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For other uses, see Stroke (disambiguation).
MCA Territory Infarct.svg
CT scan of the brain showing a right-hemispheric ischemic stroke.
Classification and external resources
ICD-10 I61-I64ner
ICD-9 434.91
OMIM 601367
DiseasesDB 2247
MedlinePlus 000726
Patient UK Stroke
MeSH D020521

Stroke, also known as cerebrovascular accident (CVA), cerebrovascular insult (CVI), or brain attack, is when poor blood flow to the brain results in cell death. There are two main types of stroke: ischemic due to lack of blood flow and hemorrhagic due to bleeding. They result in part of the brain not functioning properly.[1] Signs and symptoms of a stroke may include an inability to move or feel on one side of the body, problems understanding or speaking, feeling like the world is spinning, or loss of one vision to one side among others.[2][3] Signs and symptoms often appear soon after the stroke has occurred. If symptoms last less than one or two hours it is known as a transient ischemic attack (TIA).[3] Hemorrhagic strokes may also be associated with a severe headache.[3] The symptoms of a stroke can be permanent.[1] Long term complications may include pneumonia or loss of bladder control.[3]

The main risk factor for stroke is high blood pressure.[4] Other risk factors include tobacco smoking, obesity, high blood cholesterol, diabetes mellitus, previous TIA, and atrial fibrillation among others.[2][4] An ischemic stroke is typically caused by blockage of a blood vessel.[5] A hemorrhagic stroke is caused by bleeding either directly into the brain or into the space surrounding the brain.[5][6] Bleeding may occur due to a brain aneurysm.[5] Diagnosis is typically with medical imaging such as a CT scan or MRI scan along with a physical exam. Other tests such as an electrocardiogram (ECG) and blood tests are done to determine risk factors and rule out other possible causes. Low blood sugar may cause similar symptoms.[7]

Prevention includes decreasing risk factors as well as possibly aspirin, statins, surgery to open up the arteries to the brain in those with problematic narrowing, and warfarin in those with atrial fibrillation.[2] A stroke often requires emergency care.[1] An ischemic stroke, if detected within three to four and half hours, may be treatable with a medication that can break down the clot. Aspirin should be used. Some hemorrhagic strokes benefit from surgery. Treatment to try recover lost function is called stroke rehabilitation and ideally takes place in a stroke unit; however, these are not available in much of the world.[2]

In 2010 approximately 17 million people had a stroke and 33 million people had previously had a stroke and were still alive. Between 1990 and 2010 the number of strokes which occurred each year decreased by approximately 10% in the developed world and increased by 10% in the developing world.[8] In 2013, stroke was the second most frequent cause of death after coronary artery disease, accounting for 6.4 million deaths (12% of the total).[9] About 3.3 million deaths resulted from ischemic stroke while 3.2 million deaths resulted from hemorrhagic stroke.[9] About half of people who have had a stroke live less than one year.[2] Overall, two thirds of strokes occurred in those over 65 years old.[8]








  3. Systemic hypoperfusion (general decrease in blood supply, e.g., in shock)[13]
  4. Venous thrombosis.[14]





An intracranial hemorrhage is the accumulation of blood anywhere within the cranial vault. The main types of intracranial 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).

A cerebral hemorrhage is bleeding within the brain tissue. A cerebral hemorrhage can be due to either intraparenchymal hemorrhage or intraventricular hemorrhage (blood in the ventricular system). Most of the hemorrhagic stroke syndromes have specific symptoms particularly headaches, or have evidence of a previous head injury).

Signs and symptoms


Early recognition

Various systems have been proposed to increase recognition of stroke. Different findings are able to predict the presence or absence of stroke to different degrees. Sudden-onset face weakness, arm drift (i.e., 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 increasing the likelihood by 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).[20] 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),[21] as advocated by the Department of Health (United Kingdom) and the Stroke Association, the American Stroke Association, the National Stroke Association (US), the Los Angeles Prehospital Stroke Screen (LAPSS)[22] and the Cincinnati Prehospital Stroke Scale (CPSS).[23] Use of these scales is recommended by professional guidelines.[24]






  • 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



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

Associated symptoms




Thrombotic 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 cause of death in people under 20 with sickle-cell anemia.[31] Air pollution may also increase stroke risk.[32]

Embolic stroke




Causes of stroke related to the heart can be distinguished between high and low-risk:[34]

Cerebral hypoperfusion

Cerebral hypoperfusion is the reduction of blood flow to all parts of the body. It is most commonly due to heart failure from cardiac arrest or arrhythmias, or from reduced cardiac output as a result of myocardial infarction, pulmonary embolism, pericardial effusion, or bleeding.[citation needed] 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 vulnerable "watershed" areas - border zone regions supplied by the major cerebral arteries. A watershed stroke refers to the condition when blood supply to these areas is compromised. Blood flow to these areas does not necessarily stop, but instead it may lessen to the point where brain damage can occur.

Venous thrombosis


Intracerebral hemorrhage


Silent stroke

A silent stroke is a stroke that does not have any outward symptoms, and the patients are typically unaware they have had a stroke. Despite not causing identifiable symptoms, a silent stroke still damages the brain, and places the patient at increased risk for both transient ischemic attack and major stroke in the future. Conversely, those who have had a major stroke are also at risk of having silent strokes.[36] In a broad study in 1998, more than 11 million people were estimated to have experienced a stroke in the United States. Approximately 770,000 of these strokes were symptomatic and 11 million were first-ever silent MRI infarcts or hemorrhages. Silent strokes typically cause lesions which are detected via the use of neuroimaging such as MRI. Silent strokes are estimated to occur at five times the rate of symptomatic strokes.[37][38] The risk of silent stroke increases with age, but may also affect younger adults and children, especially those with acute anemia.[37][39]




Ischemic stroke occurs because of a loss of blood supply to part of the brain, initiating the ischemic cascade.[40] 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 fibrinolytics such as alteplase 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.[41] 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, break off, enter the cerebral circulation, then lodge in and block brain blood vessels. Since blood vessels in the brain are now blocked, the brain becomes low in energy, and thus it resorts into using anaerobic metabolism within the region of brain tissue affected by ischemia. Anaerobic metabolism produces less adenosine triphosphate (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-base balance in the brain. The ischemia area is referred to as the "ischemic penumbra".[42]






Bleeding within the skull cavity can occur from various causes. Subdural and epidural bleeding mostly are the result of trauma.[45] Hemorrhagic strokes arise from bleeding within the brain parenchyma or intraventricular spaces, and are classified based on their underlying pathology. Some examples of hemorrhagic stroke are hypertensive hemorrhage, ruptured aneurysm, ruptured AV fistula, transformation of prior ischemic infarction, and drug induced bleeding.[46] They 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.[31][47] Inflammation contributes to the secondary brain injury after hemorrhage.[47]




Physical examination



For diagnosing ischemic stroke in the emergency setting:[49]

  • 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.[50]


Underlying cause




Given the disease burden of strokes, prevention is an important public health concern.[51] Primary prevention is less effective than secondary prevention (as judged by the number needed to treat to prevent one stroke per year).[51] Recent guidelines detail the evidence for primary prevention in stroke.[52] In those who are otherwise healthy, aspirin does not appear beneficial and thus is not recommended.[53] In people who have had a myocardial infarction or those with a high cardiovascular risk, it provides some protection against a first stroke.[54][55] In those who have previously had a stroke, treatment with medications such as aspirin, clopidogrel and dipyridamole may be beneficial.[54] The U.S. Preventive Services Task Force (USPSTF) recommends against screening for carotid artery stenosis in those without symptoms.[56]

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[57][58]). Other modifiable risk factors include high blood cholesterol levels, diabetes mellitus, cigarette smoking[59][60] (active and passive), heavy alcohol consumption[61] and drug use,[62] lack of physical activity, obesity, processed red meat consumption[63] and unhealthy diet.[64] 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).[65] Drugs, most commonly amphetamines and cocaine, can induce stroke through damage to the blood vessels in the brain and/or acute hypertension.[66][67]

No high-quality studies have shown the effectiveness of interventions aimed at weight reduction, promotion of regular exercise, reducing alcohol consumption or smoking cessation.[68] Nonetheless, given the large body of circumstantial evidence, best medical management for stroke includes advice on diet, exercise, smoking and alcohol use.[69] 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 (high blood pressure) accounts for 35-50% of stroke risk.[70] Blood pressure reduction of 10 mmHg systolic or 5 mmHg diastolic reduces the risk of stroke by ~40%.[71] Lowering blood pressure has been conclusively shown to prevent both ischemic and hemorrhagic strokes.[72][73] It is equally important in secondary prevention.[74] Even patients older than 80 years and those with isolated systolic hypertension benefit from antihypertensive therapy.[75][76][77] 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 and cost should be considered.[78][79] The routine use of beta-blockers following a stroke or TIA has not been shown to result in benefits.[80]

Blood lipids

High cholesterol levels have been inconsistently associated with (ischemic) stroke.[73][81] Statins have been shown to reduce the risk of stroke by about 15%.[82] Since earlier meta-analyses of other lipid-lowering drugs did not show a decreased risk,[83] statins might exert their effect through mechanisms other than their lipid-lowering effects.[82]

Diabetes mellitus


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.[54] 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.[86] Thienopyridines (clopidogrel, ticlopidine) "might be slightly more effective" than aspirin and have a decreased risk of gastrointestinal bleeding, but are more expensive.[87] Their exact role remains controversial. Ticlopidine is associated with higher rates of skin rash, diarrhea, low blood neutrophil count and thrombotic thrombocytopenic purpura.[87] Dipyridamole can be added to aspirin therapy to provide a small additional benefit, even though headache is a common side effect.[88] Low-dose aspirin is also effective for stroke prevention after having a myocardial infarction.[55]

Those with atrial fibrillation have a 5% a year risk of stroke, and this risk is higher in those with valvular atrial fibrillation.[89] Depending on the stroke risk, anticoagulation with medications such as warfarin or aspirin is useful for prevention.[90] Except in people with atrial fibrillation, oral anticoagulants are not advised for stroke prevention —any benefit is offset by bleeding risk.[91]

In primary prevention however, antiplatelet drugs did not reduce the risk of ischemic stroke but increased the risk of major bleeding.[92][93] Further studies are needed to investigate a possible protective effect of aspirin against ischemic stroke in women.[94][95]


Carotid endarterectomy or carotid angioplasty can be used to remove atherosclerotic narrowing (stenosis) of the carotid artery. There is evidence supporting this procedure in selected cases.[69] Endarterectomy for a significant stenosis has been shown to be useful in the prevention of further strokes in those who have already had one.[96] Carotid artery stenting has not been shown to be equally useful.[97][98] Patients are selected for surgery based on age, gender, degree of stenosis, time since symptoms and patients' preferences.[69] 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.[99][100]

Screening for carotid artery narrowing has not been shown to be a useful screening test in the general population.[101] Studies of surgical intervention for carotid artery stenosis without symptoms have shown only a small decrease in the risk of stroke.[102][103] 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.[69]


Nutrition, specifically the Mediterranean-style diet, has the potential for decreasing the risk of having a stroke by more than half.[104] It does not appear that lowering levels of homocysteine with folic acid affects the risk of stroke.[105][106]



Previous stroke or TIA

Keeping blood pressure below 140/90 mmHg is recommended.[108] Anticoagulation can prevent recurrent ischemic strokes. Among people with nonvalvular atrial fibrillation, anticoagulation can reduce stroke by 60% while antiplatelet agents can reduce stroke by 20%.[109] However, a recent meta-analysis suggests harm from anti-coagulation started early after an embolic stroke.[110] Stroke prevention treatment for atrial fibrillation is determined according to the CHADS/CHADS2 system. The most widely used anticoagulant to prevent thromboembolic stroke in patients with nonvalvular atrial fibrillation is the oral agent warfarin while a number of newer agents including dabigatran are alternatives which do not require prothrombin time monitoring.[108]

Anticoagulants, when used following stroke, should not be stopped for dental procedures.[111]

If studies show carotid stenosis, and the person 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.


Ischemic stroke

Definitive therapy is aimed at removing the blockage by breaking the clot down (thrombolysis), or by removing it mechanically (thrombectomy). The philosophical premise underlying the importance of rapid stroke intervention was crystallized as Time is Brain! in the early 1990s.[112] Years later, that same idea, that rapid cerebral blood flow restoration results in fewer brain cells dying, has been proved and quantified.[113]

Tight blood sugar control in the first few hours does not improve outcomes and may cause harm.[114] High blood pressure is also not typically lowered as this has not been found to be helpful.[115]


Thrombolysis, such as with recombinant tissue plasminogen activator (rtPA), in acute ischemic stroke, when given within three hours of symptom onset results in an overall benefit of 10% with respect to living without disability.[116][117] It does not, however, improve chances of survival.[116] Benefit is greater the earlier it is used.[118] Between three and four and a half hours the effects are less clear.[119][120][121] A 2014 review found a 5% increase in the number of people living without disability at three to six months; however, there was a 2% increased risk of death in the short term.[117] After four and a half hours thrombolysis worsens outcomes.[119] These benefits or lack of benefits occurred regardless of the age of the person treated.[122] There is no reliable way to determine who will have an intracranial hemorrhage post treatment versus who will not.[123]

Its use 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[124] which showed that tPA improves the chances for a good neurological outcome. When administered within the first three hours thrombolysis improves functional outcome without affecting mortality.[125] 6.4% of people with large strokes developed substantial brain hemorrhage as a complication from being given tPA thus part of the reason for increased short term mortality.[126] Additionally, the American Academy of Emergency Medicine states 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.[127] Intra-arterial fibrinolysis, where a catheter is passed up an artery into the brain and the medication is injected at the site of thrombosis, has been found to improve outcomes in people with acute ischemic stroke.[128]


Large territory strokes can cause significant brain swelling with secondary brain injury in surrounding tissue. This phenomenon is mainly encountered in strokes of the middle cerebral artery territory, and is also called "malignant cerebral infarction" because it carries a dismal prognosis. Relief of the pressure may be attempted with medication, but some require hemicraniectomy, the temporary surgical removal of the skull on one side of the head. This decreases the risk of death, although some more people survive with disability who would otherwise have died.[129]

Hemorrhagic stroke

People 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. People are monitored for changes in the level of consciousness, and their blood pressure, blood sugar, and oxygenation are kept at optimum levels.[citation needed]

Stroke unit





A rehabilitation team is usually multidisciplinary as it involves staff with different skills working together to help the patient. These include physicians trained in rehabilitation medicine, clinical pharmacists, nursing staff, physiotherapists, occupational therapists, speech and language therapists, and orthotists. Some teams may also include psychologists and social workers, since at least one third of the people 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.


For most people with stroke, physical therapy (PT), occupational therapy (OT) and speech-language pathology (SLP) are the cornerstones of the rehabilitation process. Often, assistive technology such as wheelchairs, walkers and canes may be beneficial. Many mobility problems can be improved by the use of ankle foot orthoses.[131] PT and OT have overlapping areas of expertise, however PT focuses on joint range of motion and strength by performing exercises and re-learning functional tasks such as bed mobility, transferring, walking and other gross motor functions. Physiotherapists can also work with patients to improve awareness and use of the hemiplegic side. Rehabilitation involves working on the ability to produce strong movements or the ability to perform tasks using normal patterns. Emphasis is often concentrated on functional tasks and patient’s goals. One example physiotherapists employ to promote motor learning involves constraint-induced movement therapy. Through continuous practice the patient relearns to use and adapt the hemiplegic limb during functional activities to create lasting permanent changes.[132] OT is involved in 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 the speech production disorders: dysarthria[133] and apraxia of speech,[134] aphasia,[135] cognitive-communication impairments and/or dysphagia (problems with swallowing).


Treatment of spasticity related to stroke often involves early mobilizations, commonly performed by a physiotherapist, combined with elongation of spastic muscles and sustained stretching through various positionings.[26] Gaining initial improvement in range of motion is often achieved through rhythmic rotational patterns associated with the affected limb.[26] After full range has been achieved by the therapist, the limb should be positioned in the lengthened positions to prevent against further contractures, skin breakdown, and disuse of the limb with the use of splints or other tools to stabilize the joint.[26] Cold in the form of ice wraps or ice packs have been proven to briefly reduce spasticity by temporarily dampening neural firing rates.[26] Electrical stimulation to the antagonist muscles or vibrations has also been used with some success.[26]


Some current and future therapy methods include the use of virtual reality and video games for rehabilitation. These forms of rehabilitation offer potential for motivating patients to perform specific therapy tasks that many other forms do not.[136] Many clinics and hospitals are adopting the use of these off-the-shelf devices for exercise, social interaction and rehabilitation because they are affordable, accessible and can be used within the clinic and home.[136]

Other novel non-invasive rehabilitation methods are currently being developed to augment physical therapy to improve motor function of stroke patients, such as transcranial magnetic stimulation (TMS) and transcranial direct-current stimulation (tDCS)[137] and robotic therapies.[138]

A stroke can also reduce people's general fitness.[139] Reduced fitness can reduce capacity for rehabilitation as well as general health.[140] A systematic review found that there are inadequate long-term data about the effects of exercise and training on death, dependence and disability after a stroke.[139] However, cardiorespiratory training added to walking programs in rehabilitation can improve speed, tolerance and independence during walking.[139]


Disability affects 75% of stroke survivors enough to decrease their employability.[141] Stroke can affect people physically, mentally, emotionally, or a combination of the three. The results of stroke vary widely depending on size and location of the lesion.[142] Dysfunctions correspond to areas in the brain that have been damaged.



Disruption in self-identity, relationships with others, and emotional well-being can lead to social consequences after stroke due to the lack of ability to communicate. Many people who experience communication impairments after a stroke find it more difficult to cope with the social issues rather than physical impairments. Broader aspects of care must address the emotional impact speech impairment has on those who experience difficulties with speech after a stroke.[144] Those who experience a stroke are at risk for paralysis which could result in a self disturbed body image which may also lead to other social issues.[145]

30 to 50% of stroke survivors suffer post-stroke depression, which is characterized by lethargy, irritability, sleep disturbances, lowered self-esteem and withdrawal.[146] Depression can reduce motivation and worsen outcome, but can be treated with antidepressants.

Emotional lability, another consequence of stroke, causes the person 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 person's actual emotions, a more severe form of emotional lability causes the affected person to laugh and cry pathologically, without regard to context or emotion.[141] Some people show the opposite of what they feel, for example crying when they are happy.[147] Emotional lability occurs in about 20% of those who have had a stroke.

Cognitive deficits resulting from stroke include perceptual disorders, aphasia,[148] dementia,[149] and problems with attention[150] and memory.[151] A stroke sufferer may be unaware of his or her own disabilities, a condition called anosognosia. In a condition called hemispatial neglect, the affected person is unable to attend to anything on the side of space opposite to the damaged hemisphere.




Disability-adjusted life year for cerebral vascular disease per 100,000 inhabitants in 2004.[155]
  no data

Stroke was the second most frequent cause of death worldwide in 2011, accounting for 6.2 million deaths (~11% of the total).[156] Approximately 17 million people had a stroke in 2010 and 33 million people have previously had a stroke and were still alive.[8] Between 1990 and 2010 the number of strokes decrease by approximately 10% in the developed world and increased by 10% in the developing world.[8] Overall, two thirds of strokes occurred in those over 65 years old.[8] South Asians are at particularly high risk for stroke, accounting for 40% of global stroke deaths.[157]

It is ranked after heart disease and before cancer.[2] In the United States stroke is a leading cause of disability, and recently declined from the third leading to the fourth leading cause of death.[158] 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.[159] 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.[31][146] 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 childhood.

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.[160] 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,[31] yet 60% of deaths from stroke occur in women.[147] Since women live longer, they are older on average when they have their strokes and thus more often killed.[31] Some risk factors for stroke apply only to women. Primary among these are pregnancy, childbirth, menopause, and the treatment thereof (HRT).



Episodes of stroke and familial stroke have been reported from the 2nd millennium BC onward in ancient Mesopotamia and Persia.[161] 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.[162][163] The word stroke was used as a synonym for apoplectic seizure as early as 1599,[164] 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.[31][162] Wepfer also identified the main arteries supplying the brain, the vertebral and carotid arteries, and identified the cause of a type of ischemic stroke known as a cerebral infarction when he suggested that apoplexy might be caused by a blockage to those vessels.[31] Rudolf Virchow first described the mechanism of thromboembolism as a major factor.[165]

The term cerebrovascular accident was introduced in 1927, reflecting a "growing awareness and acceptance of vascular theories and (...) recognition of the consequences of a sudden disruption in the vascular supply of the brain".[166] Its use is now discouraged by a number of neurology textbooks, reasoning that the connotation of fortuitousness carried by the word accident insufficiently highlights the modifiability of the underlying risk factors.[167][168][169] Cerebrovascular insult may be used interchangeably.[170]

The term brain attack was introduced for use to underline the acute nature of stroke according to the American Stroke Association,[170] who since 1990 have used the term,[171] and is used colloquially to refer to both ischemic as well as hemorrhagic stroke.[172]


Angioplasty and stenting

Angioplasty and stenting have begun to be looked at as possible viable options in treatment of acute ischemic stroke. 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 randomized controlled trial is needed to more completely evaluate the possible therapeutic advantage of this preventative measure.[173]

Mechanical thrombectomy

Removal of the clot may be attempted in those where it occurs within a large blood vessel and may be an option for those who either are not eligible for or do not improve with intravenous thrombolytics.[174] Significant complications occur in about 7%.[175]


Drugs that scavenge reactive oxygen species, inhibit programmed cell death, or inhibit excitatory neurotransmitters have been shown experimentally to reduce tissue injury caused by 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 phenylbutylnitrone, is reported to be neuroprotective in stroke.[176] 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.[31] Benefit of NXY-059 is questionable.[177]

Hyperbaric oxygen therapy has been studied as a possible protective measure, but is currently not thought to be beneficial.[178]

See also


  1. ^ a b c "What Is a Stroke?". March 26, 2014. Retrieved 26 February 2015. 
  2. ^ a b c d e f g h i j k l m Donnan GA, Fisher M, Macleod M, Davis SM (May 2008). "Stroke". Lancet 371 (9624): 1612–23. doi:10.1016/S0140-6736(08)60694-7. PMID 18468545. 
  3. ^ a b c d "What Are the Signs and Symptoms of a Stroke?". March 26, 2014. Retrieved 27 February 2015. 
  4. ^ a b "Who Is at Risk for a Stroke?". March 26, 2014. Retrieved 27 February 2015. 
  5. ^ a b c "Types of Stroke". March 26, 2014. Retrieved 27 February 2015. 
  6. ^ Feigin VL, Rinkel GJ, Lawes CM, Algra A, Bennett DA, van Gijn J, Anderson CS (2005). "Risk factors for subarachnoid hemorrhage: an updated systematic review of epidemiological studies". Stroke 36 (12): 2773–80. doi:10.1161/01.STR.0000190838.02954.e8. PMID 16282541. 
  7. ^ "How Is a Stroke Diagnosed?". March 26, 2014. Retrieved 27 February 2015. 
  8. ^ a b c d e Feigin VL, Forouzanfar MH, Krishnamurthi R, Mensah GA, Connor M, Bennett DA, Moran AE, Sacco RL, Anderson L, Truelsen T, O'Donnell M, Venketasubramanian N, Barker-Collo S, Lawes CM, Wang W, Shinohara Y, Witt E, Ezzati M, Naghavi M, Murray C (2014). "Global and regional burden of stroke during 1990-2010: findings from the Global Burden of Disease Study 2010". Lancet 383 (9913): 245–54. doi:10.1016/S0140-6736(13)61953-4. PMID 24449944. 
  11. ^ World Health Organisation (1978). Cerebrovascular Disorders (Offset Publications). Geneva: World Health Organization. ISBN 92-4-170043-2. OCLC 4757533. 
  13. ^ Shuaib A, Hachinski VC (September 1991). "Mechanisms and management of stroke in the elderly". CMAJ 145 (5): 433–43. PMC 1335826. PMID 1878825. 
  19. ^ Osterweil,, Neil. "Methamphetamine induced ischemic strokes". Medpagetoday. Retrieved 24 August 2013. 
  27. ^ "Thrombus". MedlinePlus. U.S. National Library of Medicine. 
  28. ^ "Circle of Willis". The Internet Stroke Center. 
  29. ^ "Brain anaurysm - Introduction". NHS Choices. 
  30. ^ Fisher CM (1968-12-18). "The arterial lesions underlying lacunes". Acta Neuropathologica 12 (1): 1–15. doi:10.1007/BF00685305. PMID 5708546. 
  31. ^ a b c d e f g h National Institute of Neurological Disorders and Stroke (NINDS) (1999). "Stroke: Hope Through Research". National Institutes of Health. 
  32. ^ Shah, A. S. V.; Lee, K. K.; McAllister, D. A.; Hunter, A.; Nair, H.; Whiteley, W.; Langrish, J. P.; Newby, D. E.; Mills, N. L. (24 March 2015). "Short term exposure to air pollution and stroke: systematic review and meta-analysis". BMJ 350 (mar23 11): h1295–h1295. doi:10.1136/bmj.h1295. 
  33. ^ a b Robbins and Cotran Pathologic Basis of Disease, Professional Edition. (8th ed. ed.). Philadelphia, Pa: Elsevier. 2009. ISBN 978-1-4377-0792-2.  |first1= missing |last1= in Authors list (help)
  35. ^ "Hypertension". 
  36. ^ Miwa K, Hoshi T, Hougaku H, Tanaka M, Furukado S, Abe Y, Okazaki S, Sakaguchi M, Sakoda S, Kitagawa K (2010). "Silent cerebral infarction is associated with incident stroke and TIA independent of carotid intima-media thickness". Intern. Med. 49 (9): 817–22. doi:10.2169/internalmedicine.49.3211. PMID 20453400. 
  37. ^ a b Herderscheê D, Hijdra A, Algra A, Koudstaal PJ, Kappelle LJ, van Gijn J (September 1992). "Silent stroke in patients with transient ischemic attack or minor ischemic stroke. The Dutch TIA Trial Study Group". Stroke 23 (9): 1220–4. doi:10.1161/01.STR.23.9.1220. PMID 1519274. 
  38. ^ Leary MC, Saver JL (2003). "Annual incidence of first silent stroke in the United States: a preliminary estimate". Cerebrovasc. Dis. 16 (3): 280–5. doi:10.1159/000071128. PMID 12865617. 
  39. ^ Vermeer SE, Koudstaal PJ, Oudkerk M, Hofman A, Breteler MM (January 2002). "Prevalence and risk factors of silent brain infarcts in the population-based Rotterdam Scan Study". Stroke 33 (1): 21–5. doi:10.1161/hs0102.101629. PMID 11779883. 
  40. ^ Deb P, Sharma S, Hassan KM (June 2010). "Pathophysiologic mechanisms of acute ischemic stroke: An overview with emphasis on therapeutic significance beyond thrombolysis". Pathophysiology : the official journal of the International Society for Pathophysiology / ISP 17 (3): 197–218. doi:10.1016/j.pathophys.2009.12.001. PMID 20074922. 
  41. ^ Richard S. Snell (2006). Clinical neuroanatomy, 6. ed. Lippincott Williams & Wilkins, Philadelphia. pp. 478–485. ISBN 978-963-226-293-2. 
  42. ^ Brunner and Suddarth's Textbook on Medical-Surgical Nursing, 11th Edition
  43. ^ Kristián, T; Siesjö, BK (1996). "Calcium-related damage in ischemia.". Life sciences 59 (5-6): 357–67. PMID 8761323. 
  44. ^ Chan, PH (January 2001). "Reactive oxygen radicals in signaling and damage in the ischemic brain.". Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism 21 (1): 2–14. PMID 11149664. 
  45. ^ Longo, ed. Dan L. Longo ... [et et al. (2012). Harrison's principles of internal medicine. (18th ed. ed.). New York: McGraw-Hill. pp. Chapter 370. ISBN 978-0071748896. 
  53. ^ "Use of Aspirin for Primary Prevention of Heart Attack and Stroke". FDA. 05/02/2014. Retrieved 11 June 2014.  Check date values in: |date= (help)
  56. ^ Jonas, Daniel E.; Feltner, Cynthia; Amick, Halle R.; Sheridan, Stacey; Zheng, Zhi-Jie; Watford, Daniel J.; Carter, Jamie L.; Rowe, Cassandra J.; Harris, Russell (Jul 8, 2014). "Screening for Asymptomatic Carotid Artery Stenosis: A Systematic Review and Meta-analysis for the U.S. Preventive Services Task Force.". Annals of internal medicine 161: 336. doi:10.7326/M14-0530. PMID 25004169. 
  57. ^ Medical Research Council Working Party (July 1985). "MRC trial of treatment of mild hypertension: principal results". British Medical Journal 291 (6488): 97–104. doi:10.1136/bmj.291.6488.97. PMC 1416260. PMID 2861880. 
  62. ^ Sloan MA, Kittner SJ, Rigamonti D, Price TR (September 1991). "Occurrence of stroke associated with use/abuse of drugs". Neurology 41 (9): 1358–64. doi:10.1212/WNL.41.9.1358. PMID 1891081. 
  63. ^ Larsson SC, Virtamo J, Wolk A (2011). "Red meat consumption and risk of stroke in Swedish men". American Journal of Clinical Nutrition 94 (2): 417–421. doi:10.3945/ajcn.111.015115. PMID 21653800. 
  64. ^ "Stroke Risk Factors". American Heart Association. 2007. Retrieved January 22, 2007. 
  65. ^ Gorelick PB (1987). "Alcohol and stroke". Stroke; a Journal of Cerebral Circulation 18 (1): 268–71. doi:10.1161/01.STR.18.1.268. PMID 3810763. 
  70. ^ Whisnant JP (1996). "Effectiveness versus efficacy of treatment of hypertension for stroke prevention". Neurology 46 (2): 301–7. doi:10.1212/WNL.46.2.301. PMID 8614485. 
  71. ^ Law MR, Morris JK, Wald NJ (May 19, 2009). "Use of blood pressure lowering drugs in the prevention of cardiovascular disease: meta-analysis of 147 randomised trials in the context of expectations from prospective epidemiological studies". BMJ (Clinical research ed.) 338: b1665. doi:10.1136/bmj.b1665. PMC 2684577. PMID 19454737. 
  72. ^ Psaty BM, Lumley T, Furberg CD, Schellenbaum G, Pahor M, Alderman MH, Weiss NS (2003). "Health outcomes associated with various antihypertensive therapies used as first-line agents: a network meta-analysis". JAMA 289 (19): 2534–44. doi:10.1001/jama.289.19.2534. PMID 12759325. 
  73. ^ a b "Cholesterol, diastolic blood pressure, and stroke: 13,000 strokes in 450,000 people in 45 prospective cohorts. Prospective studies collaboration". Lancet 346 (8991–8992): 1647–53. 1995. doi:10.1016/S0140-6736(95)92836-7. PMID 8551820. 
  74. ^ Gueyffier F, Boissel JP, Boutitie F, Pocock S, Coope J, Cutler J, Ekbom T, Fagard R, Friedman L, Kerlikowske K, Perry M, Prineas R, Schron E (1997). "Effect of antihypertensive treatment in patients having already suffered from stroke. Gathering the evidence. The INDANA (INdividual Data ANalysis of Antihypertensive intervention trials) Project Collaborators". Stroke 28 (12): 2557–62. doi:10.1161/01.STR.28.12.2557. PMID 9412649. 
  75. ^ Gueyffier F, Bulpitt C, Boissel JP, Schron E, Ekbom T, Fagard R, Casiglia E, Kerlikowske K, Coope J (1999). "Antihypertensive drugs in very old people: a subgroup meta-analysis of randomised controlled trials. INDANA Group". Lancet 353 (9155): 793–6. doi:10.1016/S0140-6736(98)08127-6. PMID 10459960. 
  76. ^ Staessen JA, Gasowski J, Wang JG, Thijs L, Den Hond E, Boissel JP, Coope J, Ekbom T, Gueyffier F, Liu L, Kerlikowske K, Pocock S, Fagard RH (2000). "Risks of untreated and treated isolated systolic hypertension in the elderly: meta-analysis of outcome trials". Lancet 355 (9207): 865–72. doi:10.1016/S0140-6736(99)07330-4. PMID 10752701. 
  77. ^ Beckett NS, Peters R, Fletcher AE, Staessen JA, Liu L, Dumitrascu D, Stoyanovsky V, Antikainen RL, Nikitin Y, Anderson C, Belhani A, Forette F, Rajkumar C, Thijs L, Banya W, Bulpitt CJ (2008). "Treatment of Hypertension in Patients 80 Years of Age or Older". N. Engl. J. Med. 358 (18): 1887–98. doi:10.1056/NEJMoa0801369. PMID 18378519. 
  80. ^ De Lima, LG; Saconato, H; Atallah, AN; da Silva, EM (Oct 15, 2014). "Beta-blockers for preventing stroke recurrence.". The Cochrane database of systematic reviews 10: CD007890. doi:10.1002/14651858.CD007890.pub3. PMID 25317988. 
  87. ^ a b Hankey GJ, Sudlow CL, Dunbabin DW (2000). Hankey, Graeme, ed. "Thienopyridine derivatives (ticlopidine, clopidogrel) versus aspirin for preventing stroke and other serious vascular events in high vascular risk patients". Cochrane Database Syst Rev (2): CD001246. doi:10.1002/14651858.CD001246. PMID 10796426. 
  96. ^ Rothwell PM, Eliasziw M, Gutnikov SA, Fox AJ, Taylor DW, Mayberg MR, Warlow CP, Barnett HJ (2003). "Analysis of pooled data from the randomised controlled trials of endarterectomy for symptomatic carotid stenosis". Lancet 361 (9352): 107–16. doi:10.1016/S0140-6736(03)12228-3. PMID 12531577. 
  98. ^ Ederle J, Featherstone RL, Brown MM (2007). Brown, Martin M, ed. "Percutaneous transluminal angioplasty and stenting for carotid artery stenosis". Cochrane Database Syst Rev (4): CD000515. doi:10.1002/14651858.CD000515.pub3. PMID 17943745. 
  101. ^ U.S. Preventive Services Task Force (2007). "Screening for carotid artery stenosis: U.S. Preventive Services Task Force recommendation statement". Ann. Intern. Med. 147 (12): 854–9. doi:10.7326/0003-4819-147-12-200712180-00005. PMID 18087056. 
  103. ^ Chambers BR, Donnan GA (2005). Chambers, Brian R, ed. "Carotid endarterectomy for asymptomatic carotid stenosis". Cochrane Database Syst Rev (4): CD001923. doi:10.1002/14651858.CD001923.pub2. PMID 16235289. 
  104. ^ Spence JD (2006). "Nutrition and stroke prevention". Stroke; a Journal of Cerebral Circulation 37 (9): 2430–5. doi:10.1161/ PMID 16873712. 
  105. ^ Zhou YH, Tang JY, Wu MJ, Lu J, Wei X, Qin YY, Wang C, Xu JF, He J (2011). Wright, James M, ed. "Effect of folic acid supplementation on cardiovascular outcomes: a systematic review and meta-analysis". PLoS ONE 6 (9): e25142. Bibcode:2011PLoSO...625142Z. doi:10.1371/journal.pone.0025142. PMC 3182189. PMID 21980387. 
  106. ^ Clarke R, Halsey J, Lewington S, Lonn E, Armitage J, Manson JE, Bønaa KH, Spence JD, Nygård O, Jamison R, Gaziano JM, Guarino P, Bennett D, Mir F, Peto R, Collins R (Oct 11, 2010). "Effects of lowering homocysteine levels with B vitamins on cardiovascular disease, cancer, and cause-specific mortality: Meta-analysis of 8 randomized trials involving 37 485 individuals". Archives of Internal Medicine 170 (18): 1622–31. doi:10.1001/archinternmed.2010.348. PMID 20937919. 
  107. ^ Bushnell C, McCullough LD, Awad IA, Chireau MV, Fedder WN, Furie KL, Howard VJ, Lichtman JH, Lisabeth LD, Piña IL, Reeves MJ, Rexrode KM, Saposnik G, Singh V, Towfighi A, Vaccarino V, Walters MR (2014). "Guidelines for the prevention of stroke in women: a statement for healthcare professionals from the American Heart Association/American Stroke Association". Stroke; a Journal of Cerebral Circulation 45 (5): 1545–88. doi:10.1161/01.str.0000442009.06663.48. PMID 24503673. 
  108. ^ a b Kernan WN, Ovbiagele B, Black HR, Bravata DM, Chimowitz MI, Ezekowitz MD, Fang MC, Fisher M, Furie KL, Heck DV, Johnston SC, Kasner SE, Kittner SJ, Mitchell PH, Rich MW, Richardson D, Schwamm LH, Wilson JA (May 1, 2014). "Guidelines for the Prevention of Stroke in Patients With Stroke and Transient Ischemic Attack: A Guideline for Healthcare Professionals From the American Heart Association/American Stroke Association.". Stroke; a journal of cerebral circulation 45 (7): 2160–236. doi:10.1161/STR.0000000000000024. PMID 24788967. 
  109. ^ 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. doi:10.7326/0003-4819-146-12-200706190-00007. PMID 17577005. 
  111. ^ Armstrong MJ, Gronseth G, Anderson DC, Biller J, Cucchiara B, Dafer R, Goldstein LB, Schneck M, Messé SR (May 28, 2013). "Summary of evidence-based guideline: Periprocedural management of antithrombotic medications in patients with ischemic cerebrovascular disease: Report of the Guideline Development Subcommittee of the American Academy of Neurology". Neurology 80 (22): 2065–2069. doi:10.1212/WNL.0b013e318294b32d. PMC 3716407. PMID 23713086. 
  112. ^ Gomez CR: Time is Brain! J Stroke and Cerebrovasc Dis 3:1-2. 1993, additional Time
  113. ^ Saver JL (2006). "Time is brain - quantified". Stroke 37 (1): 263–6. doi:10.1161/01.STR.0000196957.55928.ab. PMID 16339467. 
  114. ^ Bellolio MF, Gilmore RM, Stead LG (2011-09-07). Bellolio, M Fernanda, ed. "Insulin for glycaemic control in acute ischaemic stroke". Cochrane database of systematic reviews (Online) 9 (9): CD005346. doi:10.1002/14651858.CD005346.pub3. PMID 21901697. 
  115. ^ Bath, PM; Krishnan, K (28 October 2014). "Interventions for deliberately altering blood pressure in acute stroke.". The Cochrane database of systematic reviews 10: CD000039. doi:10.1002/14651858.CD000039.pub3. PMID 25353321. 
  116. ^ a b Wardlaw, JM; Murray, V; Berge, E; del Zoppo, GJ (Jul 29, 2014). "Thrombolysis for acute ischaemic stroke.". The Cochrane database of systematic reviews 7: CD000213. doi:10.1002/14651858.CD000213.pub3. PMID 25072528. 
  117. ^ a b Emberson, J; Lees, KR; Lyden, P; Blackwell, L; Albers, G; Bluhmki, E; Brott, T; Cohen, G; Davis, S; Donnan, G; Grotta, J; Howard, G; Kaste, M; Koga, M; von Kummer, R; Lansberg, M; Lindley, RI; Murray, G; Olivot, JM; Parsons, M; Tilley, B; Toni, D; Toyoda, K; Wahlgren, N; Wardlaw, J; Whiteley, W; Del Zoppo, GJ; Baigent, C; Sandercock, P; Hacke, W; for the Stroke Thrombolysis Trialists' Collaborative, Group (Aug 5, 2014). "Effect of treatment delay, age, and stroke severity on the effects of intravenous thrombolysis with alteplase for acute ischaemic stroke: a meta-analysis of individual patient data from randomised trials.". Lancet 384: 1929–1935. doi:10.1016/S0140-6736(14)60584-5. PMID 25106063. 
  119. ^ a b "Thrombolytics for acute stroke". Dynamed. Sep 15, 2014. Retrieved 4 October 2014. at 3-4.5 hours after stroke onset t-PA increases risk of symptomatic intracranial hemorrhage but effect on functional outcomes is inconsistent 
  120. ^ "Thrombolysis in acute ischaemic stroke: time for a rethink?". BMJ 350 (h1075). Mar 17, 2015. doi:10.1136/bmj.h1075. 
  121. ^ "Canadian Association of Emergency Physicians Position Statement on Acute Ischemic Stroke" (PDF). 20155. Retrieved 7 April 2015.  Check date values in: |date= (help)
  122. ^ Wardlaw JM, Murray V, Berge E, del Zoppo G, Sandercock P, Lindley RL, Cohen G (May 23, 2012). "Recombinant tissue plasminogen activator for acute ischaemic stroke: an updated systematic review and meta-analysis". Lancet. Online first (9834): 2364–72. doi:10.1016/S0140-6736(12)60738-7. PMC 3386494. PMID 22632907. 
  123. ^ Whiteley WN, Slot KB, Fernandes P, Sandercock P, Wardlaw J (November 2012). "Risk factors for intracranial hemorrhage in acute ischemic stroke patients treated with recombinant tissue plasminogen activator: a systematic review and meta-analysis of 55 studies". Stroke; a journal of cerebral circulation 43 (11): 2904–9. doi:10.1161/STROKEAHA.112.665331. PMID 22996959. 
  125. ^ Wardlaw JM, Murray V, Berge E, Del Zoppo GJ (2009-10-07). Wardlaw, Joanna M, ed. "Thrombolysis for acute ischaemic stroke". Cochrane database of systematic reviews (Online) (4): CD000213. doi:10.1002/14651858.CD000213.pub2. PMID 19821269. 
  129. ^ Simard JM, Sahuquillo J, Sheth KN, Kahle KT, Walcott BP (April 2011). "Managing malignant cerebral infarction". Curr Treat Options Neurol 13 (2): 217–29. doi:10.1007/s11940-010-0110-9. PMC 3243953. PMID 21190097. 
  130. ^ "Organised inpatient (stroke unit) care for stroke". Cochrane Database of Systematic Reviews. Sep 11, 2013. doi:10.1002/14651858.CD000197.pub3. 
  131. ^
  132. ^ O'Sullivan 2007, pp. 471, 484, 737, 740
  133. ^ Mackenzie C (April 2011). "Dysarthria in stroke: a narrative review of its description and the outcome of intervention". Int J Speech Lang Pathol 13 (2): 125–36. doi:10.3109/17549507.2011.524940. PMID 21480809. 
  134. ^ West C, Hesketh A, Vail A, Bowen A (2005). West, Carolyn, ed. "Interventions for apraxia of speech following stroke". Cochrane Database Syst Rev (4): CD004298. doi:10.1002/14651858.CD004298.pub2. PMID 16235357. 
  135. ^ Kelly H, Brady MC, Enderby P (2010). Brady, Marian C, ed. "Speech and language therapy for aphasia following stroke". Cochrane Database Syst Rev (5): CD000425. doi:10.1002/14651858.CD000425.pub2. PMID 20464716. 
  136. ^ a b B. Lange, S. Flynn & A. Rizzo, B.; Flynn, S.; Rizzo, A. (2009). "Initial usability assessment of off-the-shelf video game consoles for clinical game-based motor rehabilitation". Physical Therapy Reviews 14 (5): 355–362. doi:10.1179/108331909X12488667117258. 
  137. ^ Fregni F, Pascual-Leone A (2007). "Technology Insight: noninvasive brain stimulation in neurology—perspectives on the therapeutic potential of rTMS and tDCS". Nature Clinical Practice Neurology 3 (7): 383–393. doi:10.1038/ncpneuro0530. PMID 17611487. 
  138. ^ Balasubramanian S, Klein J, Burdet E (2010). "Robot-assisted rehabilitation of hand function". Current Opinion in Neurology 23 (6): 661–70. doi:10.1097/WCO.0b013e32833e99a4. PMID 20852421. 
  139. ^ a b c Brazzelli M, Saunders DH, Greig CA, Mead GE (2011). "Physical fitness training for stroke patients". The Cochrane Database of Systematic Reviews (11): CD003316. doi:10.1002/14651858.CD003316.pub4. PMID 22071806. 
  143. ^ editors, Tom A. Schweizer, R. Loch Macdonald, (2014). The behavioral consequences of stroke. New York, NY [u.a.]: Springer. pp. 119–133. ISBN 978-1-4614-7671-9. 
  144. ^ Mackenzie, Catherine (2011). "Dysarthria in stroke: A narrative review of its description and the outcome of intervention". International Journal of Speech-Language Pathology: 125–136. 
  145. ^ Ackley, Betty; Ladwig, Gail B.; Kelley, Helen (2010). Nursing diagnosis handbook: an evidence-based guide to planning care (9th ed.). Maryland Heights, MO.: Mosby. 
  146. ^ a b Senelick Richard C., Rossi, Peter W., Dougherty, Karla (1994). Living with Stroke: A Guide for Families. Contemporary Books, Chicago. ISBN 0-8092-2607-3. OCLC 40856888 42835161. 
  147. ^ a b Villarosa, Linda; Singleton, Lafayette; Johnson, Kirk A. (1993). The Black health library guide to stroke. New York: Henry Holt and Co. ISBN 0-8050-2289-9. OCLC 26929500. 
  148. ^ Hamilton RH, Chrysikou EG, Coslett B (July 2011). "Mechanisms of aphasia recovery after stroke and the role of noninvasive brain stimulation". Brain Lang 118 (1–2): 40–50. doi:10.1016/j.bandl.2011.02.005. PMC 3109088. PMID 21459427. 
  149. ^ Leys D, Hénon H, Mackowiak-Cordoliani MA, Pasquier F (November 2005). "Poststroke dementia". Lancet Neurol 4 (11): 752–9. doi:10.1016/S1474-4422(05)70221-0. PMID 16239182. 
  150. ^ Coulthard E, Singh-Curry V, Husain M (December 2006). "Treatment of attention deficits in neurological disorders". Current Opinion in Neurology 19 (6): 613–8. doi:10.1097/01.wco.0000247605.57567.9a. PMID 17102702. 
  151. ^ Lim C, Alexander MP (December 2009). "Stroke and episodic memory disorders". Neuropsychologia 47 (14): 3045–58. doi:10.1016/j.neuropsychologia.2009.08.002. PMID 19666037. 
  152. ^ Murray ED, Buttner N, Price BH (2012). "Depression and Psychosis in Neurological Practice". In Bradley WG, Daroff RB, Fenichel GM, Jankovic J. Bradley's neurology in clinical practice. 1 (6th ed.). Philadelphia, PA: Elsevier/Saunders. pp. 100–1. ISBN 1-4377-0434-4. 
  153. ^ 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. doi:10.1161/01.STR.28.8.1585. PMID 9259753. 
  154. ^ 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. doi:10.1136/bmj.315.7122.1582. PMC 2127973. PMID 9437276. 
  156. ^ "The top 10 causes of death". WHO. 
  157. ^ Indian Heart Association Why South Asians Facts Web. May 8 2015.<>
  158. ^ Towfighi A, Saver JL (August 2011). "Stroke declines from third to fourth leading cause of death in the United States: historical perspective and challenges ahead". Stroke 42 (8): 2351–5. doi:10.1161/STROKEAHA.111.621904. PMID 21778445. 
  159. ^ Ellekjaer 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. doi:10.1161/01.STR.28.11.2180. PMID 9368561. Retrieved 2008-01-22. 
  160. ^ Bongers TN, de Maat MP, van Goor ML, Bhagwanbali V, van Vliet HH, Gómez García EB, Dippel DW, Leebeek FW (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. 
  161. ^ Ashrafian H (2010). "Familial stroke 2700 years ago". Stroke 41 (4): e187. doi:10.1161/STROKEAHA.109.573170. PMID 20185778. 
  162. ^ 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. doi:10.1161/01.STR.27.8.1427. PMID 8711815. 
  163. ^ Kopito, Jeff (September 2001). "A Stroke in Time". 6 (9). [dead link]
  165. ^ Schiller F (April 1970). "Concepts of stroke before and after Virchow". Med Hist 14 (2): 115–31. doi:10.1017/S0025727300015325. PMC 1034034. PMID 4914683. 
  166. ^ Stanley Finger; François Boller; Kenneth L. Tyler (2010). Handbook of Clinical Neurology. North-Holland Publishing Company. p. 401. ISBN 978-0-444-52009-8. Retrieved 1 October 2013. 
  167. ^ John W. Scadding (December 2011). Clinical Neurology. CRC Press. p. 488. ISBN 978-0-340-99070-4. Retrieved 1 October 2013. 
  168. ^ Joseph I. Sirven; Barbara L. Malamut (2008). Clinical Neurology of the Older Adult. Lippincott Williams & Wilkins. p. 243. ISBN 978-0-7817-6947-1. Retrieved 1 October 2013. 
  169. ^ David Myland Kaufman; Mark J Milstein (5 December 2012). Kaufman's Clinical Neurology for Psychiatrists. Elsevier Health Sciences. p. 892. ISBN 978-1-4557-4004-8. Retrieved 1 October 2013. 
  170. ^ a b Mosby's Medical Dictionary, 8th edition. Elsevier. 2009. 
  171. ^ "What is a Stroke/Brain Attack?" (PDF). National Stroke Association. Retrieved 27 February 2014. 
  172. ^ Segen's Medical Dictionary. Farlex, Inc. 2010. 
  173. ^ Derdeyn CP, Chimowitz MI; Chimowitz (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. PMC 2040119. PMID 17826637. 
  174. ^ Tenser MS, Amar AP, Mack WJ; Amar; Mack (December 2011). "Mechanical thrombectomy for acute ischemic stroke using the MERCI retriever and penumbra aspiration systems". World neurosurgery 76 (6 Suppl): S16–23. doi:10.1016/j.wneu.2011.07.003. PMID 22182267. 
  175. ^ Ortega-Lopez Y, Llanos-Mendez A (2010). "[Mechanical thrombectomy with MERCI device. Ischaemic stroke]". Andalusian Agency for Health Technology Assessment. 
  176. ^ Lees KR, Zivin JA, Ashwood T, Davalos A, Davis SM, Diener HC, Grotta J, Lyden P, Shuaib A, Hårdemark HG, Wasiewski WW; Zivin; Ashwood; Davalos; Davis; Diener; Grotta; Lyden; Shuaib; Hårdemark; Wasiewski; Stroke-Acute Ischemic NXY Treatment (SAINT I) Trial Investigators (February 2006). "NXY-059 for acute ischemic stroke". The New England Journal of Medicine 354 (6): 588–600. doi:10.1056/NEJMoa052980. PMID 16467546. 
  177. ^ Koziol JA, Feng AC; Feng (October 2006). "On the analysis and interpretation of outcome measures in stroke clinical trials: lessons from the SAINT I study of NXY-059 for acute ischemic stroke". Stroke; a journal of cerebral circulation 37 (10): 2644–7. doi:10.1161/01.STR.0000241106.81293.2b. PMID 16946150. 
  178. ^ Bennett, MH; Weibel, S; Wasiak, J; Schnabel, A; French, C; Kranke, P (12 November 2014). "Hyperbaric oxygen therapy for acute ischaemic stroke.". The Cochrane database of systematic reviews 11: CD004954. doi:10.1002/14651858.CD004954.pub3. PMID 25387992. 

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