ring) of the mitral valve, patent foramen ovale (PFO), atrial septal aneurysm, atrial septal aneurysm with patent foramen ovale, left ventricular aneurysm without thrombus, isolated left atrial "smoke" on
or atrial fibrillation), complex atheroma in the
or proximal arch
Systemic hypoperfusion
Systemic hypoperfusion is the reduction of blood flow to all parts of the body. It is most commonly due to
failure from
or arrhythmias, or from reduced
as a result of myocardial infarction, , , or bleeding.
(low blood oxygen content) may precipitate the hypoperfusion. Because the reduction in blood flow is global, all parts of the brain may be affected, especially "watershed" areas - border zone regions supplied by the major cerebral arteries. Blood flow to these areas does not necessarily stop, but instead it may lessen to the point where brain damage can occur. This phenomenon is also referred to as "last meadow" to point to the fact that in irrigation the last meadow receives the least amount of water.
Venous thrombosis
leads to stroke due to locally increased venous pressure, which exceeds the pressure generated by the arteries. Infarcts are more likely to undergo hemorrhagic transformation (leaking of blood into the damaged area) than other types of ischemic stroke.
Intracerebral hemorrhage
It generally occurs in small arteries or arterioles and is commonly due to hypertension, intracranial vascular malformations (including
or ), cerebral , or infarcts into which secondary haemorrhage has occurred. Other potential causes are trauma, , ,
(e.g. amphetamines or ). The hematoma enlarges until pressure from surrounding tissue limits its growth, or until it decompresses by emptying into the ,
or the pial surface. A third of intracerebral bleed is into the brain's ventricles. ICH has a
of 44 percent after 30 days, higher than ischemic stroke or even the very deadly subarachnoid hemorrhage (which, however, also may be classified as a type of stroke).
Ischemic stroke occurs due to a loss of blood supply to part of the brain, initiating the . Brain tissue ceases to function if deprived of oxygen for more than 60 to 90 seconds and after approximately three hours, will suffer irreversible injury possibly leading to death of the tissue, i.e., . (This is why TPA's (e.g. , Altapase) are given only until three hours since the onset of the stroke.) Atherosclerosis may disrupt the blood supply by narrowing the lumen of blood vessels leading to a reduction of blood flow, by causing the formation of blood clots within the vessel, or by releasing showers of small
through the disintegration of atherosclerotic plaques. Embolic infarction occurs when emboli formed elsewhere in the circulatory system, typically in the heart as a consequence of atrial fibrillation, or in the carotid arteries. These break off, enter the cerebral circulation, then lodge in and occlude brain blood vessels. Since blood vessels in the brain are now occluded, the brain becomes low in energy, and thus it resorts into using
within the region of brain tissue affected by ischemia. Unfortunately, this kind of respiration produces less ATP but releases a by-product called . Lactic acid is an irritant which could potentially destroy cells since it is an acid and disrupts the normal acid-bace balance in the brain. The ischemia area is referred to as the "ischemic ".
Then, as oxygen or glucose becomes depleted in ischemic brain tissue, the production of
compounds such as adenosine triphosphate (ATP) fails, leading to failure of energy-dependent processes (such as ion pumping) necessary for tissue cell survival. This sets off a series of interrelated events that result in cellular injury and death. A major cause of neuronal injury is release of the excitatory neurotransmitter glutamate. The concentration of glutamate outside the cells of the nervous system is normally kept low by so-called uptake carriers, which are powered by the concentration gradients of ions (mainly Na+) across the cell membrane. However, stroke cuts off the supply of oxygen and glucose which powers the ion pumps maintaining these gradients. As a result the transmembrane ion gradients run down, and glutamate transporters reverse their direction, releasing glutamate into the extracellular space. Glutamate acts on receptors in nerve cells (especially NMDA receptors), producing an influx of calcium which activates enzymes that digest the cells' proteins, lipids and nuclear material. Calcium influx can also lead to the failure of , which can lead further toward energy depletion and may trigger cell death due to apoptosis.
Ischemia also induces production of
and other . These react with and damage a number of cellular and extracellular elements. Damage to the blood vessel lining or endothelium is particularly important. In fact, many antioxidant neuroprotectants such as
work at the level of the endothelium and not in the brain per se. Free radicals also directly initiate elements of the apoptosis cascade by means of .
These processes are the same for any type of ischemic tissue and are referred to collectively as the ischemic cascade. However, brain tissue is especially vulnerable to ischemia since it has little respiratory reserve and is completely dependent on , unlike most other organs.
Brain tissue survival can be improved to some extent if one or more of these processes is inhibited. Drugs that scavenge , inhibit , or inhibit excitotoxic neurotransmitters, for example, have been shown experimentally to reduce tissue injury due to ischemia. Agents that work in this way are referred to as being neuroprotective. Until recently, human
with neuroprotective agents have failed, with the probable exception of deep . However, more recently NXY-059, the disulfonyl derivative of the radical-scavenging spintrap phenylbutylnitrone, is reported to be neuroprotective in stroke. This agent appears to work at the level of the blood vessel lining or endothelium. Unfortunately, after producing favorable results in one large-scale clinical trial, a second trial failed to show favorable results.
In addition to injurious effects on brain cells, ischemia and infarction can result in loss of structural integrity of brain tissue and blood vessels, partly through the release of matrix metalloproteases, which are zinc- and calcium-dependent enzymes that break down collagen, , and other elements of . Other proteases also contribute to this process. The loss of vascular structural integrity results in a breakdown of the protective
that contributes to , which can cause secondary progression of the brain injury.
As is the case with any type of , the
is activated by cerebral infarction and may under some circumstances exacerbate the injury caused by the infarction. Inhibition of the
has been shown experimentally to reduce tissue injury due to cerebral infarction, but this has not proved out in clinical studies.
Head CT showing deep intracerebral hemorrhage due to bleeding within the , approximately 30 hours old.
Hemorrhagic strokes result in tissue injury by causing compression of tissue from an expanding hematoma or hematomas. This can distort and injure tissue. In addition, the pressure may lead to a loss of blood supply to affected tissue with resulting infarction, and the blood released by brain hemorrhage appears to have direct toxic effects on brain tissue and vasculature.
Stroke is diagnosed through several techniques: a neurological examination, CT scans (most often without contrast enhancements) or , , and . The diagnosis of stroke itself is clinical, with assistance from the imaging techniques. Imaging techniques also assist in determining the subtypes and cause of stroke. There is yet no commonly used
for the stroke diagnosis itself, though blood tests may be of help in finding out the likely cause of stroke.
For diagnosing ischemic stroke in the emergency setting:
CT scans (without contrast enhancements)
sensitivity= 83%
specificity= 98%
For diagnosing hemorrhagic stroke in the emergency setting:
CT scans (without contrast enhancements)
sensitivity= 89%
specificity= 100%
sensitivity= 81%
specificity= 100%
For detecting chronic hemorrhages, MRI scan is more sensitive.
For the assessment of stable stroke, nuclear medicine scans SPECT and PET/CT may be helpful. SPECT documents cerebral blood flow and PET with FDG isotope the metabolic activity of the neurons.
When a stroke has been diagnosed, various other studies may be performed to determine the underlying etiology. With the current treatment and diagnosis options available, it is of particular importance to determine whether there is a peripheral source of emboli. Test selection may vary, since the cause of stroke varies with age,
and the clinical presentation. Commonly used techniques include:
(to detect ) or dissection of the precerebral arteries
(to identify
and resultant clots in the heart which may spread to the brain vessels through the bloodstream)
study to identify intermittent arrhythmias
of the cerebral vasculature (if a bleed is thought to have originated from an
blood tests to determine hypercholesterolemia,
and some rarer causes such as
Given the disease burden of stroke,
is an important
is less effective than secondary prevention (as judged by the
to prevent one stroke per year). Recent guidelines detail the evidence for primary prevention in stroke. Because stroke may indicate underlying atherosclerosis, it is important to determine the patient's risk for other cardiovascular diseases such as . Conversely, aspirin prevents against first stroke in patients who have suffered a myocardial infarction or patients with a high cardiovascular risk.
The most important modifiable risk factors for stroke are high blood pressure and atrial fibrillation (although magnitude of this effect is small: the evidence from the Medical Research Council trials is that 833 patients have to be treated for 1 year to prevent one stroke). Other modifiable risk factors include high blood cholesterol levels, diabetes, cigarette smoking (active and passive), heavy
and drug use, lack of ,
and unhealthy diet. Alcohol use could predispose to ischemic stroke, and intracerebral and subarachnoid hemorrhage via multiple mechanisms (for example via hypertension, atrial fibrillation, rebound
disturbances). The drugs most commonly associated with stroke are cocaine,
causing hemorrhagic stroke, but also
cough and cold drugs containing .
No high quality studies have shown the effectiveness of interventions aimed at weight reduction, promotion of regular exercise, reducing alcohol consumption or . Nonetheless, given the large body of circumstantial evidence, best medical management for stroke includes advice on diet, exercise, smoking and alcohol use. Medication or
is the most common method
can be a useful surgical method of preventing stroke.
accounts for 35-50% of stroke risk.
studies suggest that even a small blood pressure reduction (5 to 6 mmHg systolic, 2 to 3 mmHg diastolic) would result in 40% fewer strokes. Lowering blood pressure has been conclusively shown to prevent both ischemic and hemorrhagic strokes. It is equally important in secondary prevention. Even patients older than 80 years and those with
benefit from antihypertensive therapy. Studies show that intensive antihypertensive therapy results in a greater risk reduction. The available evidence does not show large differences in stroke prevention between antihypertensive drugs —therefore, other factors such as protection against other forms of cardiovascular disease should be considered and cost.
Patients with atrial fibrillation have a risk of 5% each year to develop stroke, and this risk is even higher in those with valvular atrial fibrillation. Depending on the stroke risk, anticoagulation with medications such as
or aspirin is warranted for stroke prevention.
High cholesterol levels have been inconsistently associated with (ischemic) stroke.
have been shown to reduce the risk of stroke by about 15%. Since earlier meta-analyses of other
did not show a decreased risk, statins might exert their effect through mechanisms other than their lipid-lowering effects.
Patients with diabetes mellitus are 2 to 3 times more likely to develop stroke, and they commonly have hypertension and . Intensive disease control has been shown to reduce microvascular complications such as nephropathy and retinopathy but not macrovascular complications such as stroke.
Oral anticoagulants such as
have been the mainstay of stroke prevention for over 50 years. However, several studies have shown that aspirin and antiplatelet drugs are highly effective in
after a stroke or transient ischemic attack. Low doses of aspirin (for example 75–150&mg) are as effective as high doses but have fewer side- the lowest effective dose remains unknown.
(, ) are modestly more effective than aspirin and have a decreased risk of , but they are more expensive. Their exact role remains controversial. Ticlopidine has more , ,
can be added to aspirin therapy to provide a small additional benefit, even though headache is a common side-effect. Low-dose aspirin is also effective for stroke prevention after sustaining a myocardial infarction. &
are not advised for stroke prevention —any benefit is offset by bleeding risk.
In primary prevention however, antiplatelet drugs did not reduce the risk of ischemic stroke while increasing the risk of major bleeding. Further studies are needed to investigate a possible protective effect of aspirin against ischemic stroke in women.
Surgical procedures such as carotid endarterectomy or carotid
can be used to remove significant atherosclerotic narrowing (stenosis) of the carotid artery, which supplies blood to the brain. There is a large body of evidence supporting this procedure in selected cases. Endarterectomy for a significant stenosis has been shown to be useful in the secondary prevention after a previous symptomatic stroke. Carotid artery stenting has not been shown to be equally useful. Patients are selected for surgery based on age, gender, degree of stenosis, time since symptoms and patients' preferences. Surgery is most efficient when not delayed too long —the risk of recurrent stroke in a patient who has a 50% or greater stenosis is up to 20% after 5 years, but endarterectomy reduces this risk to around 5%. The number of procedures needed to cure one patient was 5 for early surgery (within two weeks after the initial stroke), but 125 if delayed longer than 12 weeks.
Screening for carotid artery narrowing has not been shown to be a useful
test in the general population. Studies of surgical intervention for carotid artery stenosis without symptoms have shown only a small decrease in the risk of stroke. To be beneficial, the complication rate of the surgery should be kept below 4%. Even then, for 100 surgeries, 5 patients will benefit by avoiding stroke, 3 will develop stroke despite surgery, 3 will develop stroke or die due to the surgery itself, and 89 will remain stroke-free but would also have done so without intervention.
Nutrition, specifically the Mediterranean-style diet, has the potential of more than halving stroke risk.
With regards to lowering , a
of previous trials has concluded that lowering homocysteine with
and other supplements may reduce stroke risk. However, the two largest
included in the meta-analysis had conflicting results. One repo whereas the other was negative.
The European Society of Cardiology and the European Association for Cardiovascular Prevention and Rehabilitation have developed an interactive tool for prediction and managing the risk of heart attack and stroke in Europe. HeartScore is aimed at supporting clinicians in optimising individual cardiovascular risk reduction. The Heartscore Programme is available in 12 languages and offers web based or PC version ().
Ideally, people who have had a stroke are admitted to a "stroke unit", a ward or dedicated area in hospital staffed by nurses and therapists with experience in stroke treatment. It has been shown that people admitted to a stroke unit have a higher chance of surviving than those admitted elsewhere in hospital, even if they are being cared for by doctors with experience in stroke.
When an acute stroke is suspected by history and physical examination, the goal of early assessment is to determine the cause. Treatment varies according to the underlying cause of the stroke, thromboembolic (ischemic) or hemorrhagic. A non-contrast head
can rapidly identify a hemorrhagic stroke by imaging bleeding in or around the brain. If no bleeding is seen, a presumptive diagnosis of ischemic stroke is made.
Ischemic stroke is caused by a
(blood clot) occluding blood flow to an artery supplying the brain. Definitive therapy is aimed at removing the blockage by breaking the clot down (), or by removing it mechanically (). The more rapidly blood flow is restored to the brain, the fewer brain cells die.
Other medical therapies are aimed at minimizing clot enlargement or preventing new clots from forming. To this end, treatment with medications such as ,
may be given to prevent platelets from aggregating.
In addition to definitive therapies, management of acute stroke includes control of blood sugars, ensuring the patient has adequate oxygenation and adequate intravenous fluids. Patients may be positioned with their heads flat on the stretcher, rather than sitting up, to increase blood flow to the brain. It is common for the
immediately following a stroke. Although high blood pressure may cause some strokes, hypertension during acute stroke is desirable to allow adequate blood flow to the brain.
In increasing numbers of primary stroke centers, pharmacologic thrombolysis ("clot busting") with the drug
(tPA), is used to dissolve the clot and unblock the artery. However, the use of tPA in acute stroke is controversial. On one hand, it is endorsed by the
and the American Academy of Neurology as the recommended treatment for acute stroke within three hours of onset of symptoms as long as there are not other contraindications (such as abnormal lab values, high blood pressure, or recent surgery). This position for tPA is based upon the findings of two studies by one group of investigators which showed that tPA improves the chances for a good neurological outcome. When administered within the first three hours, 39% of all patients who were treated with tPA had a good outcome at three months, only 26% of placebo controlled patients had a good functional outcome. A recent study using
for thrombolysis in ischemic stroke suggests clinical benefit with administration 3 to 4.5 hours after stroke onset. However, in the NINDS trial 6.4% of patients with large strokes developed substantial brain hemorrhage as a complication from being given tPA. tPA is often misconstrued as a "magic bullet" and it is important for patients to be aware that despite the study that supports its use, some of the data were flawed and the safety and efficacy of tPA is controversial. A recent study found the mortality to be higher among patients receiving tPA versus those who did not. Additionally, it is the position of the
that objective evidence regarding the efficacy, safety, and applicability of tPA for acute ischemic stroke is insufficient to warrant its classification as .
Merci Retriever L5.
Another intervention for acute ischemic stroke is removal of the offending thrombus directly. This is accomplished by inserting a catheter into the , directing it into the , and deploying a corkscrew-like device to ensnare the clot, which is then withdrawn from the body. Mechanical embolectomy devices have been demonstrated effective at restoring blood flow in patients who were unable to receive
or for whom the drugs were ineffective, though no differences have been found between newer and older versions of the devices. The devices have only been tested on patients treated with mechanical clot embolectomy within eight hours of the onset of symptoms.
have begun to be looked at as possible viable options in treatment of acute ischemic stroke. In a
of six uncontrolled, single-center trials, involving a total of 300 patients, of intra-cranial stenting in symptomatic intracranial arterial stenosis, the rate of technical success (reduction to stenosis of &50%) ranged from 90-98%, and the rate of major peri-procedural complications ranged from 4-10%. The rates of restenosis and/or stroke following the treatment were also favorable. This data suggests that a large,
is needed to more completely evaluate the possible therapeutic advantage of this treatment.
Main article:
Most of the data concerning ’s effectiveness in treating ischemic stroke is limited to animal studies. These studies have focused primarily on ischemic as opposed to hemorrhagic stroke, as hypothermia has been associated with a lower clotting threshold. In these animal studies investigating the effect of temperature decline following ischemic stroke, hypothermia has been shown to be an effective all-purpose neuroprotectant. This promising data has led to the initiation of a variety of human studies. At the time of this article’s publishing, this research has yet to return results. However, in terms of feasibility, the use of hypothermia to control
(ICP) after an ischemic stroke was found to be both safe and practical. The device used in this study was called the .
Anticoagulation can prevent recurrent stroke. Among patients with nonvalvular atrial fibrillation, anticoagulation can reduce stroke by 60% while antiplatelet agents can reduce stroke by 20%.. However, a recent meta-analysis suggests harm from anti-coagulation started early after an embolic stroke. Stroke prevention treatment for atrial fibrillation is determined according to the .
If studies show carotid stenosis, and the patient has residual function in the affected side, carotid endarterectomy (surgical removal of the stenosis) may decrease the risk of recurrence if performed rapidly after stroke.
Patients with
evaluation to detect and treat the cause of the bleeding, although many may not need surgery. Anticoagulants and antithrombotics, key in treating ischemic stroke, can make bleeding worse and cannot be used in intracerebral hemorrhage. Patients are monitored and their blood pressure, blood sugar, and oxygenation are kept at optimum levels.
is the process by which patients with disabling strokes undergo treatment to help them return to normal life as much as possible by regaining and relearning the skills of everyday living. It also aims to help the survivor understand and adapt to difficulties, prevent secondary complications and educate family members to play a supporting role.
A rehabilitation team is usually multidisciplinary as it involves staff with different skills working together to help the patient. These include nursing staff, physiotherapy, occupational therapy, , and usually a
trained in . Some teams may also include , , and
since at least one third of the patients manifest . Validated instruments such as the
may be used to assess the likelihood of a stroke patient being able to manage at home with or without support subsequent to discharge from hospital.
is fundamental in maintaining , feeding, hydration, positioning, and monitoring
such as temperature, pulse, and blood pressure. Stroke rehabilitation begins almost immediately.
For most stroke patients,
(PT) and occupational therapy (OT) are the cornerstones of the rehabilitation process, but in many countries
is used, too. Often,
such as a , walkers, canes, and
may be beneficial. PT and OT have overlapping areas of working but their main
PT involves re-learning functions as transferring, walking and other gross motor functions. OT focusses on exercises and training to help relearn everyday activities known as the
(ADLs) such as eating, drinking, dressing, bathing, cooking, reading and writing, and toileting.
is appropriate for patients with problems understanding speech or written words, problems forming speech and problems with swallowing.
Patients may have particular problems, such as complete or partial inability to swallow, which can cause swallowed material to pass into the lungs and cause . The condition may improve with time, but in the interim, a
may be inserted, enabling liquid food to be given directly into the stomach. If swallowing is still unsafe after a week, then a
(PEG) tube is passed and this can remain indefinitely.
Stroke rehabilitation should be started as immediately as possible and can last anywhere from a few days to over a year. Most return of function is seen in the first few days and weeks, and then improvement falls off with the "window" considered officially by
rehabilitation units and others to be closed after six months, with little chance of further improvement. However, patients have been known to continue to improve for years, regaining and strengthening abilities like writing, walking, running, and talking. Daily rehabilitation exercises should continue to be part of the stroke patient's routine. Complete recovery is unusual but not impossible and most patients will improve to some extent&: a correct diet and exercise are known to help the brain to self-recover.
Disability affects 75% of stroke survivors enough to decrease their employability. Stroke can affect patients physically, mentally, emotionally, or a combination of the three. The results of stroke vary widely depending on size and location of the lesion. Dysfunctions correspond to areas in the brain that have been damaged.
Some of the physical disabilities that can result from stroke include paralysis, numbness, , , , apraxia (inability to perform learned movements), difficulties carrying out daily activities, appetite loss, , , and . If the stroke is severe enough, or in a certain location such as parts of the brainstem,
or death can result.
Emotional problems resulting from stroke can result from direct damage to emotional centers in the brain or from frustration and difficulty adapting to new limitations. Post-stroke emotional difficulties include , ,
(failure to express emotions), , , and .
30 to 50% of stroke survivors suffer post stroke depression, which is characterized by lethargy, irritability, , lowered , and withdrawal.
can reduce motivation and worsen outcome, but can be treated with .
, another consequence of stroke, causes the patient to switch quickly between emotional highs and lows and to express emotions inappropriately, for instance with an excess of laughing or crying with little or no provocation. While these expressions of emotion usually correspond to the patient's actual emotions, a more severe form of emotional lability causes patients to laugh and cry pathologically, without regard to context or emotion. Some patients show the opposite of what they feel, for example crying when they are happy. Emotional lability occurs in about 20% of stroke patients.
Cognitive deficits resulting from stroke include perceptual disorders, , , and problems with attention and memory. A stroke sufferer may be unaware of his or her own disabilities, a condition called anosognosia. In a condition called , a patient is unable to attend to anything on the side of space opposite to the damaged hemisphere.
Up to 10% of all stroke patients develop , most commonly in the week sub the severity of the stroke increases the likelihood of a seizure.
Stroke could soon be the most common cause of death worldwide. Stroke is currently the second leading cause of death in the , ranking after heart disease and before cancer, and causes 10% of deaths worldwide. Geographic disparities in stroke incidence have been observed, including the existence of a "" in the , but causes of these disparities have not been explained.
from 30 years of age, and
varies by age. Advanced age is one of the most significant stroke risk factors. 95% of strokes occur in people age 45 and older, and two-thirds of strokes occur in those over the age of 65. A person's risk of dying if he or she does have a stroke also increases with age. However, stroke can occur at any age, including in fetuses.
Family members may have a genetic tendency for stroke or share a lifestyle that contributes to stroke. Higher levels of
are more common amongst people who have had ischemic stroke for the first time. The results of this study found that the only significant genetic factor was the person's . Having had a stroke in the past greatly increases one's risk of future strokes.
Men are 25% more likely to suffer strokes than women, yet 60% of deaths from stroke occur in women. Since women live longer, they are older on average when they have their strokes and thus more often killed (NIMH 2002). Some risk factors for stroke apply only to women. Primary among these are pregnancy, childbirth, menopause and the treatment thereof ().
Hippocrates first described the sudden paralysis that is often associated with stroke.
(460 to 370 BC) was first to describe the phenomenon of sudden
that is often associated with . , from the
word meaning "struck down with violence,” first appeared in Hippocratic writings to describe this phenomenon.
The word stroke was used as a synonym for apoplectic
as early as 1599, and is a fairly literal translation of the Greek term.
In 1658, in his Apoplexia,
() identified the cause of
stroke when he suggested that people who had
of apoplexy had bleeding in their brains. Wepfer also identified the main
supplying the brain, the
arteries, and identified the cause of
stroke [also known as ] when he suggested that
might be caused by a blockage to those vessels.
first described the mechanism of
as a major factor.
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From Wikiversity
A stroke (syn. Cerebral Vascular Accident
or "CVA") is a sudden, focal, neurological deficit or loss of
brain function. Most stroke experts prefer the term "stroke" to
"CVA", but both are used commonly to refer to this acquired
neurological disorder.
A Stroke can be due to ischaemia or due to haemorrhage,
ishcaemia being more common. The common effect of all strokes is
damage to brain cells. This can be transient or permanent. Strokes
have many different clinical presentations.
The term "brain attack" has been advocated for
use in the United States for stroke, just as the term "heart
attack" is used for myocardial infarction. Many hospitals have
multidisciplinary "stroke teams" specifically for swift treatment
of stroke.
2.1 Ischemic Stroke
Thrombotic Stroke
Cardioembolic Stroke
2.1.4 Systemic
hypoperfusion (Watershed stroke)
2.2 Hemorrhagic stroke
2.2.1 Intracerebral
hemorrhage
2.2.2 Subarachnoid
hemorrhage
Risk factor reduction
9 External Links
10 Further Reading
Approximately 700,000 Americans per year experience a stroke. It
is the third leading cause of death and the leading cause of
long-term adult disability in the United States.[1] On average, a stroke occurs every
45 seconds and someone dies from a stroke every 3 minutes.[2]
Risk factors for stroke include atherosclerosis, advanced age,
blood pressure), , high cholesterol,
cigarette smoking, atrial fibrillation, ethnic identity, and some
blood clotting disorders.
This illustration serves to show the reader the general
circular shape of the roadmap of arteries that supply the brain.
This is an x-ray image of the head after a radio-opaque dye was
injected into the arterial system, the image is called an
angiogram. For more detailed discussion of anatomy, see Circle of
Strokes can be classified as ischemic or
hemorrhagic. In ischemic strokes, all or part of
the brain is deprived of blood and oxygen, usually through the
blockage of an artery. In hemorrhagic strokes, loss of blood supply
plays a part, but the initial event is bleeding into the brain
causing increased pressure on the brain, and irritation to brain
Ischemic strokes make up about 87% of all strokes and can be
due to occlusion or an artery by a thrombus or by generalized low
blood flow (hypoperfusion). Lacunae, or small vessel
ischemic strokes, are responsible for about 20% of all strokes and
are common in hypertension and .
Atherosclerosis is responsible for the majority of
ischemic strokes. The etiology of atherosclerosis-related strokes
is very similar to that of heart attacks. An atherosclerotic plaque
in a cerebral artery can gradually develop an associated thrombus
or rupture suddenly causing a rapid occlusion, or the thrombus can
break off and lodge in a vessel even deeper in the brain.
"Thrombotic stroke" usually refers to in-situ thrombus, "embolic
stroke" to thrombi that travel from distant sites.
Thrombotic and thromboembolic strokes can originate in either
large or small blood vessels, and are usually due to abnormalities
in the vessel (most commonly atherosclerosis). Atheroembolism can
occur within the cerebral circulation or can originate outside the
cerebral circulation. One of the most important etiologies is
carotid artery disease. Lacunae are also a subset of thrombotic
Embolism of thrombi from outside the cerebral circulation are
responsible for a large and important subset of ischemic strokes.
In these cases a thrombus (blood clot) travels from its origin and
lodges in a cerebral artery. Most of these strokes are of cardiac
origin (Cardioembolic).
Atrial fibrillation: The majority of embolic strokes
originating in the heart are due to atrial fibrillation. In fact,
about 16% of strokes are associated with atrial fibrillation, and
the presence of atrial fibrillation increases stroke risk by about
5-11% per year, depending on other risk factors. [4]The relative stasis of blood in
the left atrium leads to blood clot formation, and these clots can
be expelled from the heart to enter the cerebral circulation.
Mural thrombi: anything that causes blood flow in the heart to
slow can cause thrombus formation. This includes thrombi formed in
the atrial appendage and thrombi formed in the left ventricle in
patients with heart failure.
Valvular heart disease: this includes rheumatic heart disease,
infective endocarditis, and presence of a prosthetic heart
Paradoxical embolism: this occurs primarily when a deep venous
thrombosis (DVT) in the leg breaks off, passing through a patent
foramen ovale (PFO) into the left ventricle, and then to the
Systemic hypoperfusion is the reduction of blood flow to all
parts of the body. It is most commonly due to various types of shock. Hypoxemia (low blood oxygen
content) may precipitate the hypoperfusion. Because the reduction
in blood flow is global, all parts of the brain may be affected,
especially "watershed" areas --- border zone regions supplied by
the major cerebral arteries. Blood flow to these areas does not
necessarily stop, but instead it may lessen to the point where
brain damage can occur.
A hemorrhagic stroke, is a form of stroke that occurs when a
blood vessel in the brain ruptures or bleeds. There are two types
of hemorrhagic stroke: intracerebral hemorrhage, and subarachnoid
hemorrhage (SAH). Traumatic hemorrhage, including epidural
hemorrhage, subdural hemorrhage, and some SAH are usually
considered separately.
Hemorrhagic strokes are usually classed as either intracerebral
hemorrhage or subarachnoid hemorrhage. Uncontrolled
hypertension is a leading cause of hemorrhagic stroke. Weaknesses
in brain arteries, (for example, aneurysms) can cause hemorrhagic
strokes even when the pressure of the blood inside the arteries is
not excessive. Because the brain is enclosed within a rigid
structure (the skull), even a small amount of bleeding can cause a
dramatic increase in pressure on the brain. This can lead to
herniation, in which part of the brain is compressed
through the base of the skull, causing rapid coma and death.
Intracerebral hemorrhage (ICH) is bleeding directly into the
brain tissue, forming a gradually enlarging hematoma (pool of
blood). It generally occurs in small arteries or arterioles and is
commonly due to , trauma, and vascular
malformations. The hematoma enlarges until pressure from
surrounding tissue limits its growth, or until it decompresses by
emptying into the ventricular system. ICH has a mortality rate of
44 percent after 30 days, higher than ischemic stroke or even the
very deadly subarachnoid hemorrhage.
Subarachnoid hemorrhage (SAH) is bleeding into the cerebrospinal
fluid (CSF) surrounding the brain. The two most common causes of
SAH are rupture of aneurysms and bleeding}