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Stroke
Classification and external resources

CT scan slice of the brain showing a right-hemispheric ischemic stroke (left side of image).
ICD-10 I61.-I64.
ICD-9 434.91
OMIM 601367
DiseasesDB 2247
MedlinePlus 000726
eMedicine neuro/9 emerg/558 emerg/557 pmr/187
MeSH D020521

A stroke (sometimes called a cerebrovascular accident (CVA)) is the rapidly developing loss of brain function(s) due to disturbance in the blood supply to the brain, caused by a blocked or burst blood vessel. This can be due to ischemia (lack of glucose and oxygen supply) caused by thrombosis or embolism or due to a hemorrhage.[1] As a result, the affected area of the brain is unable to function, leading to inability to move one or more limbs on one side of the body, inability to understand or formulate speech, or inability to see one side of the visual field.[2]

A stroke is a medical emergency and can cause permanent neurological 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.[3] Risk factors for stroke include advanced age, hypertension (high blood pressure), previous stroke or transient ischemic attack (TIA), diabetes, high cholesterol, cigarette smoking and atrial fibrillation.[4] High blood pressure is the most important modifiable risk factor of stroke.[2]

A stroke is occasionally treated with thrombolysis ("clot buster"), but usually with supportive care (speech and language therapy, physiotherapy and occupational therapy) in a "stroke unit" and secondary prevention with antiplatelet drugs (aspirin and often dipyridamole), blood pressure control, statins, and in selected patients with carotid endarterectomy and anticoagulation.[2]

Contents

Definition

The traditional definition of stroke, devised by the World Health Organization in the 1970s,[5] 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 transient ischemic attack, which is a related syndrome of stroke symptoms that resolve completely within 24 hours.[2] 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 heart attack and acute coronary syndrome respectively), that reflect the urgency of stroke symptoms and the need to act swiftly.[6]

Classification

A slice of brain from the autopsy of a person who suffered an acute middle cerebral artery (MCA) stroke

Strokes can be classified into two major categories: ischemic and hemorrhagic.[7] 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 blood vessel or an abnormal vascular structure. 80% of strokes are due to ischemia; 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.[2]

Ischemic stroke

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),[2]

3. Systemic hypoperfusion (general decrease in blood supply, e.g. in shock)[8]

4. Venous thrombosis.[9]

Stroke without an obvious explanation is termed "cryptogenic" (of unknown origin); this constitutes 30-40% of all ischemic strokes.[2][10]

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 the initial symptoms; based on the extent of the symptoms, the stroke episode is classified as total anterior circulation infarct (TACI), partial anterior circulation infarct (PACI), lacunar infarct (LACI) or posterior circulation infarct (POCI). These four entities predict the extent of the stroke, the area of the brain affected, the underlying cause, and the prognosis.[11][12] The TOAST (Trial of Org 10172 in Acute Stroke Treatment) classification is based on clinical symptoms as well as results of further investigations; on this basis, a stroke is classified as being due to (1) thrombosis or embolism due to atherosclerosis of a large artery, (2) embolism of cardiac origin, (3) occlusion of a small blood vessel, (4) other determined cause, (5) undetermined cause (two possible causes, no cause identified, or incomplete investigation).[2][13]

Hemorrhagic stroke

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 intra-axial hemorrhage (blood inside the brain) and extra-axial hemorrhage (blood inside the skull but outside the brain). Intra-axial hemorrhage is due to intraparenchymal hemorrhage or intraventricular hemorrhage (blood in the ventricular system). The main types of extra-axial hemorrhage are epidural hematoma (bleeding between the dura mater and the skull), subdural hematoma (in the subdural space) and subarachnoid hemorrhage (between the arachnoid mater and pia mater). Most of the hemorrhagic stroke syndromes have specific symptoms (e.g. headache, previous head injury). Intracerebral hemorrhage (ICH) is bleeding directly into the brain tissue, forming a gradually enlarging hematoma (pooling of blood).[citation needed]

Signs and symptoms

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 headache, apart from subarachnoid hemorrhage and cerebral venous thrombosis and occasionally intracerebral hemorrhage.

Early recognition

Various systems have been proposed to increase recognition of stroke by patients, relatives and emergency first responders. A systematic review, updating a previous systematic review from 1994, looked at a number of trials to evaluate how well different physical examination 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 (+ likelihood ratio 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 (– likelihood ratio of 0.39).[14] 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),[15] as advocated by the Department of Health (United Kingdom) and The Stroke Association, the Los Angeles Prehospital Stroke Screen (LAPSS)[16] and the Cincinnati Prehospital Stroke Scale (CPSS).[17] Use of these scales is recommended by professional guidelines.[18]

For people referred to the emergency room, 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 recommended for this purpose; it is based on features from the medical history and physical examination.[18][19]

Subtypes

If the area of the brain affected contains one of the three prominent Central nervous system pathways—the spinothalamic tract, corticospinal tract, and dorsal column (medial lemniscus), symptoms may include:

In most cases, the symptoms affect only one side of the body (unilateral). 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 spinal cord and any lesion there can also produce these symptoms.

In addition to the above CNS pathways, the brainstem also consists of the 12 cranial nerves. 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 (ptosis) and weakness of ocular muscles
  • decreased reflexes: gag, swallow, pupil reactivity to light
  • decreased sensation and muscle weakness of the face
  • balance problems and nystagmus
  • altered breathing and heart rate
  • weakness in sternocleidomastoid muscle with inability to turn head to one side
  • weakness in tongue (inability to protrude and/or move from side to side)

If the cerebral cortex is involved, the CNS pathways can again be affected, but also can produce the following symptoms:

If the cerebellum is involved, the patient may have the following:

  • trouble walking
  • altered movement coordination
  • vertigo and or disequilibrium

Associated symptoms

Loss of consciousness, 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.

Causes

Thrombotic stroke

In thrombotic stroke a thrombus (blood clot) usually forms around atherosclerotic 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:

Sickle cell anemia, which can cause blood cells 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.[20]

Embolic stroke

An embolic stroke refers to the blockage of an artery by an embolus, 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 fat (e.g. from bone marrow in a broken bone), air, cancer cells or clumps of bacteria (usually from infectious endocarditis).

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 heart (especially in atrial fibrillation) but may originate from elsewhere in the arterial tree. In paradoxical embolism, a deep vein thrombosis embolises through an atrial or ventricular septal defect in the heart into the brain.

Cardiac causes can be distinguished between high and low-risk:[21]

Systemic hypoperfusion

Systemic hypoperfusion is the reduction of blood flow to all parts of the body. It is most commonly due to cardiac pump failure from cardiac arrest or arrhythmias, or from reduced cardiac output as a result of myocardial infarction, pulmonary embolism, pericardial effusion, or bleeding. 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. 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

Cerebral venous sinus 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.[9]

Intracerebral hemorrhage

It generally occurs in small arteries or arterioles and is commonly due to hypertension, intracranial vascular malformations (including cavernous angiomas or arteriovenous malformations), cerebral amyloid angiopathy, or infarcts into which secondary haemorrhage has occurred.[2] Other potential causes are trauma, bleeding disorders, amyloid angiopathy, illicit drug use (e.g. amphetamines or cocaine). The hematoma enlarges until pressure from surrounding tissue limits its growth, or until it decompresses by emptying into the ventricular system, CSF or the pial surface. A third of intracerebral bleed is into the brain's ventricles. ICH has a mortality rate 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[2]).

Pathophysiology

Ischemic

Ischemic stroke occurs due to a loss of blood supply to part of the brain, initiating the ischemic cascade.[22] 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., infarction. (This is why TPA's (e.g. Streptokinase, 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 emboli 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 anaerobic respiration 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. 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 penumbra".[23]

Then, as oxygen or glucose becomes depleted in ischemic brain tissue, the production of high energy phosphate 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 mitochondria, which can lead further toward energy depletion and may trigger cell death due to apoptosis.

Ischemia also induces production of oxygen free radicals and other reactive oxygen species. 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 uric acid and NXY-059 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 redox signaling.[20]

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 aerobic metabolism, 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 reactive oxygen species, inhibit apoptosis, 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 clinical trials with neuroprotective agents have failed, with the probable exception of deep barbiturate coma. However, more recently NXY-059, the disulfonyl derivative of the radical-scavenging spintrap phenylbutylnitrone, is reported to be neuroprotective in stroke.[24] 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.[20]

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, hyaluronic acid, and other elements of connective tissue. Other proteases also contribute to this process. The loss of vascular structural integrity results in a breakdown of the protective blood brain barrier that contributes to cerebral edema, which can cause secondary progression of the brain injury.

As is the case with any type of brain injury, the immune system is activated by cerebral infarction and may under some circumstances exacerbate the injury caused by the infarction. Inhibition of the inflammatory response has been shown experimentally to reduce tissue injury due to cerebral infarction, but this has not proved out in clinical studies.

Hemorrhagic

Head CT showing deep intracerebral hemorrhage due to bleeding within the cerebellum, 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.[20]

Diagnosis

Stroke is diagnosed through several techniques: a neurological examination, CT scans (most often without contrast enhancements) or MRI scans, Doppler ultrasound, and arteriography. 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 blood test for the stroke diagnosis itself, though blood tests may be of help in finding out the likely cause of stroke.[25]

Imaging

For diagnosing ischemic stroke in the emergency setting:[26]

  • CT scans (without contrast enhancements)
sensitivity= 16%
specificity= 96%
  • MRI scan
sensitivity= 83%
specificity= 98%

For diagnosing hemorrhagic stroke in the emergency setting:

  • CT scans (without contrast enhancements)
sensitivity= 89%
specificity= 100%
  • MRI scan
sensitivity= 81%
specificity= 100%

For detecting chronic hemorrhages, MRI scan is more sensitive.[27]

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.

Underlying etiology

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, comorbidity and the clinical presentation. Commonly used techniques include:

Prevention

Given the disease burden of stroke, prevention is an important public health concern.[28] Primary prevention is less effective than secondary prevention (as judged by the number needed to treat to prevent one stroke per year).[28] Recent guidelines detail the evidence for primary prevention in stroke.[29] Because stroke may indicate underlying atherosclerosis, it is important to determine the patient's risk for other cardiovascular diseases such as coronary heart disease. Conversely, aspirin prevents against first stroke in patients who have suffered a myocardial infarction or patients with a high cardiovascular risk.[30][31]

Risk factors

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[32][33]). Other modifiable risk factors include high blood cholesterol levels, diabetes, cigarette smoking[34][35] (active and passive), heavy alcohol consumption[36] and drug use,[37] lack of physical activity, obesity and unhealthy diet.[38] Alcohol use could predispose to ischemic stroke, and intracerebral and subarachnoid hemorrhage via multiple mechanisms (for example via hypertension, atrial fibrillation, rebound thrombocytosis and platelet aggregation and clotting disturbances).[39] The drugs most commonly associated with stroke are cocaine, amphetamines causing hemorrhagic stroke, but also over-the-counter cough and cold drugs containing sympathomimetics.[40][41]

No high quality studies have shown the effectiveness of interventions aimed at weight reduction, promotion of regular exercise, reducing alcohol consumption or smoking cessation.[42] Nonetheless, given the large body of circumstantial evidence, best medical management for stroke includes advice on diet, exercise, smoking and alcohol use.[43] Medication or drug therapy is the most common method of stroke prevention; carotid endarterectomy can be a useful surgical method of preventing stroke.

Blood pressure

Hypertension accounts for 35-50% of stroke risk.[44] Epidemiological 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.[45] Lowering blood pressure has been conclusively shown to prevent both ischemic and hemorrhagic strokes.[46][47] It is equally important in secondary prevention.[48] Even patients older than 80 years and those with isolated systolic hypertension benefit from antihypertensive therapy.[49][50][51] Studies show that intensive antihypertensive therapy results in a greater risk reduction.[52] 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.[52][53]

Atrial fibrillation

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.[54] Depending on the stroke risk, anticoagulation with medications such as coumarins or aspirin is warranted for stroke prevention.[55]

Blood lipids

High cholesterol levels have been inconsistently associated with (ischemic) stroke.[47][56] Statins have been shown to reduce the risk of stroke by about 15%.[57] Since earlier meta-analyses of other lipid-lowering drugs did not show a decreased risk,[58] statins might exert their effect through mechanisms other than their lipid-lowering effects.[57]

Diabetes mellitus

Patients with diabetes mellitus are 2 to 3 times more likely to develop stroke, and they commonly have hypertension and hyperlipidemia. Intensive disease control has been shown to reduce microvascular complications such as nephropathy and retinopathy but not macrovascular complications such as stroke.[59][60]

Anticoagulation drugs

Oral anticoagulants such as warfarin 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 secondary prevention after a stroke or transient ischemic attack[30]. Low doses of aspirin (for example 75–150 mg) are as effective as high doses but have fewer side-effects; the lowest effective dose remains unknown.[61] Thienopyridines (clopidogrel, ticlopidine) are modestly more effective than aspirin and have a decreased risk of gastrointestinal bleeding, but they are more expensive.[62] Their exact role remains controversial. Ticlopidine has more skin rash, diarrhea, neutropenia and thrombotic thrombocytopenic purpura.[62] Dipyridamole can be added to aspirin therapy to provide a small additional benefit, even though headache is a common side-effect.[63] Low-dose aspirin is also effective for stroke prevention after sustaining a myocardial infarction.[31] > Oral anticoagulants are not advised for stroke prevention —any benefit is offset by bleeding risk.[64]

In primary prevention however, antiplatelet drugs did not reduce the risk of ischemic stroke while increasing the risk of major bleeding.[65][66] Further studies are needed to investigate a possible protective effect of aspirin against ischemic stroke in women.[67][68]

Surgery

Surgical procedures such as carotid endarterectomy or carotid angioplasty 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.[43] Endarterectomy for a significant stenosis has been shown to be useful in the secondary prevention after a previous symptomatic stroke.[69] Carotid artery stenting has not been shown to be equally useful.[70][71] Patients are selected for surgery based on age, gender, degree of stenosis, time since symptoms and patients' preferences.[43] 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.[72][73]

Screening for carotid artery narrowing has not been shown to be a useful screening test in the general population.[74] Studies of surgical intervention for carotid artery stenosis without symptoms have shown only a small decrease in the risk of stroke.[75][76] 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.[43]

Nutritional and metabolic interventions

Nutrition, specifically the Mediterranean-style diet, has the potential of more than halving stroke risk.[77]

With regards to lowering homocysteine, a meta-analysis of previous trials has concluded that lowering homocysteine with folic acid and other supplements may reduce stroke risk.[78] However, the two largest randomized controlled trials included in the meta-analysis had conflicting results. One reported positve results;[79] whereas the other was negative.[80]

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 ([1]).

Treatment

Stroke unit

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.[2]

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 CT scan 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.

Treatment of ischemic stroke

Ischemic stroke is caused by a thrombus (blood clot) occluding blood flow to an artery supplying the brain. Definitive therapy is aimed at removing the blockage by breaking the clot down (thrombolysis), or by removing it mechanically (thrombectomy). The more rapidly blood flow is restored to the brain, the fewer brain cells die.[81]

Other medical therapies are aimed at minimizing clot enlargement or preventing new clots from forming. To this end, treatment with medications such as aspirin, clopidogrel and dipyridamole may be given to prevent platelets from aggregating[30].

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 blood pressure to be elevated 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.

Thrombolysis

In increasing numbers of primary stroke centers, pharmacologic thrombolysis ("clot busting") with the drug tissue plasminogen activator (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 American Heart Association 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[82] 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 alteplase for thrombolysis in ischemic stroke suggests clinical benefit with administration 3 to 4.5 hours after stroke onset.[83] 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.[84] Additionally, it is the position of the American Academy of Emergency Medicine that objective evidence regarding the efficacy, safety, and applicability of tPA for acute ischemic stroke is insufficient to warrant its classification as standard of care.[85]

Mechanical thrombectomy

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 femoral artery, directing it into the cerebral circulation, 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 thrombolytic drugs or for whom the drugs were ineffective,[86][87][88][89] though no differences have been found between newer and older versions of the devices.[90] The devices have only been tested on patients treated with mechanical clot embolectomy within eight hours of the onset of symptoms.

Angioplasty and stenting

Angioplasty and stenting have begun to be looked at as possible viable options in treatment of acute ischemic stroke. In a systematic review 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.[91] This data suggests that a large, randomized controlled trial is needed to more completely evaluate the possible therapeutic advantage of this treatment.

Therapeutic hypothermia

Most of the data concerning therapeutic hypothermia’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.[92] 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 intracranial pressure (ICP) after an ischemic stroke was found to be both safe and practical. The device used in this study was called the Arctic Sun.[93]

Secondary prevention of ischemic stroke

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%.[94]. However, a recent meta-analysis suggests harm from anti-coagulation started early after an embolic stroke.[95] Stroke prevention treatment for atrial fibrillation is determined according to the CHADS/CHADS2 system.

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.

Treatment of hemorrhagic stroke

Patients with intracerebral hemorrhage require neurosurgical 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.

Care and rehabilitation

Stroke rehabilitation 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, speech and language therapy, and usually a physician trained in rehabilitation medicine. Some teams may also include psychologists, social workers, and pharmacists since at least one third of the patients manifest post stroke depression. Validated instruments such as the Barthel scale 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.

Good nursing care is fundamental in maintaining skin care, feeding, hydration, positioning, and monitoring vital signs such as temperature, pulse, and blood pressure. Stroke rehabilitation begins almost immediately.

For most stroke patients, physical therapy (PT) and occupational therapy (OT) are the cornerstones of the rehabilitation process, but in many countries Neurocognitive Rehabilitation is used, too. Often, assistive technology such as a wheelchair, walkers, canes, and orthosis may be beneficial. PT and OT have overlapping areas of working but their main attention fields are; 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 Activities of daily living (ADLs) such as eating, drinking, dressing, bathing, cooking, reading and writing, and toileting. Speech and language therapy 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 aspiration pneumonia. The condition may improve with time, but in the interim, a nasogastric tube may be inserted, enabling liquid food to be given directly into the stomach. If swallowing is still unsafe after a week, then a percutaneous endoscopic gastrostomy (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 U.S. state 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.

Prognosis

Disability affects 75% of stroke survivors enough to decrease their employability.[96] 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.[97] Dysfunctions correspond to areas in the brain that have been damaged.

Some of the physical disabilities that can result from stroke include paralysis, numbness, pressure sores, pneumonia, incontinence, apraxia (inability to perform learned movements), difficulties carrying out daily activities, appetite loss, speech loss, vision loss, and pain. If the stroke is severe enough, or in a certain location such as parts of the brainstem, coma 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 anxiety, panic attacks, flat affect (failure to express emotions), mania, apathy, and psychosis.

30 to 50% of stroke survivors suffer post stroke depression, which is characterized by lethargy, irritability, sleep disturbances, lowered self esteem, and withdrawal.[98] Depression can reduce motivation and worsen outcome, but can be treated with antidepressants.

Emotional lability, 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.[96] Some patients show the opposite of what they feel, for example crying when they are happy.[99] Emotional lability occurs in about 20% of stroke patients.

Cognitive deficits resulting from stroke include perceptual disorders, speech problems, dementia, 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 hemispatial neglect, 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 seizures, most commonly in the week subsequent to the event; the severity of the stroke increases the likelihood of a seizure.[100][101]

Epidemiology

Stroke could soon be the most common cause of death worldwide.[102] Stroke is currently the second leading cause of death in the Western world, ranking after heart disease and before cancer,[2] and causes 10% of deaths worldwide.[103] Geographic disparities in stroke incidence have been observed, including the existence of a "stroke belt" in the southeastern United States, but causes of these disparities have not been explained.

The incidence of stroke increases exponentially from 30 years of age, and etiology varies by age.[104] 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.[98][20] 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 Von Willebrand factor are more common amongst people who have had ischemic stroke for the first time.[105] The results of this study found that the only significant genetic factor was the person's blood type. 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,[20] yet 60% of deaths from stroke occur in women.[99] Since women live longer, they are older on average when they have their strokes and thus more often killed (NIMH 2002).[20] Some risk factors for stroke apply only to women. Primary among these are pregnancy, childbirth, menopause and the treatment thereof (HRT).

History

Hippocrates first described the sudden paralysis that is often associated with stroke.

Hippocrates (460 to 370 BC) was first to describe the phenomenon of sudden paralysis that is often associated with ischemia. Apoplexy, from the Greek word meaning "struck down with violence,” first appeared in Hippocratic writings to describe this phenomenon.[106][107]

The word stroke was used as a synonym for apoplectic seizure as early as 1599,[108] and is a fairly literal translation of the Greek term.

In 1658, in his Apoplexia, Johann Jacob Wepfer (1620–1695) identified the cause of hemorrhagic stroke when he suggested that people who had died of apoplexy had bleeding in their brains.[106][20] Wepfer also identified the main arteries supplying the brain, the vertebral and carotid arteries, and identified the cause of ischemic stroke [also known as cerebral infarction] when he suggested that apoplexy might be caused by a blockage to those vessels.[20]

Rudolf Virchow first described the mechanism of thromboembolism as a major factor.[109]

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  85. ^ "Position Statement on the Use of Intravenous Thrombolytic Therapy in the Treatment of Stroke". American Academy of Emergency Medicine. http://www.aaem.org/positionstatements/thrombolytictherapy.shtml. Retrieved 2008-01-25. 
  86. ^ Flint AC, Duckwiler GR, Budzik RF, Liebeskind DS, Smith WS (2007). "Mechanical thrombectomy of intracranial internal carotid occlusion: pooled results of the MERCI and Multi MERCI Part I trials". Stroke 38 (4): 1274–80. doi:10.1161/01.STR.0000260187.33864.a7. PMID 17332445. 
  87. ^ Smith WS, Sung G, Starkman S, et al. (2005). "Safety and efficacy of mechanical embolectomy in acute ischemic stroke: results of the MERCI trial". Stroke 36 (7): 1432–8. doi:10.1161/01.STR.0000171066.25248.1d. PMID 15961709. http://stroke.ahajournals.org/cgi/content/full/36/7/1432. 
  88. ^ Lutsep HL, Rymer MM, Nesbit GM (2008). "Vertebrobasilar revascularization rates and outcomes in the MERCI and multi-MERCI trials". J Stroke Cerebrovasc Dis 17 (2): 55–7. doi:10.1016/j.jstrokecerebrovasdis.2007.11.003. PMID 18346645. 
  89. ^ Smith WS (June 1, 2006). "Safety of mechanical thrombectomy and intravenous tissue plasminogen activator in acute ischemic stroke. Results of the multi Mechanical Embolus Removal in Cerebral Ischemia (MERCI) trial, part I". AJNR Am J Neuroradiol 27 (6): 1177–82. PMID 16775259. http://www.ajnr.org/cgi/content/full/27/6/1177. 
  90. ^ Smith WS, Sung G, Saver J, et al. (2008). "Mechanical thrombectomy for acute ischemic stroke: final results of the Multi MERCI trial". Stroke 39 (4): 1205–12. doi:10.1161/STROKEAHA.107.497115. PMID 18309168. 
  91. ^ Derdeyn CP, Chimowitz MI (August 2007). "Angioplasty and stenting for atherosclerotic intracranial stenosis: rationale for a randomized clinical trial". Neuroimaging Clin. N. Am. 17 (3): 355–63, viii–ix. doi:10.1016/j.nic.2007.05.001. 
  92. ^ Krieger DW, De Georgia MA, Abou-Chebl A, et al. (August 2001). "Cooling for acute ischemic brain damage (cool aid): an open pilot study of induced hypothermia in acute ischemic stroke". Stroke 32 (8): 1847–54. PMID 11486115. http://stroke.ahajournals.org/cgi/content/full/32/8/1847. 
  93. ^ Schwab S, Schwarz S, Spranger M, Keller E, Bertram M, Hacke W (December 1998). "Moderate hypothermia in the treatment of patients with severe middle cerebral artery infarction". Stroke 29 (12): 2461–6. PMID 9836751. http://stroke.ahajournals.org/cgi/pmidlookup?view=long&pmid=9836751. 
  94. ^ Hart RG, Pearce LA, Aguilar MI (2007). "Meta-analysis: antithrombotic therapy to prevent stroke in patients who have nonvalvular atrial fibrillation". Ann. Intern. Med. 146 (12): 857–67. PMID 17577005. 
  95. ^ Paciaroni M, Agnelli G, Micheli S, Caso V (2007). "Efficacy and safety of anticoagulant treatment in acute cardioembolic stroke: a meta-analysis of randomized controlled trials". Stroke 38 (2): 423–30. doi:10.1161/01.STR.0000254600.92975.1f. PMID 17204681.  ACP JC synopsis
  96. ^ a b Coffey C. Edward, Cummings Jeffrey L, Starkstein Sergio, Robinson Robert (2000). Stroke - the American Psychiatric Press Textbook of Geriatric Neuropsychiatry (Second ed.). Washington DC: American Psychiatric Press. pp. 601–617. 
  97. ^ Stanford Hospital & Clinics. "Cardiovascular Diseases: Effects of Stroke". http://www.stanfordhospital.com/healthLib/atoz/cardiac/effects.html. Retrieved 2005. 
  98. ^ a b Senelick Richard C., Rossi, Peter W., Dougherty, Karla (1994). Living with Stroke: A Guide for Families. Contemporary Books, Chicago. ISBN 0809226073. OCLC 42835161 40856888 42835161. 
  99. ^ a b Villarosa, Linda, Ed., Singleton, LaFayette, MD, Johnson, Kirk A. (1993). Black Health Library Guide to Stroke. Henry Holt and Company, New York. 
  100. ^ Reith J, Jørgensen HS, Nakayama H, Raaschou HO, Olsen TS (August 1997). "Seizures in acute stroke: predictors and prognostic significance. The Copenhagen Stroke Study". Stroke 28 (8): 1585–9. PMID 9259753. http://stroke.ahajournals.org/cgi/pmidlookup?view=long&pmid=9259753. 
  101. ^ Burn J, Dennis M, Bamford J, Sandercock P, Wade D, Warlow C (December 1997). "Epileptic seizures after a first stroke: the Oxfordshire Community Stroke Project". BMJ 315 (7122): 1582–7. PMID 9437276. PMC 2127973. http://bmj.com/cgi/pmidlookup?view=long&pmid=9437276. 
  102. ^ Murray CJ, Lopez AD (1997). "Mortality by cause for eight regions of the world: Global Burden of Disease Study". Lancet 349 (9061): 1269–76. doi:10.1016/S0140-6736(96)07493-4. PMID 9142060. 
  103. ^ (PDF) The World health report 2004. Annex Table 2: Deaths by cause, sex and mortality stratum in WHO regions, estimates for 2002.. Geneva: World Health Organization. 2004. http://www.who.int/entity/whr/2004/en/report04_en.pdf. 
  104. ^ Ellekjær, H; Holmen J, Indredavik B, Terent A (November 1, 1997). "Epidemiology of Stroke in Innherred, Norway, 1994 to 1996 : Incidence and 30-Day Case-Fatality Rate". Stroke 28 (11): 2180–2184. PMID 9368561. http://stroke.ahajournals.org/cgi/content/abstract/strokeaha%3B28/11/2180. Retrieved 2008-01-22. 
  105. ^ Bongers T, de Maat M, van Goor M et al. (2006). "High von Willebrand factor levels increase the risk of first ischemic stroke: influence of ADAMTS13, inflammation, and genetic variability". Stroke 37 (11): 2672–7. doi:10.1161/01.STR.0000244767.39962.f7. PMID 16990571. 
  106. ^ a b Thompson JE (August 1, 1996). "The evolution of surgery for the treatment and prevention of stroke. The Willis Lecture". Stroke 27 (8): 1427–34. PMID 8711815. http://stroke.ahajournals.org/cgi/content/full/27/8/1427. 
  107. ^ Kopito, Jeff (September 2001). "A Stroke in Time" (). MERGINET.com 6 (9). http://www.webasx.com/articles/strokeintime.html. 
  108. ^ R. Barnhart, ed. The Barnhart Concise Dictionary of Etymology (1995)
  109. ^ Schiller F (April 1970). "Concepts of stroke before and after Virchow". Med Hist 14 (2): 115–31. PMID 4914683. 

Further reading

  • J. P. Mohr, Dennis Choi, James Grotta, Philip Wolf (2004). Stroke: Pathophysiology, Diagnosis, and Management. New York: Churchill Livingstone. ISBN 0-443-06600-0. OCLC 52990861 50477349 52990861. 
  • Charles P. Warlow, Jan van Gijn, Martin S. Dennis, Joanna M. Wardlaw, John M. Bamford, Graeme J. Hankey, Peter A. G. Sandercock, Gabriel Rinkel, Peter Langhorne, Cathie Sudlow, Peter Rothwell (2008). Stroke: Practical Management (3rd ed.). Wiley-Blackwell. ISBN 1-4051-2766-X. 

Study guide

Up to date as of January 14, 2010

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.

Contents

Epidemiology

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][3]

Risk factors for stroke include atherosclerosis, advanced age, hypertension (high blood pressure), diabetes mellitus, 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 Willis.

Etiology

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 tissue.

Ischemic Stroke

  • 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 diabetes mellitus. 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 Stroke

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 stroke.

Embolic Stroke

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).

Cardioembolic Stroke
  • 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 valve.
  • 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 brain.

Systemic hypoperfusion (Watershed stroke)

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.

Hemorrhagic stroke

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.[5] 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

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 hypertension, 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.[6]

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 from vascular malformations. Bleeding into the CSF from a ruptured aneurysm occurs very quickly, causing rapidly increased intracranial pressure. The initial bleed can be brief, but rebleeding is common. Death or deep coma ensues if the bleeding continues. SAH has a 37-45% mortality for patients 45 and older.[7][8]Cerebral aneurysms can be associated with other disorders, such as adult polycystic kidney disease.

Risk Factors

Many factors are generally agreed to cause a higher risk for a stroke.[9]

  • Previous stroke
  • Atherosclerosis: many of the risk factors listed below are also risk factors for atherosclerosis. Other marker for atherosclerosis include peripheral artery disease and coronary artery disease.
  • Hypertension is the most powerful risk factor for ischemic stroke, and the primary risk factor for intracerebral hemorrhagic stroke. [10][11]
  • Smoking: cigarette smoking significantly increases stroke risk, and the risk is dependent on the amount of smoking.[12] Cigar and pipe smoke also increase stroke risk but to a lesser degree.
  • Transient Ischemic Attack: Occurrence of TIA is a strong risk factor for stroke. In one study, 5% of patients with TIA developed stroke within 2 days, 10% within 90 days.[13] TIA should be considered a medical emergency; rapid response reduces the risk of stroke.
  • Atrial Fibrillation (AF): The average yearly risk for stroke in untreated AF is 5%, but can be as high as 12%.[14]
  • Diabetes mellitus: Diabetes is a major stroke risk.[15]
  • Age: the risk of stroke in adults increases significantly over the age of 55, and continues to increase thereafter.
  • Ethnicity: African Americans have twice the risk of a first stroke as whites.
  • Carotid stenosis (asymptomatic)
  • Cocaine: cocaine use is a significant risk for stroke and heart attack.
  • Blood disorders (e.g. sickle-cell disease, anti-cardiolipin syndrome)
  • Estrogen: recent studies have reported a small but significant increase in stroke risk in women receiving hormone replacement therapy (HRT). In one large study, it was reported that there was an approximate 37% increased risk for all types of strokes (95% confidence interval 9% to 73%). The observed risk for hemorrhagic stroke may have been reduced (64%) for estrogen-treated women, but the observed reduction was judged to be non-significant at the 95% confidence level. For ischemic stroke, estrogen-treated women had an observed 55% increased risk (95% confidence interval 19% to 101%). This equates to approximately 12 additional strokes per 10,000 person-years.[16]. The statistical significance of the reported increase in stroke risk has been disputed[17]. Oral contraceptive pills (OCPs) may confer some risk, especially when combined with other risks such as smoking, however the risk from the currently used low-dose OCPs is quite low.[18]
  • Pregnancy: there is a small but significant increase in stroke risk during, and just after pregnancy.

Symptoms

The symptoms of stroke depend on what part of the brain is affected. A friend or family member may be the first to notice. Symptoms can include:

  • Sudden numbness or weakness of the face, arm, or leg, especially one-sided
  • Sudden confusion, trouble speaking, or trouble understanding
  • Sudden trouble walking, dizziness, or loss of balance or coordination
  • Sudden trouble seeing in 1 or both eyes
  • Sudden severe headache
  • Difficulty swallowing or drooling

Diagnosis

A stroke is diagnosed first by a medical professional taking a proper history and physical exam. Addtional tests include:

  • Computed tomography (CT) scan
  • Magnetic resonance imaging (MRI)
  • Cerebral angiography

Treatment

Stroke is a medical emergency. Permanent neurologic damage or death can sometimes be avoided, but only if stroke is promptly diagnosed and treated.

Thrombolysis

Presentation to a specialized stroke center within 3 hours of the start of symptoms may allow for the reversal of the stroke by adminstration by clot-disolving medications, or thrombolytics. Tissue Plasminogen Activator (tPA) is the usual agent. Studies have shown that tPA given within 6 hours of the onset of stroke symptoms significantly reduces death and dependency, but there is a significant risk of bleeding, especially intracranial hemorrhage. If given within 3 hours, outcomes are improved, and risk is reduced.[19][20]

Prevention

Prevention of stroke involves reducing modifiable risk factors, and falls broadly into two categories: prevention of first stroke (primary prevention), and prevention of further strokes (secondary prevention). Also, some risk factors are modifiable (e.g. smoking), and some are not (e.g. age). Prevention, especially secondary prevention, involves certain medications.

Risk factor reduction

  • Keeping blood pressure below 120/80 reduces the risk of both primary and recurrent stroke, although in the elderly, lower blood pressures might increase the risk of myocardial infarction.[10][11]
  • Quitting smoking decreases risk significantly 2 years after quitting cigarettes.[12]
  • Transient ischemic attack (TIA) is a brief period of stroke symptoms, and is a warning sign of impending stroke. Seeking emergency medical attention reduces the risk of stroke after TIA.
  • The risk of stroke due to atrial fibrillation can be significantly reduced with the use of oral anticoagulants (i.e. warfarin).[21][22]
  • Diabetes is a major stroke risk factor. The role of good blood sugar control in the prevention of stroke in diabetics is still being investigated. Aggressive treatment of cholesterol and blood pressure in diabetics is essential. Certain medications help prevent strokes in diabetics.[23][24]
  • High Cholesterol: treatment of high cholesterol and other blood lipid disorders reduces the rate of first stroke and recurrent stroke. [25]

Medications

  • Aspirin
  • Plavix
  • Aggrenox
  • Warfarin
  • HMG-CoA reductase inhibitors (Statins)
  • Angiogensin converting enzyme (ACE) inhibitors

References

  1. Centers for Disease Control and Prevention (CDC). Prevalence of disabilities and associated health conditions among adults: United States, 1999. MMWR Morb Mortal Wkly Rep. 2001; 50: 120–125
  2. Circulation. 2007;115:e69-e171.
  3. http://circ.ahajournals.org/cgi/content/full/CIRCULATIONAHA.106.179918
  4. Robert G. Hart, MD Jonathan L. Halperin, MD. Atrial Fibrillation and Stroke Concepts and Controversies. Stroke. 2001;32:803.
  5. Goldman: Cecil Textbook of Medicine, 22nd ed., Copyright © 2004 W. B. Saunders Company
  6. Caplan LR (1992). "Intracerebral hemorrhage". Lancet 339 (8794): 656-8. PMID 1347346.  
  7. El-Saed A, Kuller LH, Newman AB, Lopez O, Costantino J, McTigue K, Cushman M, Kronmal R. Geographic variations in stroke incidence and mortality among older populations in four US communities. Stroke. 2006; 37: 1975–1979.
  8. Rosamond WD, Folsom AR, Chambless LE, Wang CH, McGovern PG, Howard G, Copper LS, Shahar E. Stroke incidence and survival among middle-aged adults: 9-year follow-up of the Atherosclerotic Risk in Communities (ARIC) Cohort. Stroke. 1999; 30: 736–743
  9. Goldstein LB. Adams R. Alberts MJ. Appel LJ. Brass LM. Bushnell CD. Culebras A. DeGraba TJ. Gorelick PB. Guyton JR. Hart RG. Howard G. Kelly-Hayes M. Nixon JV. Sacco RL. American Heart Association. American Stroke Association Stroke Council. Primary prevention of ischemic stroke: a guideline from the American Heart Association/American Stroke Association Stroke Council: cosponsored by the Atherosclerotic Peripheral Vascular Disease Interdisciplinary Working Group; Cardiovascular Nursing Council; Clinical Cardiology Council; Nutrition, Physical Activity, and Metabolism Council; and the Quality of Care and Outcomes Research Interdisciplinary Working Group. Circulation. 113(24):e873-923, 2006 Jun 20
  10. 10.0 10.1 ALLHAT Officers and Coordinators for the ALLHAT Collaborative Research Group. The Antihypertensive and Lipid-Lowering Treatment to Prevent Heart Attack Trial.Major outcomes in high-risk hypertensive patients randomized to angiotensin-converting enzyme inhibitor or calcium channel blocker vs diuretic: The Antihypertensive and Lipid-Lowering Treatment to Prevent Heart Attack Trial (ALLHAT).JAMA. 288(23):2981-97, 2002 Dec 18.
  11. 11.0 11.1 Seshadri S, Beiser A, Kelly-Hayes M, Kase CS, Au R, Kannel WB, Wolf PA. The lifetime risk of stroke: Estimates from the Framingham study. Stroke. 2006; 37: 345–350
  12. 12.0 12.1 Wolf PA, D’Agostino RB, Kannel WB, Bonita R, Belanger AJ. Cigarette smoking as a risk factor for stroke: the Framingham study. JAMA. 1988; 259: 1025–1029
  13. Johnston SC, Gress DR, Browner WS, Sidney S. Short-term prognosis after emergency department diagnosis of TIA. JAMA. 2000; 284: 2901–2906
  14. Hylek E. M., Go A. S., Chang Y., Jensvold N. G., Henault L. E., Selby J. V., Singer D. E. N Engl J Med 2003; 349:1019-1026, Sep 11, 2003
  15. Stroke in Patients With Diabetes and Hypertension. Samy I. McFarlane, MD, MPH, Domenic A. Sica, MD, James R. Sowers, MD. J Clin Hypertens (Greenwich). 2005;7(5):286-292.
  16. Hendrix SL, Wassertheil-Smoller S, Johnson KC, Howard BV, Kooperberg C, Rossouw JE, Trevisan M, Aragaki A, Baird AE, Bray PF, Buring JE, Criqui MH, Herrington D, Lynch JK, Rapp SR, Torner J, WHI investigators. Effects of conjugated equine estrogen on stroke in the Women’s Health Initiative. Circulation. 2006; 113: 2425–2434
  17. A critique of Women’s Health Initiative Studies (2002-2006) by James H. Clark in Nucl Recept Signal. 2006; 4: e023.
  18. Sasitorn Siritho, MD; Amanda G. Thrift, PhD; John J. McNeil, PhD; Roger X. You, PhD; Stephen M. Davis, MD Geoffrey A. Donnan, MD. Risk of Ischemic Stroke Among Users of the Oral Contraceptive Pill. The Melbourne Risk Factor Study (MERFS) Group. Stroke, Vol 22, 312-318
  19. Gregory W. Albers, MD; Wayne M. Clark, MD; Kenneth P. Madden, MD, PhD Scott A. Hamilton, PhD.ATLANTIS Trial:Results for Patients Treated Within 3 Hours of Stroke Onset 2002;33:493
  20. Joanna Wardlaw, Eivind Berge, Gergory delZoppo and Takenori Yamaguchi. Thrombolysis for acute ischemic stroke. Stroke. 2004;35:2914-2915.
  21. Stroke Prevention in Atrial Fibrillation Investigators. Stroke prevention in atrial fibrillation study: Final results. Circulation 1991; 84:527. Aspirin alone only minimally reduces stroke risk.
  22. Petersen, P, Boysen, G, Godtfredsen, J, et al. Placebo-controlled, randomized trial of warfarin and aspirin for prevention of thromboembolic complications in chronic atrial fibrillation. The Copenhagen AFASAK Study. Lancet 1989; 1:175.
  23. Timothy M. E. Davis, FRACP; Helen Millns, PhD; Irene M. Stratton, MSc; Rury R. Holman, FRCP; Robert C. Turner, MD, FRCP; for the UK Prospective Diabetes Study Group. Risk Factors for Stroke in Type 2 Diabetes Mellitus, United Kingdom Prospective Diabetes Study (UKPDS) 29.Arch Intern Med. 1999;159:1097-1103.
  24. PA Wolf, RB D'Agostino, AJ Belanger and WB Kannel Probability of stroke: a risk profile from the Framingham Study. Stroke, Vol 22, 312-318
  25. Blauw GJ, Lagaay AM, Smelt AH, Westendorp RG. (1997) Stroke, statins, and cholesterol. A meta-analysis of randomized, placebo-controlled, double-blind trials with HMG-CoA reductase inhibitors. Stroke May;28(5):946-50. PMID 9158630

External Links

  1. http://circ.ahajournals.org/cgi/content/full/CIRCULATIONAHA.106.179918
  2. http://www.cdc.gov/stroke/
  3. http://www.strokeassociation.org/presenter.jhtml?identifier=1200037
  4. http://www.nlm.nih.gov/medlineplus/ency/article/000726.htm

Further Reading

This article uses content that originally appeared in the Citizendium.


Simple English

Stroke can mean one of the following:

  • Stroke (medicine), a cerebral accident, when blood supply to a part of the brain is suddenly interrupted.
  • A sunstroke.
  • Stroke (Chinese character), in graphics of Chinese characters.
  • A single line without any break, see stroke order.
  • A different name for the typographical character known as slash.
  • Stroke (engines), a single action of some engines.
  • stroke (software), a port scanning utility.
  • Local Larne (Northern Ireland) Dialect meaning either to steal ex. to stroke an item, or to get one over on someone ex. "Ah, you were well stroked there."







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