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For other uses, see Stroke (disambiguation).
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Classification and external resources
Specialty Neurology
ICD-10 I61-I64ner
ICD-9-CM 434.91
OMIM 601367
DiseasesDB 2247
MedlinePlus 000726
Patient UK Stroke
MeSH D020521

Stroke 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 vision to one side.[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) or mini-stroke.[3] A hemorrhagic stroke 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.[2][4] An ischemic stroke is typically caused by blockage of a blood vessel, though there are also less common causes.[5][6][7] A hemorrhagic stroke is caused by either bleeding directly into the brain or into the space between the brain's membranes.[5][8] Bleeding may occur due to a ruptured brain aneurysm.[5] Diagnosis is typically with medical imaging such as a CT scan or magnetic resonance imaging (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.[9]


In 2013 approximately 6.9 million people had an ischemic stroke and 3.4 million people had a hemorrhagic stroke.[10] In 2010 there were about 33 million people who 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.[11] 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).[12] About 3.3 million deaths resulted from ischemic stroke while 3.2 million deaths resulted from hemorrhagic stroke.[12] 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.[11]








  3. Systemic hypoperfusion (general decrease in blood supply, e.g., in shock)[16]
  4. cerebral venous sinus thrombosis.[17]





There are two main types of hemorrhagic stroke:[23][24]





Signs and symptoms


Early recognition


A mnemonic to remember the warning signs of stroke is FAST (facial droop, arm weakness, speech difficulty, and time to call emergency services),[27] 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)[28] and the Cincinnati Prehospital Stroke Scale (CPSS).[29] Use of these scales is recommended by professional guidelines.[30]





  • 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



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.[37] Air pollution may also increase stroke risk.[38]

Embolic stroke




Causes of stroke related to the heart can be distinguished between high and low-risk:[40]


Cerebral hypoperfusion


Venous thrombosis


Intracerebral hemorrhage



Other causes may include spasm of an artery. This may occur due to cocaine.[43]

Silent stroke











Hemorrhagic strokes are classified based on their underlying pathology. Some causes of hemorrhagic stroke are hypertensive hemorrhage, ruptured aneurysm, ruptured AV fistula, transformation of prior ischemic infarction, and drug induced bleeding.[53] They result in tissue injury by causing compression of tissue from an expanding hematoma or hematomas. 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.[37][54] Inflammation contributes to the secondary brain injury after hemorrhage.[54]




Physical examination



For diagnosing ischemic stroke in the emergency setting:[56]

  • 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.[57]


Underlying cause





Given the disease burden of strokes, prevention is an important public health concern.[59] Primary prevention is less effective than secondary prevention (as judged by the number needed to treat to prevent one stroke per year).[59] Recent guidelines detail the evidence for primary prevention in stroke.[60] In those who are otherwise healthy, aspirin does not appear beneficial and thus is not recommended.[61] In people who have had a myocardial infarction or those with a high cardiovascular risk, it provides some protection against a first stroke.[62][63] In those who have previously had a stroke, treatment with medications such as aspirin, clopidogrel, and dipyridamole may be beneficial.[62] The U.S. Preventive Services Task Force (USPSTF) recommends against screening for carotid artery stenosis in those without symptoms.[64]

Risk factors

The most important modifiable risk factors for stroke are high blood pressure and atrial fibrillation although the size of the effect is small with 833 people have to be treated for 1 year to prevent one stroke.[65][66] Other modifiable risk factors include high blood cholesterol levels, diabetes mellitus, cigarette smoking[67][68] (active and passive), drinking lots of alcohol[69] and drug use,[70] lack of physical activity, obesity, processed red meat consumption[71] and unhealthy diet.[72] 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).[73] Drugs, most commonly amphetamines and cocaine, can induce stroke through damage to the blood vessels in the brain and/or acute hypertension.[74][75]

High levels of physical activity reduce the risk of stroke by about 26%.[76] There is a lack of high quality studies looking at promotional efforts to improve lifestyle factors.[77] Nonetheless, given the large body of circumstantial evidence, best medical management for stroke includes advice on diet, exercise, smoking and alcohol use.[78] Medication is the most common method of stroke prevention; carotid endarterectomy can be a useful surgical method of preventing stroke.

Blood pressure

High blood pressure accounts for 35-50% of stroke risk.[79] Blood pressure reduction of 10 mmHg systolic or 5 mmHg diastolic reduces the risk of stroke by ~40%.[80] Lowering blood pressure has been conclusively shown to prevent both ischemic and hemorrhagic strokes.[81][82] It is equally important in secondary prevention.[83] Even patients older than 80 years and those with isolated systolic hypertension benefit from antihypertensive therapy.[84][85][86] 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.[87][88] The routine use of beta-blockers following a stroke or TIA has not been shown to result in benefits.[89]

Blood lipids

High cholesterol levels have been inconsistently associated with (ischemic) stroke.[82][90] Statins have been shown to reduce the risk of stroke by about 15%.[91] Since earlier meta-analyses of other lipid-lowering drugs did not show a decreased risk,[92] statins might exert their effect through mechanisms other than their lipid-lowering effects.[91]

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.[62] 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.[95] Thienopyridines (clopidogrel, ticlopidine) might be slightly more effective than aspirin and have a decreased risk of gastrointestinal bleeding, but are more expensive.[96] Clopidogrel has less side effects than ticlopidine.[96] Dipyridamole can be added to aspirin therapy to provide a small additional benefit, even though headache is a common side effect.[97] Low-dose aspirin is also effective for stroke prevention after having a myocardial infarction.[63]

Those with atrial fibrillation have a 5% a year risk of stroke, and this risk is higher in those with valvular atrial fibrillation.[98] Depending on the stroke risk, anticoagulation with medications such as warfarin or aspirin is useful for prevention.[99] Except in people with atrial fibrillation, oral anticoagulants are not advised for stroke prevention —any benefit is offset by bleeding risk.[100]

In primary prevention however, antiplatelet drugs did not reduce the risk of ischemic stroke but increased the risk of major bleeding.[101][102] Further studies are needed to investigate a possible protective effect of aspirin against ischemic stroke in women.[103][104]


Carotid endarterectomy or carotid angioplasty can be used to remove atherosclerotic narrowing of the carotid artery. There is evidence supporting this procedure in selected cases.[78] Endarterectomy for a significant stenosis has been shown to be useful in preventing further strokes in those who have already had one.[105] Carotid artery stenting has not been shown to be equally useful.[106][107] People are selected for surgery based on age, gender, degree of stenosis, time since symptoms and the person's preferences.[78] 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.[108][109]

Screening for carotid artery narrowing has not been shown to be a useful test in the general population.[110] Studies of surgical intervention for carotid artery stenosis without symptoms have shown only a small decrease in the risk of stroke.[111][112] 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.[78]


Nutrition, specifically the Mediterranean-style diet, has the potential for decreasing the risk of having a stroke by more than half.[113] It does not appear that lowering levels of homocysteine with folic acid affects the risk of stroke.[114][115]



Previous stroke or TIA

Keeping blood pressure below 140/90 mmHg is recommended.[117] 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%.[118] However, a recent meta-analysis suggests harm from anticoagulation started early after an embolic stroke.[119] Stroke prevention treatment for atrial fibrillation is determined according to the CHA2DS2–VASc score. 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.[117]

Anticoagulants, when used following stroke, should not be stopped for dental procedures.[120]



Ischemic stroke

Aspirin reduces the overall risk of recurrence by 13% with greater benefit early on.[121] Definitive therapy within the first few hours 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 summed up as Time is Brain! in the early 1990s.[122] Years later, that same idea, that rapid cerebral blood flow restoration results in fewer brain cells dying, has been proved and quantified.[123]

Tight blood sugar control in the first few hours does not improve outcomes and may cause harm.[124] High blood pressure is also not typically lowered as this has not been found to be helpful.[125][126] Cerebrolysin, a mix of pig brain tissue used to treat acute ischemic stroke in many Asian and European countries, does not improve outcomes and may increase the risk of severe adverse events.[127]


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.[128][129] It does not, however, improve chances of survival.[128] Benefit is greater the earlier it is used.[128] Between three and four and a half hours the effects are less clear.[130][131][132] 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.[129] After four and a half hours thrombolysis worsens outcomes.[130] These benefits or lack of benefits occurred regardless of the age of the person treated.[133] There is no reliable way to determine who will have an intracranial bleed post-treatment versus who will not.[134]

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[135] 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.[136] 6.4% of people with large strokes developed substantial brain bleeding as a complication from being given tPA thus part of the reason for increased short term mortality.[137] 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.[138] 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.[139]


Surgical removal of the blood clot causing the ischemic stroke may improve outcomes if done within 7 hours of the start of symptoms in those with an anterior circulation large artery clot.[140][141] It however does not change the risk of death.[142]


Hemorrhagic stroke



Stroke unit



Stroke rehabilitation is the process by which those 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.[citation needed]



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.[147] PT and OT have overlapping areas of expertise; however, PT focuses on joint range of motion and strength by performing exercises and relearning 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.[148] 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 people with the speech production disorders: dysarthria[149] and apraxia of speech,[150] aphasia,[151] cognitive-communication impairments and/or 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.[32] Gaining initial improvement in range of motion is often achieved through rhythmic rotational patterns associated with the affected limb.[32] 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.[32] Cold in the form of ice wraps or ice packs have been proven to briefly reduce spasticity by temporarily dampening neural firing rates.[32] Electrical stimulation to the antagonist muscles or vibrations has also been used with some success.[32]


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.[152] 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.[152]

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)[153] and robotic therapies.[154]

A stroke can also reduce people's general fitness.[155] Reduced fitness can reduce capacity for rehabilitation as well as general health.[156] 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.[155] However, cardiorespiratory training added to walking programs in rehabilitation can improve speed, tolerance and independence during walking.[155]





Disability affects 75% of stroke survivors enough to decrease their employability.[159] 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.[160] Dysfunctions correspond to areas in the brain that have been damaged.




30 to 50% of stroke survivors suffer post-stroke depression, which is characterized by lethargy, irritability, sleep disturbances, lowered self-esteem and withdrawal.[164] Depression can reduce motivation and worsen outcome, but can be treated with social and family support, psychotherapy and, in severe cases, 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.[159] Some people show the opposite of what they feel, for example crying when they are happy.[165] Emotional lability occurs in about 20% of those who have had a stroke. Those with a right hemisphere stroke are more likely to have an empathy problems which can make communication harder.[166]

Cognitive deficits resulting from stroke include perceptual disorders, aphasia,[167] dementia,[168] and problems with attention[169] and memory.[170] 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.




Stroke deaths per million persons in 2012
Disability-adjusted life year for cerebral vascular disease per 100,000 inhabitants in 2004.[174]

Stroke was the second most frequent cause of death worldwide in 2011, accounting for 6.2 million deaths (~11% of the total).[175] Approximately 17 million people had a stroke in 2010 and 33 million people have previously had a stroke and were still alive.[11] Between 1990 and 2010 the number of strokes decreased by approximately 10% in the developed world and increased by 10% in the developing world.[11] Overall, two-thirds of strokes occurred in those over 65 years old.[11] South Asians are at particularly high risk of stroke, accounting for 40% of global stroke deaths.[176]

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.[177] 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.[178] 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.[37][164] 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.[179] 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,[37] yet 60% of deaths from stroke occur in women.[165] Since women live longer, they are older on average when they have their strokes and thus more often killed.[37] 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.[180] 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.[181][182] The word stroke was used as a synonym for apoplectic seizure as early as 1599,[183] 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.[37][181] 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.[37] Rudolf Virchow first described the mechanism of thromboembolism as a major factor.[184]

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".[185] 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.[186][187][188] Cerebrovascular insult may be used interchangeably.[189]

The term brain attack was introduced for use to underline the acute nature of stroke according to the American Stroke Association,[189] who since 1990 have used the term,[190] and is used colloquially to refer to both ischemic as well as hemorrhagic stroke.[191]


Angioplasty and stenting


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.[193] Significant complications occur in about 7%.[194]


Neuroprotective agents including antioxidants which combat reactive oxygen species, or inhibit programmed cell death, or inhibit excitatory neurotransmitters have been shown experimentally to reduce tissue injury caused by ischemia. Until recently, human clinical trials with neuroprotective agents have failed, with the probable exception of deep barbiturate-induced coma. Disufenton sodium, the disulfonyl derivative of the radical-scavenging phenylbutylnitrone, was reported to be neuroprotective.[195] This agent is thought to work at the level of the blood vessel lining. However the favourable results evidenced from one large-scale trial were not reproduced in a second trial.[37] So that the benefit of disufenton sodium is questionable.[196]


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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 50477349. 
  • 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. 

External links