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{{short description|Death of a region of brain cells due to poor blood flow}}
{{otheruses}}
{{Other uses}}
 
{{pp-semi-indef}}
{{Infobox_Disease
{{cs1 config|name-list-style=vanc|display-authors=6}}
| Name = Stroke
{{Infobox medical condition (new)
| Image =
| Captionname = Stroke
| image = MCA Territory Infarct.svg
| DiseasesDB = 2247
| caption = [[CT scan]] of the brain showing a massive, prior right-sided [[ischemic]] stroke from blockage of an artery. Changes on a CT may not be visible early on.<ref>{{cite web | vauthors = Gaillard F |title=Ischaemic stroke |url=https://radiopaedia.org/articles/ischaemic-stroke |website=radiopaedia.org |date=11 April 2011 |access-date=3 June 2018 |language=en}}</ref>
| ICD10 = {{ICD10|I|61||i|60}}-{{ICD10|I|64||i|60}}
| ICD9field = {{ICD9|435}}-{{ICD9|436}}[[Neurology]], stroke medicine
| synonyms = Cerebrovascular accident (CVA), cerebrovascular insult (CVI), cerebrovascular lesion (CVL), brain attack
| ICDO =
| symptoms = [[hemiplegia|Inability to move or feel]] on one side of the body, [[receptive aphasia|problems understanding]] or [[expressive aphasia|speaking]], [[dizziness]], [[Homonymous hemianopsia|loss of vision to one side]]<ref name=Donnan2008/><ref name=HLB2014S/>
| OMIM = 601367
| complications = [[Persistent vegetative state]]<ref>{{cite book | vauthors = Martin G |title=Palliative Care Nursing: Quality Care to the End of Life, Third Edition|date=2009|publisher=Springer Publishing Company|isbn=978-0-8261-5792-8|page=290|url=https://books.google.com/books?id=rTexGiX5bqoC&pg=PA290|language=en|url-status=live|archive-url=https://web.archive.org/web/20170803132127/https://books.google.com/books?id=rTexGiX5bqoC&pg=PA290|archive-date=2017-08-03}}</ref>
| MedlinePlus = 000726pi
| onset =
| eMedicineSubj = neuro
| duration =
| eMedicineTopic = 9
| causes = [[brain ischemia|Ischemic]] (blockage) and [[intracranial hemorrhage|hemorrhagic]] (bleeding)<ref name=HLB2014W/>
| eMedicine_mult = {{eMedicine2|emerg|558}} {{eMedicine2|emerg|557}} {{eMedicine2|pmr|187}}
| risks = Age,<ref>{{cite web | url=https://www.nhs.uk/conditions/stroke/causes/ | title=Stroke - Causes | date=24 October 2017 }}</ref> [[hypertension|high blood pressure]], [[tobacco smoking]], [[obesity]], [[hypercholesterolemia|high blood cholesterol]], [[diabetes mellitus]], previous [[Transient ischemic attack|TIA]], [[end-stage kidney disease]], [[atrial fibrillation]]<ref name=Donnan2008/><ref name=HLB2014C/><ref name="Hu2018"/>
| MeshID =
| diagnosis = Based on symptoms with [[medical imaging]] typically used to rule out bleeding<ref name=HLB2014D/><ref name=AFP2009/>
| differential = [[Low blood sugar]]<ref name=HLB2014D/>
| prevention =
| treatment = Based on the type<ref name=Donnan2008/>
| medication =
| prognosis = Average life expectancy 1 year<ref name=Donnan2008/>
| frequency = 42.4 million (2015)<ref name=GBD2015Pre/>
| deaths = 6.3 million (2015)<ref name=GBD2015De/>
}}
<!-- Definition and symptoms -->
 
'''Stroke''' is a medical condition in which poor [[cerebral circulation|blood flow]] to a part of the [[brain]] causes [[cell death]].<ref name=HLB2014W/> There are two main types of stroke: [[brain ischemia|ischemic]], due to lack of blood flow, and [[intracranial hemorrhage|hemorrhagic]], due to [[bleeding]].<ref name="HLB2014W" /> Both cause parts of the brain to stop functioning properly.<ref name="HLB2014W">{{cite web|title=What Is a Stroke?|url=http://www.nhlbi.nih.gov/health/health-topics/topics/stroke|website=www.nhlbi.nih.gov/|access-date=26 February 2015|date=March 26, 2014|url-status=dead|archive-url=https://web.archive.org/web/20150218230259/http://www.nhlbi.nih.gov/health/health-topics/topics/stroke/|archive-date=18 February 2015}}</ref>
A '''stroke''', also known as '''cerebrovascular accident''' ('''CVA'''),<ref name="umich">{{cite web | title=Stroke (Cerebrovascular Accident) | work=Adult Health Advisor 2005.4 | publisher=[[University of Michigan Health System]] | date=2005-04-29 | url=http://www.med.umich.edu/1libr/aha/aha_strnos_crs.htm | accessdate = 2006-10-12}}</ref> is an [[Acute (medical)|acute]] neurological injury in which the [[blood]] supply to a part of the [[brain]] is interrupted. That is, a stroke involves the sudden loss of neuronal function due to disturbance in cerebral [[perfusion]]. This disturbance in perfusion is commonly arterial, but can be venous.
 
Signs and symptoms of stroke may include an [[hemiplegia|inability to move or feel on one side of the body]], [[receptive aphasia|problems understanding]] or [[expressive aphasia|speaking]], [[dizziness]], or [[homonymous hemianopsia|loss of vision to one side]].<ref name="Donnan2008" /><ref name="HLB2014S" /> Signs and symptoms often appear soon after the stroke has occurred.<ref name="HLB2014S" /> If symptoms last less than 24 hours, the stroke is a [[transient ischemic attack]] (TIA), also called a mini-stroke.<ref name="HLB2014S">{{cite web|title=What Are the Signs and Symptoms of a Stroke?|url=https://www.nhlbi.nih.gov/health/stroke/symptoms|website=www.nhlbi.nih.gov|access-date=27 February 2015|date=March 26, 2014|url-status=live|archive-url=https://web.archive.org/web/20150227083736/http://www.nhlbi.nih.gov/health/health-topics/topics/stroke/signs|archive-date=27 February 2015}}</ref> [[subarachnoid hemorrhage|Hemorrhagic stroke]] may also be associated with a [[thunderclap headache|severe headache]].<ref name="HLB2014S" /> The symptoms of stroke can be permanent.<ref name="HLB2014W" /> Long-term complications may include [[pneumonia]] and [[Urinary incontinence|loss of bladder control]].<ref name="HLB2014S" />
The part of the brain with disturbed perfusion no longer receives adequate amounts of oxygen and glucose. This initiates the [[ischemic cascade]] which causes brain cells to die or be seriously damaged, impairing local brain function. Stroke is a [[medical emergency]] and can cause permanent neurologic damage or even death if not promptly diagnosed and treated. It is the third leading cause of [[death]] and the leading cause of adult disability in the [[United States]] and industrialized [[European]] nations. On average, a stroke occurs every 45 seconds and someone dies every 3 minutes.
 
<!-- Causes, diagnosis and pathophysiology -->
Risk factors include [[Old age|advanced age]], male gender, [[hypertension]] (high blood pressure), [[diabetes mellitus]], [[hypercholesterolemia|high cholesterol]], [[cigarette smoking]], [[atrial fibrillation]], [[migraine]] with aura, and [[thrombophilia]]. Cigarette smoking is the most important modifiable risk factor of stroke.
The most significant [[risk factor]] for stroke is [[hypertension|high blood pressure]].<ref name=HLB2014C>{{cite web|title=Who Is at Risk for a Stroke?|url=https://www.nhlbi.nih.gov/health/stroke/causes|website=www.nhlbi.nih.gov|access-date=27 February 2015|date=March 26, 2014|url-status=live|archive-url=https://web.archive.org/web/20150227085058/http://www.nhlbi.nih.gov/health/health-topics/topics/stroke/atrisk|archive-date=27 February 2015}}</ref> Other risk factors include [[hypercholesterolemia|high blood cholesterol]], [[tobacco smoking]], [[obesity]], [[diabetes mellitus]], a previous [[transient ischemic attack|TIA]], [[end-stage kidney disease]], and [[atrial fibrillation]].<ref name=Donnan2008/><ref name=HLB2014C/><ref name="Hu2018">{{cite journal | vauthors = Hu A, Niu J, Winkelmayer WC | title = Oral Anticoagulation in Patients With End-Stage Kidney Disease on Dialysis and Atrial Fibrillation | journal = Seminars in Nephrology | volume = 38 | issue = 6 | pages = 618–628 | date = November 2018 | pmid = 30413255 | pmc = 6233322 | doi = 10.1016/j.semnephrol.2018.08.006 }}</ref> Ischemic stroke is typically caused by blockage of a blood vessel, though there are also less common causes.<ref name=HLB2014T/><ref>{{cite book| vauthors = Roos KL |title=Emergency Neurology |date=2012 |publisher=Springer Science & Business Media |isbn=978-0-387-88584-1 |page=360 |url= https://books.google.com/books?id=0jH7TZW8WVAC&pg=PA360 |language=en|url-status=live|archive-url= https://web.archive.org/web/20170108190342/https://books.google.com/books?id=0jH7TZW8WVAC&pg=PA360 |archive-date=2017-01-08}}</ref><ref>{{cite book| vauthors = Wityk RJ, Llinas RH |title=Stroke|date=2007|publisher=ACP Press|isbn=978-1-930513-70-9|page=296|url=https://books.google.com/books?id=Ispt6JRBgU4C&pg=PA296|language=en|url-status=live|archive-url=https://web.archive.org/web/20170108185918/https://books.google.com/books?id=Ispt6JRBgU4C&pg=PA296|archive-date=2017-01-08}}</ref> Hemorrhagic stroke is caused by either [[intracerebral hemorrhage|bleeding directly into the brain]] or [[subarachnoid hemorrhage|into the space between]] the [[meninges|brain's membranes]].<ref name=HLB2014T>{{cite web|title=Types of Stroke|url=http://www.nhlbi.nih.gov/health/health-topics/topics/stroke/types|website=www.nhlbi.nih.gov|access-date=27 February 2015|date=March 26, 2014|url-status=dead|archive-url=https://web.archive.org/web/20150319163549/http://www.nhlbi.nih.gov/health/health-topics/topics/stroke/types|archive-date=19 March 2015}}</ref><ref name=Feigin05>{{cite journal | vauthors = Feigin VL, Rinkel GJ, Lawes CM, Algra A, Bennett DA, van Gijn J, Anderson CS | title = Risk factors for subarachnoid hemorrhage: an updated systematic review of epidemiological studies | journal = Stroke | volume = 36 | issue = 12 | pages = 2773–80 | date = December 2005 | pmid = 16282541 | doi = 10.1161/01.STR.0000190838.02954.e8 | doi-access = free }}</ref> Bleeding may occur due to a ruptured [[intracranial aneurysm|brain aneurysm]].<ref name=HLB2014T/> Diagnosis is typically based on a [[physical exam]] and supported by [[medical imaging]] such as a [[CT scan]] or [[magnetic resonance imaging|MRI scan]].<ref name=HLB2014D/> A CT scan can rule out bleeding, but may not necessarily rule out ischemia, which early on typically does not show up on a CT scan.<ref name=AFP2009>{{cite journal | vauthors = Yew KS, Cheng E | title = Acute stroke diagnosis | journal = American Family Physician | volume = 80 | issue = 1 | pages = 33–40 | date = July 2009 | pmid = 19621844 | pmc = 2722757 }}</ref> Other tests such as an [[electrocardiogram]] (ECG) and [[blood test]]s are done to determine risk factors and possible causes.<ref name=HLB2014D/> [[Low blood sugar]] may cause similar symptoms.<ref name=HLB2014D>{{cite web|title=How Is a Stroke Diagnosed?|url=https://www.nhlbi.nih.gov/health/stroke/diagnosis|website=www.nhlbi.nih.gov|access-date=27 February 2015|date=March 26, 2014|url-status=live|archive-url=https://web.archive.org/web/20150227083640/http://www.nhlbi.nih.gov/health/health-topics/topics/stroke/diagnosis|archive-date=27 February 2015}}</ref>
 
<!-- Prevention and treatment -->
The term "'''brain attack'''" is starting to come into use in the United States for stroke, just as the term "heart attack" is used for [[myocardial infarction]], where a cutoff of blood causes [[necrosis]] to the tissue of the [[heart]]. Many hospitals have "brain attack" teams within their [[neurology]] departments specifically for swift treatment of stroke..{{Fact|date=February 2007}}
Prevention includes decreasing risk factors, [[carotid endarterectomy|surgery to open up the arteries to the brain]] in those with problematic [[carotid stenosis|carotid narrowing]], and [[anticoagulant]] medication in people with [[atrial fibrillation]].<ref name=Donnan2008/> [[Aspirin]] or [[statin]]s may be recommended by physicians for prevention.<ref name=Donnan2008/> Stroke is a medical emergency.<ref name=HLB2014W/> Ischemic strokes, if detected within three to four-and-a-half hours, may be treatable with [[thrombolytic drug|medication]] that can [[thrombolysis|break down the clot]],<ref name=Donnan2008/> while hemorrhagic strokes sometimes benefit from [[neurosurgery|surgery]].<ref name=Donnan2008/> Treatment to attempt recovery of lost function is called [[stroke rehabilitation]], and ideally takes place in a stroke unit; however, these are not available in much of the world.<ref name=Donnan2008>{{cite journal | vauthors = Donnan GA, Fisher M, Macleod M, Davis SM | title = Stroke | journal = Lancet | volume = 371 | issue = 9624 | pages = 1612–23 | date = May 2008 | pmid = 18468545 | doi = 10.1016/S0140-6736(08)60694-7 | s2cid = 208787942 }}{{subscription required}}</ref>
 
<!-- Epidemiology -->
==Types of stroke==
In 2023, 15 million people worldwide had a stroke.<ref name="who24">{{cite web |title=Stroke, cerebrovascular accident |url=https://www.emro.who.int/health-topics/stroke-cerebrovascular-accident/index.html |publisher=World Health Organization |access-date=12 March 2024 |date=2024}}</ref> In 2021, stroke was the third biggest cause of death, responsible for approximately 10% of total deaths.<ref>{{Cite web |title=The top 10 causes of death |url=https://www.who.int/news-room/fact-sheets/detail/the-top-10-causes-of-death |access-date=2024-08-12 |website=www.who.int |language=en}}</ref> In 2015, there were about 42.4&nbsp;million people who had previously had stroke and were still alive.<ref name=GBD2015Pre>{{cite journal | author = ((GBD 2015 Disease and Injury Incidence and Prevalence Collaborators)) | title = Global, regional, and national incidence, prevalence, and years lived with disability for 310 diseases and injuries, 1990-2015: a systematic analysis for the Global Burden of Disease Study 2015 | journal = Lancet | volume = 388 | issue = 10053 | pages = 1545–1602 | date = October 2016 | pmid = 27733282 | pmc = 5055577 | doi = 10.1016/S0140-6736(16)31678-6 }}</ref> Between 1990 and 2010 the annual incidence of stroke decreased by approximately 10% in the [[developed world]], but increased by 10% in the developing world.<ref name=Fei2013/> In 2015, stroke was the second most [[List of causes of death by rate|frequent cause of death]] after [[coronary artery disease]], accounting for 6.3&nbsp;million deaths (11% of the total).<ref name=GBD2015De>{{cite journal | author = ((GBD 2015 Mortality and Causes of Death Collaborators)) | title = Global, regional, and national life expectancy, all-cause mortality, and cause-specific mortality for 249 causes of death, 1980-2015: a systematic analysis for the Global Burden of Disease Study 2015 | journal = Lancet | volume = 388 | issue = 10053 | pages = 1459–1544 | date = October 2016 | pmid = 27733281 | pmc = 5388903 | doi = 10.1016/S0140-6736(16)31012-1 }}</ref> About 3.0 million deaths resulted from ischemic stroke while 3.3 million deaths resulted from hemorrhagic stroke.<ref name=GBD2015De/> About half of people who have had a stroke live less than one year.<ref name=Donnan2008/> Overall, two thirds of cases of stroke occurred in those over 65 years old.<ref name=Fei2013>{{cite journal | vauthors = 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 | title = Global and regional burden of stroke during 1990-2010: findings from the Global Burden of Disease Study 2010 | journal = Lancet | volume = 383 | issue = 9913 | pages = 245–54 | date = January 2014 | pmid = 24449944 | pmc = 4181600 | doi = 10.1016/S0140-6736(13)61953-4 }}</ref>
Strokes can be classified into two major categories: ischemic and hemorrhagic. [[Ischemia]] can be due to [[thrombosis]], [[embolism]], or systemic hypoperfusion. [[Hemorrhage]] can be due to [[intracerebral hemorrhage]] or [[subarachnoid hemorrhage]]. ~80% of strokes are due to ischemia.
{{TOC limit|3}}
 
==Classification==
===Ischemic stroke===
[[File:Ischemic Stroke.svg|thumb|There are two main categories of stroke. Ischemic (top), typically caused by a blood clot in an artery (1a) resulting in brain death to the affected area (2a). Hemorrhagic (bottom), caused by blood leaking into or around the brain from a ruptured blood vessel (1b) allowing blood to pool in the affected area (2b) thus increasing the pressure on the brain.]]
In an ischemic stroke, which is the cause of approximately 80% of strokes, a [[blood vessel]] becomes occluded and the blood supply to part of the brain is totally or partially blocked. Ischemic stroke is commonly divided into thrombotic stroke, embolic stroke, systemic hypoperfusion (Watershed or Border Zone stroke), or venous thrombosis.
[[File:MCA-Stroke-Brain-Human-2.JPG|thumb|A slice of brain from the autopsy of a person who had an acute [[middle cerebral artery|middle cerebral artery (MCA)]] stroke]]
 
Stroke can be classified into two major categories: [[ischemia|ischemic]] and [[bleeding|hemorrhagic]].<ref>{{cite web|url=http://www.ninds.nih.gov/disorders/stroke/preventing_stroke.htm|title=Brain Basics: Preventing Stroke|publisher=National Institute of Neurological Disorders and Stroke|access-date=2009-10-24|url-status=dead|archive-url=https://web.archive.org/web/20091008203200/http://www.ninds.nih.gov/disorders/stroke/preventing_stroke.htm|archive-date=2009-10-08}}</ref> Ischemic stroke is caused by [[Perfusion#Malperfusion|interruption of the blood supply]] to the brain, while hemorrhagic stroke results from the rupture of a [[blood vessel]] or an [[cerebral arteriovenous malformation|abnormal vascular structure]].
==== Thrombotic stroke ====
In thrombotic stroke, a [[thrombus]]-forming process develops in the affected artery. The thrombus — a built up clot — gradually narrows the lumen of the artery and impedes blood flow to distal tissue. These clots usually form around [[atherosclerosis|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 then called an "embolus." Thrombotic stroke can be divided into two types depending on the type of vessel the thrombus is formed on:
* ''Large vessel disease'' involves the common and [[internal carotid artery|internal carotids]], [[vertebral artery|vertebral]], and the [[Circle of Willis]]. Diseases that may form thrombi in the large vessels include (in descending incidence):
** [[Atherosclerosis]]
** Vasoconstriction
** [[Aortic dissection|Dissection]]
** [[Takayasu arteritis]]
** [[Giant cell arteritis]]
** Arteritis/vasculitis
** Noninflammatory vasculopathy
** [[Moyamoya syndrome]]
** [[Fibromuscular dysplasia]]
* ''Small vessel disease'' involves the intracerebral arteries, branches of the Circle of Willis, [[middle cerebral artery]], stem, and arteries arising from the distal vertebral and [[basilar artery]]. Diseases that may form thrombi in the small vessels include (in descending incidence):
** Lipohyalinosis (lipid hyaline build-up secondary to hypertension and aging) and fibrinoid degeneration (stroke involving these vessels are known as [[lacunar infarcts]])
** Microatheromas from larger arteries that extend into the smaller arteries (atheromatous branch disease)
 
About 87% of stroke is ischemic, with the rest being hemorrhagic. Bleeding can develop inside areas of ischemia, a condition known as "[[hemorrhagic transformation]]." It is unknown how many cases of hemorrhagic stroke actually start as ischemic stroke.<ref name="Donnan2008" />
====Embolic stroke====
Embolic stroke refers to the blockage of arterial access to a part of the brain by an [[embolus]] -- a traveling particle or debris in the arterial bloodstream originating from elsewhere. An embolus is most frequently a blood clot, but it can also be a plaque broken off from an [[atherosclerosis|atherosclerotic]] blood vessel or a number of other substances including fat (e.g., from bone marrow in a broken bone), air, and even [[cancer]]ous cells. Another cause is bacterial emboli released in infectious [[endocarditis]].
 
===Definition===
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 lyses and moves to a different ___location or dissipates altogether.
In the 1970s the [[World Health Organization]] defined "stroke" as a "neurological deficit of cerebrovascular cause that persists beyond 24 hours or is interrupted by death within 24 hours",<ref>{{cite book |author=World Health Organisation|title=Cerebrovascular Disorders (Offset Publications) |publisher=[[World Health Organization]] |___location=Geneva |year= 1978|isbn=978-92-4-170043-6 |oclc= 4757533}}</ref> although the word "stroke" is centuries old. 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.<ref name=Donnan2008/> With the availability of treatments that can reduce stroke severity when given early, many now prefer alternative terminology, such as "brain attack" and "acute ischemic cerebrovascular syndrome" (modeled after [[myocardial infarction|heart attack]] and [[acute coronary syndrome]], respectively), to reflect the urgency of stroke symptoms and the need to act swiftly.<ref>{{cite journal | vauthors = Kidwell CS, Warach S | title = Acute ischemic cerebrovascular syndrome: diagnostic criteria | journal = Stroke | volume = 34 | issue = 12 | pages = 2995–8 | date = December 2003 | pmid = 14605325 | doi = 10.1161/01.STR.0000098902.69855.A9 | doi-access = | s2cid = 16083887 }}</ref>
Embolic stroke can be divided into four categories:
* those with known cardiac source
* those with potential cardiac or aortic source (from [[transthoracic echocardiogram|transthoracic]] or [[transesophageal echocardiogram]])
* those with an arterial source
* those with unknown source
High risk cardiac causes include:<!--
--><ref name="ay">{{cite journal | author= Ay H; Furie KL; Singhal A; Smith WS; Sorensen AG; Koroshetz WJ | title= An evidence-based causative classification system for acute ischemic stroke | journal= Ann Neurol | year=2005 | pages=688-97 | volume=58 | issue=5 | id=PMID 16240340}}</ref>
* [[Atrial fibrillation]] and [[paroxysmal atrial fibrillation]]
* Rheumatic mitral or aortic valve disease
* Bioprosthetic and mechanical heart valves
* Atrial or ventricular thrombus
* [[Sick sinus syndrome]]
* Sustained [[atrial flutter]]
* Recent [[myocardial infarction]] (within one month)
* Chronic myocardial infarction together with [[ejection fraction]] <28 percent
* Symptomatic [[congestive heart failure]] with ejection fraction <30 percent
* [[Dilated cardiomyopathy]]
* [[Libman-Sacks endocarditis]]
* [[Antiphospholipid syndrome]]
* [[Marantic endocarditis]] from cancer
* [[Infective endocarditis]]
* [[Papillary fibroelastoma]]
* [[Left atrial myxoma]]
* [[Coronary artery bypass graft]] ([[CABG]]) surgery
Potential cardiac causes include:<!--
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* [[Mitral annular calcification]]
* [[Patent foramen ovale]]
* Atrial septal [[aneurysm]]
* Atrial septal aneurysm with patent foramen ovale
* Left ventricular aneurysm without thrombus
* Isolated left atrial smoke on echocardiography (no mitral stenosis or atrial fibrillation)
* Complex atheroma in the ascending aorta or proximal arch
 
===Ischemic===
====Systemic hypoperfusion (Watershed stroke)====
{{Main|Cerebral infarction|Brain ischemia}}
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. [[Hypoxia (medical)|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.
 
During 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:
===Hemorrhagic stroke===
A hemorrhagic stroke, or [[cerebral hemorrhage]], is a form of stroke that occurs when a blood vessel in the brain ruptures or bleeds. Like ischemic strokes, hemorrhagic strokes interrupt the brain's blood supply because the bleeding vessel can no longer carry the blood to its target tissue. In addition, blood irritates brain tissue, disrupting the delicate chemical balance, and, if the bleeding continues, it can cause increased intracranial pressure which physically impinges on brain tissue and restricts blood flow into the brain. In this respect, hemorrhagic strokes are more dangerous than their more common counterpart, ischemic strokes. There are two types of hemorrhagic stroke: intracerebral hemorrhage, and subarachnoid hemorrhage.
 
# [[Thrombosis]] (obstruction of a blood vessel by a blood clot forming locally)
====Intracerebral hemorrhage====
# [[Embolism]] (obstruction due to an [[embolus]] from elsewhere in the body),<ref name=Donnan2008/>
{{main|intracerebral hemorrhage}}
# Systemic [[hypoperfusion]] (general decrease in blood supply, e.g., in [[Shock (circulatory)|shock]])<ref>{{cite journal | vauthors = Shuaib A, Hachinski VC | title = Mechanisms and management of stroke in the elderly | journal = CMAJ | volume = 145 | issue = 5 | pages = 433–43 | date = September 1991 | pmid = 1878825 | pmc = 1335826 }}</ref>
Intracerebral hemorrhage (ICH) is bleeding directly into the brain tissue, forming a gradually enlarging [[hematoma]] (pooling of blood). It generally occurs in small arteries or arterioles and is commonly due to [[hypertension]], trauma, bleeding disorders, [[amyloid angiopathy]], illicit drug use (e.g., [[amphetamines]] or [[cocaine]]), and vascular malformations. The hematoma enlarges until pressure from surrounding tissue limits its growth, or until it decompresses by emptying into the ventricular system, [[cerebrospinal fluid|CSF]] or the [[pia|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.<!--
# [[Cerebral -->venous sinus thrombosis]].<ref name="caplan"Stam2005>{{cite journal | author=vauthors = CaplanStam LRJ | title = Thrombosis of the cerebral veins Intracerebraland hemorrhagesinuses | journal = The New England Journal of LancetMedicine | yearvolume =1992 352 | issue = 17 | pages =656-8 1791–8 | volumedate =339 April 2005 | issuepmid =8794 15858188 | iddoi =PMID 134734610.1056/NEJMra042354 | s2cid = 42126852 | url = https://pure.uva.nl/ws/files/3830901/45867_208116y.pdf }}</ref>
 
Stroke without an obvious explanation is termed '''cryptogenic stroke''' ([[idiopathic disease|idiopathic]]); this constitutes 30–40% of all cases of ischemic stroke.<ref name=Donnan2008/><ref name=Guercini>{{cite journal | vauthors = Guercini F, Acciarresi M, Agnelli G, Paciaroni M | title = Cryptogenic stroke: time to determine aetiology | journal = Journal of Thrombosis and Haemostasis | volume = 6 | issue = 4 | pages = 549–54 | date = April 2008 | pmid = 18208534 | doi = 10.1111/j.1538-7836.2008.02903.x | s2cid = 20211745 | doi-access =free }}</ref>
====Subarachnoid hemorrhage====
 
{{main|subarachnoid hemorrhage}}
There are 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 that is affected, the underlying cause, and the prognosis.<ref>{{cite journal | vauthors = Bamford J, Sandercock P, Dennis M, Burn J, Warlow C | title = Classification and natural history of clinically identifiable subtypes of cerebral infarction | journal = Lancet | volume = 337 | issue = 8756 | pages = 1521–6 | date = June 1991 | pmid = 1675378 | doi = 10.1016/0140-6736(91)93206-O | s2cid = 21784682 }} Later publications distinguish between "syndrome" and "infarct", based on evidence from imaging. "Syndrome" may be replaced by "hemorrhage" if imaging demonstrates a bleed. See {{cite web |url=http://www.strokecenter.org/trials/scales/oxford.html |title=Oxford Stroke Scale |author=Internet Stroke Center |access-date=2008-11-14 |url-status=live |archive-url=https://web.archive.org/web/20081025134133/http://www.strokecenter.org/trials/scales/oxford.html |archive-date=2008-10-25 }}</ref><ref>{{cite journal | vauthors = Bamford JM | title = The role of the clinical examination in the subclassification of stroke | journal = Cerebrovascular Diseases | volume = 10 | issue = 4 | pages = 2–4 | year = 2000 | pmid = 11070389 | doi = 10.1159/000047582 | s2cid = 29493084 }}</ref>
Subarachnoid hemorrhage (SAH) is bleeding into the [[cerebrospinal fluid]] (CSF) of the [[subarachnoid space]] surrounding the brain. The two most common causes of SAH are rupture of [[aneurysms]] from the base of the brain and bleeding from [[vascular malformations]] near the pial surface. Bleeding into the CSF from a ruptured aneurysm occurs very quickly, causing rapidly increased [[intracranial pressure]]. The bleeding usually only lasts a few seconds but rebleeding is common. Death or deep coma ensues if the bleeding continues. Hemorrhage from other sources is less abrupt and may continue for a longer period of time. SAH has a 40% mortality over 30 day period.
 
The TOAST (Trial of [[Danaparoid|Org 10172]] in Acute Stroke Treatment) classification is based on clinical symptoms as well as results of further investigations; on this basis, stroke is classified as being due to
 
(1) thrombosis or embolism due to [[atherosclerosis]] of a large artery,
 
(2) an embolism originating in the [[heart]],
 
(3) complete blockage of a small blood vessel,
 
(4) other determined cause,
 
(5) undetermined cause (two possible causes, no cause identified, or incomplete investigation).<ref>{{cite journal | vauthors = Adams HP, Bendixen BH, Kappelle LJ, Biller J, Love BB, Gordon DL, Marsh EE | title = Classification of subtype of acute ischemic stroke. Definitions for use in a multicenter clinical trial. TOAST. Trial of Org 10172 in Acute Stroke Treatment | journal = Stroke | volume = 24 | issue = 1 | pages = 35–41 | date = January 1993 | pmid = 7678184 | doi = 10.1161/01.STR.24.1.35 | doi-access = free }}</ref>
 
[[Recreational drug use|Users]] of [[stimulant]]s such as [[cocaine]] and [[methamphetamine]] are at a high risk for ischemic stroke.<ref>{{cite news | vauthors = Osterweil N |title=Methamphetamine May Trigger Ischemic Stroke |url=https://www.medpagetoday.com/neurology/strokes/4761 |work=Medpage Today |date=26 December 2006 }}</ref>
 
===Hemorrhagic===
{{Main|Intracerebral hemorrhage|Subarachnoid hemorrhage}}
[[File:Parachemableedwithedema.png|thumb|[[CT scan]] of an intraparenchymal bleed (bottom arrow) with surrounding edema (top arrow)]]
 
There are two main types of hemorrhagic stroke:<ref>{{cite web|last1=Anonymous|title=Hemorrhagic stroke|url=http://www.stroke.org/understand-stroke/what-stroke/hemorrhagic-stroke|publisher=National Stroke Association|access-date=30 June 2016|url-status=live|archive-url=https://web.archive.org/web/20160627175524/http://www.stroke.org/understand-stroke/what-stroke/hemorrhagic-stroke|archive-date=27 June 2016|date=2014-07-29}}</ref><ref>{{cite web|last1=Anonymous|title=Types of Stroke|url=https://www.cdc.gov/stroke/types_of_stroke.htm|website=www.cdc.gov|publisher=Centers of Disease Control and Prevention|access-date=30 June 2016|date=6 December 2013|url-status=live|archive-url=https://web.archive.org/web/20160627061518/http://www.cdc.gov/stroke/types_of_stroke.htm|archive-date=27 June 2016}}</ref>
* [[Intracerebral hemorrhage]], which is bleeding within the brain itself (when an artery in the brain bursts, flooding the surrounding tissue with blood), due to either [[intraparenchymal hemorrhage]] (bleeding within the brain tissue) or [[intraventricular hemorrhage]] (bleeding within the brain's [[ventricular system]]).
* [[Subarachnoid hemorrhage]], which is bleeding that occurs outside of the brain tissue but still within the skull, and precisely between the [[arachnoid mater]] and [[pia mater]] (the delicate ''innermost'' layer of the three layers of the [[meninges]] that surround the brain).
The above two main types of hemorrhagic stroke are also two different forms of [[intracranial hemorrhage]], which is the accumulation of blood anywhere within the [[cranial vault]]; but the other forms of intracranial hemorrhage, such as [[epidural hematoma]] (bleeding between the skull and the [[dura mater]], which is the thick ''outermost'' layer of the meninges that surround the brain) and [[subdural hematoma]] (bleeding in the [[subdural space]]), are not considered "hemorrhagic stroke".<ref>{{cite journal | vauthors = Al-Shahi Salman R, Labovitz DL, Stapf C | title = Spontaneous intracerebral haemorrhage | journal = BMJ | volume = 339 | issue = jul24 1 | pages = b2586 | date = July 2009 | pmid = 19633038 | doi = 10.1136/bmj.b2586 | s2cid = 206891608 }}</ref>
 
Hemorrhagic stroke may occur on the background of alterations to the blood vessels in the brain, such as [[cerebral amyloid angiopathy]], [[cerebral arteriovenous malformation]] and an [[intracranial aneurysm]], which can cause intraparenchymal or subarachnoid hemorrhage.<ref name="Articles">{{Cite web |title=Articles |url=https://www.cedars-sinai.org/health-library/articles.html |access-date=2022-04-26 |website=Cedars-Sinai |language=en-US |archive-date=2020-05-30 |archive-url=https://web.archive.org/web/20200530132825/https://www.cedars-sinai.org/health-library/articles.html |url-status=dead }}</ref>
 
In addition to neurological impairment, hemorrhagic stroke usually causes specific symptoms (for instance, subarachnoid hemorrhage classically causes a severe [[headache]] known as a [[thunderclap headache]]) or reveal evidence of a previous [[head injury]].
 
==Signs and symptoms==
Stroke may be preceded by premonitory symptoms, which may indicate a stroke is imminent. These symptoms may include dizziness, [[dysarthria]] (speech disorder), exhaustion, [[hemiparesis]] (weakness on one side of the body), [[paresthesia]] (tingling, pricking, chilling, burning, numbness of the skin), pathological laughter, seizure that turns into paralysis, "thunderclap" headache, or vomiting. Premonitory symptoms are not diagnostic of a stroke, and may be a sign of other illness. Assessing onset (gradual or sudden), duration, and the presence of other associated symptoms are important, and premonitory symptoms may not appear at all or may vary depending on the type of stroke.<ref>{{cite book|last1=Odier|first1=Céline|last2=Michel|first2=Patrik|chapter=Common Stroke Syndromes|title=Textbook of Stroke Medicine|editor-last1=Brainin|editor-first1=Michael|editor-last2=Heiss|editor-first2=Wolf-Dieter|editor-last3=Tabernig|editor-first3=Susan|___location=Cambridge, UK|publisher=Cambridge University Press|date=2014|isbn=9781107047495|url=https://books.google.com/books?id=wU5CBAAAQBAJ|page=161|postscript=none}}; {{cite book|last1=Jung|first1=Simon|last2=Mattle|first2=Heinrich P.|chapter=Is it a vascular event and where is the lesion?|title=Warlow's Stroke: Practical Management|editor-last1=Hankey|editor-first1=Graeme J.|editor-last2=Macleod|editor-first2=Malcolm|editor-last3=Gorelick|editor-first3=Philip B.|editor-last4=Chen|editor-first4=Christopher|editor-last5=Caprio|editor-first5=Fan Z.|editor-last6=Mattle|editor-first6=Heinrich|___location=Hoboken, N.J.|publisher=Blackwell Publishing|date=2019|isbn=9781118492222|url=https://books.google.com/books?id=8kCFDwAAQBAJ|pages=77, 449}}</ref>
The symptoms of stroke depend on the type of stroke and the area of the brain affected. Ischemic strokes usually only affect regional areas of the brain perfused by the blocked artery. Hemorrhagic strokes can affect local areas, but often can also cause more global symptoms due to bleeding and increased intracranial pressure.
 
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 the brain affected, the more functions that are likely to be lost. Some forms of stroke can cause additional symptoms. For example, in intracranial hemorrhage, the affected area may compress other structures. Most forms of stroke are not associated with a [[headache]], apart from subarachnoid hemorrhage and cerebral venous thrombosis and occasionally intracerebral hemorrhage.<ref name="Articles"/>
..If the area of the brain affected contains one of the three prominent [[Neural pathway|Central nervous system pathways]] -- the [[spinothalamic tract]], [[corticospinal tract]], and [[dorsal column]] ([[medial lemniscus]]), symptoms may include:
* muscle weakness ([[hemiplegia]])
* numbness
* reduction in sensory or vibratory sensation
 
===Early recognition===
In most cases, the symptoms affect only one side of the body. The defect in the brain is ''usually'' on the opposite side of the body (depending on which part of the brain is affected). However, the presence of any one of these symptoms does not necessarily suggest a stroke, since these pathways also travel in the [[spinal cord]] and any lesion there can also produce these symptoms.
{{main|FAST (stroke)}}
[[File:Act FAST.svg|thumb|A [[Centers for Disease Control and Prevention]] [[infographic]] describing the FAST mnemonic for early recognition of stroke]]
Systems have been proposed to increase recognition of stroke. 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 decreased (– [[likelihood ratios in diagnostic testing|likelihood ratio]] of 0.39).<ref name="pmid15900010">{{cite journal | vauthors = Goldstein LB, Simel DL | title = Is this patient having a stroke? | journal = JAMA | volume = 293 | issue = 19 | pages = 2391–402 | date = May 2005 | pmid = 15900010 | doi = 10.1001/jama.293.19.2391 | s2cid = 20408776 }}</ref> 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.
 
A mnemonic to remember the warning signs of stroke is [[FAST (stroke)|FAST]] (facial droop, arm weakness, speech difficulty, and time to call emergency services),<ref>{{cite journal | vauthors = Harbison J, Massey A, Barnett L, Hodge D, Ford GA | title = Rapid ambulance protocol for acute stroke | journal = Lancet | volume = 353 | issue = 9168 | pages = 1935 | date = June 1999 | pmid = 10371574 | doi = 10.1016/S0140-6736(99)00966-6 | s2cid = 36692451 }}</ref> as advocated by the [[Department of Health (United Kingdom)]] and the [[Stroke Association]], the [[American Stroke Association]], and the [[National Stroke Association]] (US). FAST is less reliable in the recognition of posterior circulation stroke.<ref>{{cite journal | vauthors = Merwick Á, Werring D | title = Posterior circulation ischaemic stroke | journal = BMJ | volume = 348 | issue = may19 33 | pages = g3175 | date = May 2014 | pmid = 24842277 | doi = 10.1136/bmj.g3175 | doi-access = free | url = http://www.bmj.com/content/bmj/348/bmj.g3175.full.pdf }}</ref> The revised mnemonic ''BE FAST'', which adds balance (sudden trouble keeping balance while walking or standing) and eyesight (new onset of blurry or double vision or sudden, painless loss of sight) to the assessment, has been proposed to address this shortcoming and improve early detection of stroke even further.<ref name=BEFAST>{{cite journal |vauthors=Aroor S, Singh R, Goldstein LB |title=BE-FAST (Balance, Eyes, Face, Arm, Speech, Time): Reducing the Proportion of Strokes Missed Using the FAST Mnemonic |journal=Stroke |volume=48 |issue=2 |pages=479–481 |date=February 2017 |pmid=28082668 |doi=10.1161/STROKEAHA.116.015169}}</ref><ref>{{cite journal |vauthors=Chen X, Zhao X, Xu F, Guo M, Yang Y, Zhong L, Weng X, Liu X |title=A Systematic Review and Meta-Analysis Comparing FAST and BEFAST in Acute Stroke Patients |journal=Front Neurol |volume=12 |issue= |pages=765069 |date=2021 |pmid=35153975 |pmc=8837419 |doi=10.3389/fneur.2021.765069|doi-access=free }}</ref> Other scales for prehospital detection of stroke include the [[Los Angeles Prehospital Stroke Screen (LAPSS)]]<ref>{{cite journal | vauthors = Kidwell CS, Saver JL, Schubert GB, Eckstein M, Starkman S | title = Design and retrospective analysis of the Los Angeles Prehospital Stroke Screen (LAPSS) | journal = Prehospital Emergency Care | volume = 2 | issue = 4 | pages = 267–73 | year = 1998 | pmid = 9799012 | doi = 10.1080/10903129808958878 }}</ref> and the [[Cincinnati Stroke Scale|Cincinnati Prehospital Stroke Scale]] (CPSS),<ref>{{cite journal | vauthors = Kothari RU, Pancioli A, Liu T, Brott T, Broderick J | title = Cincinnati Prehospital Stroke Scale: reproducibility and validity | journal = Annals of Emergency Medicine | volume = 33 | issue = 4 | pages = 373–8 | date = April 1999 | pmid = 10092713 | doi = 10.1016/S0196-0644(99)70299-4 }}</ref> on which the FAST method was based.<ref>{{cite journal |vauthors=Harbison J, Hossain O, Jenkinson D, Davis J, Louw SJ, Ford GA |title=Diagnostic accuracy of stroke referrals from primary care, emergency room physicians, and ambulance staff using the face arm speech test |journal=Stroke |volume=34 |issue=1 |pages=71–6 |date=January 2003 |pmid=12511753 |doi=10.1161/01.str.0000044170.46643.5e}}</ref> Use of these scales is recommended by professional guidelines.<ref name=NICECG68>{{NICE|68|Stroke|2008}}</ref>
In addition to the above CNS pathways, the ''[[brainstem]]'' also consists of the 12 [[cranial nerves]]. A stroke affecting the brainstem therefore can produce symptoms relating to deficits in these cranial nerves:
 
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.<ref name=NICECG68/><ref>{{cite journal | vauthors = Nor AM, Davis J, Sen B, Shipsey D, Louw SJ, Dyker AG, Davis M, Ford GA | title = The Recognition of Stroke in the Emergency Room (ROSIER) scale: development and validation of a stroke recognition instrument | journal = The Lancet. Neurology | volume = 4 | issue = 11 | pages = 727–34 | date = November 2005 | pmid = 16239179 | doi = 10.1016/S1474-4422(05)70201-5 | s2cid = 2744751 }}</ref>
 
===Associated symptoms===
{{unreferenced section|date=April 2024}}
[[Unconsciousness|Loss of consciousness]], [[headache]], and [[vomiting]] usually occur more often in hemorrhagic stroke than in thrombosis because of the increased [[intracranial pressure]] from the leaking blood compressing the brain.
 
If symptoms are maximal at onset, the cause is more likely to be a subarachnoid hemorrhage or an embolic stroke.
 
===Subtypes===
If the area of the brain affected includes one of the three prominent [[Neural pathway|central nervous system pathways]]—the [[spinothalamic tract]], [[corticospinal tract]], and the [[dorsal column–medial lemniscus pathway]], symptoms may include:
* [[hemiplegia]] and [[central facial palsy|muscle weakness of the face]]
* [[numbness]]
* reduction in sensory or vibratory sensation
* initial [[flaccidity]] (reduced muscle tone), replaced by [[spasticity]] (increased muscle tone), [[hyperreflexia|excessive reflexes]], and obligatory synergies.<ref name=OSul07_719>{{cite book | vauthors = O'Sullivan SB | title = Physical Rehabilitation | chapter = Stroke | volume = 5 | veditors = O'Sullivan SB, Schmitz TJ | publisher = F.A. Davis Company | year = 2007 | ___location = Philadelphia | page = 719 }}</ref>
 
In most cases, the symptoms affect only one side of the body (unilateral). The defect in the brain is ''usually'' on the [[contralateral|opposite side]] of the body. However, since these pathways also travel in the [[spinal cord]] and any lesion there can also produce these symptoms, the presence of any one of these symptoms does not necessarily indicate stroke. In addition to the above central nervous system pathways, the [[brainstem]] gives rise to most of the twelve [[cranial nerves]]. A [[brainstem stroke syndrome|brainstem stroke]] affecting the brainstem and brain, therefore, can produce symptoms relating to deficits in these cranial nerves:{{citation needed|date=January 2017}}
* altered smell, taste, hearing, or vision (total or partial)
* drooping of eyelid ([[ptosis (eyelid)|ptosis]]) and weakness of [[Extraocular muscles|ocular muscles]]
* decreased reflexes[[reflex]]es: gag, swallow, pupil reactivity to light
* decreased sensation and muscle weakness of the face
* [[Balance disorder|balance problems]] and [[nystagmus]]
* altered breathing and heart rate
* weakness in [[sternocleidomastoid muscle]] (SCM) with inability to turn head to one side
* weakness in tongue (inability to protrudestick out the tongue and/or move it from side to side)
 
If the ''[[cerebral cortex]]'' is involved, the CNScentral nervous system pathways can again be affected, but also can also produce the following symptoms:
* [[aphasia]] (inabilitydifficulty towith speakverbal orexpression, understandauditory languagecomprehension, from[[Alexia involvement(condition)|reading]] ofand [[Agraphia|writing]]; [[Broca's area|Broca's]] or [[Wernicke's area]] typically involved)
* [[dysarthria]] ([[motor speech disorders|motor speech disorder]] resulting from neurological injury)
* [[apraxia]] (altered voluntary movements)
* [[visual field]] cut(involvement of occipital lobe)defect
* memory deficits (involvement of [[temporal lobe]])
* [[hemineglect]] (involvement of [[parietal lobe]])
* disorganized thinking, confusion, [[hypersexual]] gestures (with involvement of frontal lobe)
* [[anosognosia|lack of insight]] of his or her, usually stroke-related, disability
 
If the ''[[cerebellum]]'' is involved, the[[Ataxia#Cerebellar|ataxia]] patientmight maybe havepresent theand followingthis includes:
* troublealtered walking [[Gait abnormality|gait]]
* altered [[motor coordination|movement coordination]]
* [[Vertigo (medical)|vertigo]] and or disequilibrium
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.
 
=== Preceding signs and symptoms ===
If symptoms are maximal at onset, the cause is more likely to be a subarachnoid hemorrhage or an embolic stroke.
In the days before a stroke (generally in the previous 7 days, even the previous one), a considerable proportion of patients have a "sentinel headache": a severe and unusual headache that indicates a problem.<ref>{{cite journal | vauthors = Lebedeva ER, Ushenin AV, Gurary NM, Gilev DV, Olesen J | title = Diagnostic criteria for acute headache attributed to ischemic stroke and for sentinel headache before ischemic stroke | journal = The Journal of Headache and Pain | volume = 23 | issue = 1 | article-number = 11 | date = January 2022 | pmid = 35057731 | pmc = 8903596 | doi = 10.1186/s10194-021-01372-x | doi-access = free }}</ref> Its appearance makes it advisable to seek medical review and to consider [[Stroke#Prevention|prevention against stroke]].
 
==Causes==
 
===Thrombotic stroke===
[[File:Blausen 0836 Stroke.png|thumb|Illustration of an embolic stroke, showing a blockage lodged in a blood vessel]]
In thrombotic stroke, a thrombus<ref>{{MedlinePlusEncyclopedia|18120|Thrombus}}</ref> (blood clot) usually forms around [[atherosclerosis|atherosclerotic]] plaques. Since blockage of the artery is gradual, onset of symptomatic thrombotic stroke is slower than that of hemorrhagic stroke. A thrombus itself (even if it does not completely block the blood vessel) can lead to an embolic stroke (see below) if the thrombus breaks off and travels in the bloodstream, at which point it is called an [[embolus]]. Two types of thrombosis can cause stroke:
* ''Large vessel disease'' involves the [[Common carotid artery|common]] and [[internal carotid artery|internal carotid arteries]], the [[vertebral artery]], and the [[Circle of Willis]].<ref>{{cite web|url=http://www.strokecenter.org/professionals/brain-anatomy/blood-vessels-of-the-brain/|publisher=The Internet Stroke Center|title=Circle of Willis|url-status=live|archive-url=https://web.archive.org/web/20160205102902/http://www.strokecenter.org/professionals/brain-anatomy/blood-vessels-of-the-brain/|archive-date=2016-02-05}}</ref> Diseases that may form [[thrombi]] in the large vessels include (in descending incidence): atherosclerosis, [[vasoconstriction]] (tightening of the artery), [[Aortic dissection|aortic]], [[carotid artery dissection|carotid]] or [[vertebral artery dissection]], inflammatory diseases of the blood vessel wall ([[Takayasu arteritis]], [[giant cell arteritis]], [[vasculitis]]), noninflammatory vasculopathy, [[Moyamoya disease]] and [[fibromuscular dysplasia]]. Strokes caused by artery dissections are in the strictest sense not always caused by a 'defined disease state', such events can occur in very young people and can be caused by physical injury such as hyperextension of the neck area or often by other forms of trauma.<ref>{{cite journal | vauthors = Correia PN, Meyer IA, Eskandari A, Michel P | title = Beauty parlor stroke revisited: An 11-year single-center consecutive series | journal = International Journal of Stroke | volume = 11 | issue = 3 | pages = 356–360 | date = April 2016 | pmid = 26763920 | doi = 10.1177/1747493015620809 | s2cid = 36985608 }}</ref>
* ''[[Small vessel disease]]'' involves the smaller arteries inside the brain: branches of the [[circle of Willis]], middle cerebral artery, stem, and arteries arising from the distal vertebral and [[basilar artery]].<ref>{{cite web|url=http://www.nhs.uk/conditions/aneurysm/Pages/Introduction.aspx|publisher=[[National Health Service|NHS]] Choices|title=Brain anaurysm – Introduction|url-status=live|archive-url=https://web.archive.org/web/20160208185638/http://www.nhs.uk/conditions/aneurysm/Pages/Introduction.aspx|archive-date=2016-02-08|date=2017-10-19}}</ref> Diseases that may form thrombi in the small vessels include (in descending incidence): [[lipohyalinosis]] (build-up of fatty hyaline matter in the blood vessel as a result of high blood pressure and aging) and [[fibrinoid degeneration]] (stroke involving these vessels is known as a [[lacunar stroke]]) and microatheroma (small atherosclerotic plaques).<ref>{{cite journal | vauthors = Fisher CM | title = The arterial lesions underlying lacunes | journal = Acta Neuropathologica | volume = 12 | issue = 1 | pages = 1–15 | date = December 1968 | pmid = 5708546 | doi = 10.1007/BF00685305 | s2cid = 6942826 }}</ref>
 
Anemia causes increase blood flow in the blood circulatory system. This causes the endothelial cells of the blood vessels to express adhesion factors which encourages the clotting of blood and formation of thrombus.<ref name="pmid34207841">{{cite journal |vauthors=Heo J, Youk TM, Seo KD |title=Anemia Is a Risk Factor for the Development of Ischemic Stroke and Post-Stroke Mortality |journal=Journal of Clinical Medicine |volume=10 |issue=12 |date=June 2021 |page=2556 |pmid=34207841 |pmc=8226740 |doi=10.3390/jcm10122556 |url=|doi-access=free }}</ref> [[Sickle-cell disease|Sickle-cell anemia]], which can cause [[blood cell]]s to clump up and block blood vessels, can also lead to stroke. Stroke is the second leading cause of death in people under 20 with sickle-cell anemia.<ref name="NINDS1999"/>
 
===Embolic stroke===
An embolic stroke refers to an [[arterial embolism]] (a blockage of an artery) by an [[embolus]], a traveling 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 embolism|fat]] (e.g., from [[bone marrow]] in a [[Bone fracture|broken bone]]), air, [[cancer]] cells or clumps of [[bacteria]] (usually from infectious [[endocarditis]]).<ref name=Robbins/>
 
Because an embolus arises from elsewhere, local therapy solves the problem only temporarily. Thus, the source of the embolus must be identified. Because the embolic blockage is sudden in onset, symptoms are usually maximal at the 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]] embolizes through an [[atrial septal defect|atrial]] or [[ventricular septal defect]] in the heart into the brain.<ref name=Robbins>{{cite book| vauthors = Kumar V |title=Robbins and Cotran Pathologic Basis of Disease, Professional Edition.|year=2009|publisher=Elsevier|___location=Philadelphia|isbn=978-1-4377-0792-2|edition=8th}}</ref>
 
Causes of stroke related to the heart can be distinguished between high- and low-risk:<ref name="ay">{{cite journal | vauthors = Ay H, Furie KL, Singhal A, Smith WS, Sorensen AG, Koroshetz WJ | title = An evidence-based causative classification system for acute ischemic stroke | journal = Annals of Neurology | volume = 58 | issue = 5 | pages = 688–97 | date = November 2005 | pmid = 16240340 | doi = 10.1002/ana.20617 | s2cid = 28798146 }}</ref>
* High risk: atrial fibrillation and [[paroxysmal atrial fibrillation]], [[Rheumatic fever|rheumatic disease]] of the [[mitral valve|mitral]] or [[aortic valve]] disease, [[artificial heart valve]]s, known cardiac thrombus of the atrium or ventricle, [[sick sinus syndrome]], sustained [[atrial flutter]], recent myocardial infarction, chronic myocardial infarction together with [[ejection fraction]] <28 percent, symptomatic [[congestive heart failure]] with ejection fraction <30 percent, [[dilated cardiomyopathy]], [[Libman-Sacks endocarditis]], [[Marantic endocarditis]], [[infective endocarditis]], [[papillary fibroelastoma]], [[atrial myxoma|left atrial myxoma]], and [[coronary artery bypass graft]] (CABG) surgery.
* Low risk/potential: calcification of the annulus (ring) of the mitral valve, patent foramen ovale (PFO), atrial septal aneurysm, atrial septal aneurysm ''with'' patent foramen ovale, left ventricular aneurysm without thrombus, isolated left atrial "smoke" on [[echocardiography]] (no [[mitral stenosis]] or atrial fibrillation), and complex atheroma in the [[ascending aorta]] or proximal arch
 
Among those who have a complete blockage of one of the carotid arteries, the risk of stroke on that side is about one percent per year.<ref>{{cite journal | vauthors = Hackam DG | title = Prognosis of Asymptomatic Carotid Artery Occlusion: Systematic Review and Meta-Analysis | journal = Stroke | volume = 47 | issue = 5 | pages = 1253–7 | date = May 2016 | pmid = 27073237 | doi = 10.1161/strokeaha.116.012760 | s2cid = 3669224 | doi-access = free }}</ref>
 
A special form of embolic stroke is the [[embolic stroke of undetermined source]] (ESUS). This subset of cryptogenic stroke is defined as a non-lacunar brain infarct without proximal arterial stenosis or cardioembolic sources. About one out of six cases of ischemic stroke could be classified as ESUS.<ref>{{cite journal | vauthors = Hart RG, Catanese L, Perera KS, Ntaios G, Connolly SJ | title = Embolic Stroke of Undetermined Source: A Systematic Review and Clinical Update | journal = Stroke | volume = 48 | issue = 4 | pages = 867–872 | date = April 2017 | pmid = 28265016 | doi = 10.1161/STROKEAHA.116.016414 | s2cid = 3679562 | doi-access = free }}</ref>
 
===Cerebral hypoperfusion===
[[Shock (circulatory)|Cerebral hypoperfusion]] is the reduction of blood flow to all parts of the brain. The reduction could be to a particular part of the brain depending on the cause. It is most commonly due to [[heart failure]] from [[cardiac arrest]] or [[arrhythmia]]s, or from reduced [[cardiac output]] as a result of [[myocardial infarction]], [[pulmonary embolism]], [[pericardial effusion]], or bleeding.{{citation needed|date=October 2012}} [[Hypoxia (medical)|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 the 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===
[[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.<ref name=Stam2005/>
 
===Intracerebral hemorrhage===
It generally occurs in small arteries or arterioles and is commonly due to hypertension,<ref>{{cite journal | vauthors = Strandgaard S | title = Hypertension and stroke | journal = Journal of Hypertension Supplement | volume = 14 | issue = 3 | pages = S23-7 | date = October 1996 | pmid = 9120662 | doi = 10.1097/00004872-199610003-00005 | s2cid = 11817729 }}</ref> intracranial vascular malformations (including [[cavernous angioma]]s or [[arteriovenous malformation]]s), cerebral [[amyloid angiopathy]], or infarcts into which secondary hemorrhage has occurred.<ref name=Donnan2008/> Other potential causes are trauma, [[Hemophilia|bleeding disorders]], [[amyloid angiopathy]], [[Recreational drug use|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]], [[cerebrospinal fluid|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 [[subarachnoid hemorrhage]] (which technically may also be classified as a type of stroke<ref name=Donnan2008/>).
 
===Other===
Other causes may include spasm of an artery. This may occur due to [[cocaine]].<ref>{{cite book| vauthors = Harrigan MR, Deveikis JP |title=Handbook of Cerebrovascular Disease and Neurointerventional Technique|date=2012|publisher=Springer Science & Business Media|isbn=978-1-61779-945-7 |page=692 |url= https://books.google.com/books?id=aUh1JA82zCMC&pg=PA692 |language=en|url-status=live|archive-url=https://web.archive.org/web/20170109020750/https://books.google.com/books?id=aUh1JA82zCMC&pg=PA692|archive-date=2017-01-09}}</ref> [[Cancer]] is also another well recognized potential cause of stroke. Although, malignancy in general can increase the risk of stroke, certain types of cancer such as pancreatic, lung and gastric are typically associated with a higher thromboembolism risk. The mechanism with which cancer increases stroke risk is thought to be secondary to an acquired [[Thrombophilia|hypercoagulability]].<ref>{{cite journal | vauthors = Navi BB, Iadecola C | title = Ischemic stroke in cancer patients: A review of an underappreciated pathology | journal = Annals of Neurology | volume = 83 | issue = 5 | pages = 873–883 | date = May 2018 | pmid = 29633334 | pmc = 6021225 | doi = 10.1002/ana.25227 }}</ref> [[Air pollution]] is responsible for around 27% of deaths from strokes worldwide, according to the [[Global Burden of Disease Study]].<ref name="HEI_2024_p3-4">{{Cite book |last1=Health Effects Institute |author-link1=Health Effects Institute |url=https://www.stateofglobalair.org/resources/report/state-global-air-report-2024 |title=State of Global Air Report 2024: A Special Report on Global Exposure to Air Pollution and its Health Impacts with a Focus on Children's Health. |last2=Institute for Health Metrics and Evaluation |author-link2=Institute for Health Metrics and Evaluation |last3=UNICEF |author-link3=UNICEF |date=2024 |publisher=Health Effects Institute |page=27 |issn=2578-6873}}</ref>
 
===Silent stroke===
[[Silent stroke]] is stroke that does not have any outward symptoms, and people are typically unaware they had experienced stroke. Despite not causing identifiable symptoms, silent stroke still damages the brain and places the person at increased risk for both [[transient ischemic attack]] and major stroke in the future. Conversely, those who have had major stroke are also at risk of having silent stroke.<ref>{{cite journal | vauthors = Miwa K, Hoshi T, Hougaku H, Tanaka M, Furukado S, Abe Y, Okazaki S, Sakaguchi M, Sakoda S, Kitagawa K | title = Silent cerebral infarction is associated with incident stroke and TIA independent of carotid intima-media thickness | journal = Internal Medicine | volume = 49 | issue = 9 | pages = 817–22 | year = 2010 | pmid = 20453400 | doi = 10.2169/internalmedicine.49.3211 | doi-access = free }}</ref> In a broad study in 1998, more than 11 million people were estimated to have experienced stroke in the United States. Approximately 770,000 of these were symptomatic and 11 million were first-ever silent MRI infarcts or [[hemorrhage]]s. Silent stroke typically causes [[lesion]]s which are detected via the use of neuroimaging such as [[MRI]]. Silent stroke is estimated to occur at five times the rate of symptomatic stroke.<ref name=Dutch_TIA92>{{cite journal | vauthors = Herderscheê D, Hijdra A, Algra A, Koudstaal PJ, Kappelle LJ, van Gijn J | title = Silent stroke in patients with transient ischemic attack or minor ischemic stroke. The Dutch TIA Trial Study Group | journal = Stroke | volume = 23 | issue = 9 | pages = 1220–4 | date = September 1992 | pmid = 1519274 | doi = 10.1161/01.STR.23.9.1220 | doi-access = free }}</ref><ref>{{cite journal | vauthors = Leary MC, Saver JL | title = Annual incidence of first silent stroke in the United States: a preliminary estimate | journal = Cerebrovascular Diseases | volume = 16 | issue = 3 | pages = 280–5 | year = 2003 | pmid = 12865617 | doi = 10.1159/000071128 | s2cid = 33095581 }}</ref> The risk of silent stroke increases with age, but they may also affect younger adults and children, especially those with acute [[anemia]].<ref name=Dutch_TIA92/><ref>{{cite journal | vauthors = Vermeer SE, Koudstaal PJ, Oudkerk M, Hofman A, Breteler MM | title = Prevalence and risk factors of silent brain infarcts in the population-based Rotterdam Scan Study | journal = Stroke | volume = 33 | issue = 1 | pages = 21–5 | date = January 2002 | pmid = 11779883 | doi = 10.1161/hs0102.101629 | doi-access = free }}</ref>
 
==Pathophysiology==
 
===Ischemic===
[[File:Histopathology of thalamus infarction at approximately 24 hours, high magnification, annotated.jpg|thumb|Histopathology at high magnification of a normal neuron, and ischemic stroke at approximately 24 hours on [[H&E stain]]: The neurons become hypereosinophilic and there is an infiltrate of [[neutrophil]]s. There is slight edema and loss of normal architecture in the surrounding [[neuropil]].]]
{{more medical citations needed|section|date=June 2022}}
 
Ischemic stroke occurs because of a loss of blood supply to part of the brain, initiating the [[ischemic cascade]].<ref name=Deb>{{cite journal | vauthors = Deb P, Sharma S, Hassan KM | title = Pathophysiologic mechanisms of acute ischemic stroke: An overview with emphasis on therapeutic significance beyond thrombolysis | journal = Pathophysiology | volume = 17 | issue = 3 | pages = 197–218 | date = June 2010 | pmid = 20074922 | doi = 10.1016/j.pathophys.2009.12.001 | doi-access = free }}</ref> 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.<ref>{{cite book| vauthors = Snell RS |title= Clinical neuroanatomy, 6. ed |publisher= Lippincott Williams & Wilkins, Philadelphia|pages= 478–85|isbn= 978-963-226-293-2 |year=2006}}</ref> 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 to 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 (medicine)|penumbra]]".<ref>Brunner and Suddarth's Textbook on Medical-Surgical Nursing, 11th Edition</ref> After the initial ischemic event the penumbra transitions from a [[tissue remodeling]] characterized by damage to a remodeling characterized by repair.<ref name="pmid18463660">{{cite journal | author= Lo EH | title=A new penumbra: transitioning from injury into repair after stroke | journal=[[Nature Medicine]] | volume=14 | issue=5| pages=497–500 | year=2008 | doi = 10.1038/nm1735 | pmid=18463660| s2cid=205385488 }}</ref>
[[File:Molecular pathways outlining the role of glutamate in excitoxicity following stroke.png|thumb|300px|right|Molecular pathways outlining the role of glutamate excitoxicity following stroke]]
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 the 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<sup>+</sup>) 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|programmed cell death]].<ref name="PMID8761323">{{cite journal | vauthors = Kristián T, Siesjö BK | title = Calcium-related damage in ischemia | journal = Life Sciences | volume = 59 | issue = 5–6 | pages = 357–67 | date = 1996 | pmid = 8761323 | doi = 10.1016/0024-3205(96)00314-1 }}</ref>
 
Ischemia also induces production of [[Radical (chemistry)|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 may occur. 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.
 
==== Collateral flow ====
[[File:Impact of collateral flow on clot lysis and reperfusion. % 28a% 29 Schematic drawing of the collateral network showing anastomoses between the middle cerebral artery converted to svg by hariadhi.svg|thumb|400px|Impact of collateral flow on [[clot lysis]] and [[Reperfusion therapy|reperfusion]]]]
The brain can compensate inadequate blood flow in a single artery by the collateral system. This system relies on the efficient connection between the carotid and [[vertebral arteries]] through the [[circle of Willis]] and, to a lesser extent, the major arteries supplying the [[cerebral hemisphere]]s. However, variations in the circle of Willis, caliber of collateral vessels, and acquired [[Atheroma|arterial lesions]] such as atherosclerosis can disrupt this compensatory mechanism, increasing the risk of brain ischemia resulting from artery blockage.<ref name="MSD-2023">{{Cite web |title=Ischemic Stroke - Neurologic Disorders |url=https://www.msdmanuals.com/professional/neurologic-disorders/stroke/ischemic-stroke |access-date=2023-02-14 |website=MSD Manual Professional Edition |language=en}}</ref>
 
The extent of damage depends on the duration and severity of the ischemia. If ischemia persists for more than 5 minutes with [[perfusion]] below 5% of normal, some neurons will die. However, if ischemia is mild, the damage will occur slowly and may take up to 6 hours to completely destroy the brain tissue. In case of severe ischemia lasting more than 15 to 30 minutes, all of the affected tissue will die, leading to infarction. The rate of damage is affected by temperature, with [[hyperthermia]] accelerating damage and [[hypothermia]] slowing it down and other factors. Prompt restoration of blood flow to ischemic tissues can reduce or reverse injury, especially if the tissues are not yet irreversibly damaged. This is particularly important for the moderately ischemic areas (penumbras) surrounding areas of severe ischemia, which may still be salvageable due to collateral flow.<ref name="MSD-2023" /><ref>{{cite journal | vauthors = Iwasawa E, Ichijo M, Ishibashi S, Yokota T | title = Acute development of collateral circulation and therapeutic prospects in ischemic stroke | journal = Neural Regeneration Research | volume = 11 | issue = 3 | pages = 368–371 | date = March 2016 | pmid = 27127459 | pmc = 4828985 | doi = 10.4103/1673-5374.179033 | doi-access = free }}</ref><ref>{{cite journal | vauthors = Liu L, Ding J, Leng X, Pu Y, Huang LA, Xu A, Wong KS, Wang X, Wang Y | title = Guidelines for evaluation and management of cerebral collateral circulation in ischaemic stroke 2017 | journal = Stroke and Vascular Neurology | volume = 3 | issue = 3 | pages = 117–130 | date = September 2018 | pmid = 30294467 | doi = 10.1136/svn-2017-000135 | pmc = 6169613 }}</ref>
====Subarachnoid hemorrhage====
{{main|subarachnoid hemorrhage}}
The symptoms of SAH occur abruptly due to the sudden onset of increased intracranial pressure. Often, patients complain of a sudden, extremely severe and widespread headache. The pain may or may not radiate down into neck and legs. Vomiting may occur soon after the onset of headache. Usually the neurologic exam is nonfocal -- meaning no deficits can be identified that attributes to certain areas of the brain -- unless the bleeding also occurs into the brain. The combination of headache and vomiting is uncommon in ischemic stroke.
 
===Hemorrhagic===
====Transient ischemic attack (TIA)====
Hemorrhagic stroke is classified based on their underlying pathology. Some causes of hemorrhagic stroke are [[Hypertensive|hypertensive hemorrhage]], ruptured [[aneurysm]], ruptured [[AV fistula]], transformation of prior ischemic infarction, and drug-induced [[bleeding]].<ref name="Harrison's" /> 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]].<ref name="NINDS1999"/><ref name="Wang 2010">{{cite journal | vauthors = Wang J | title = Preclinical and clinical research on inflammation after intracerebral hemorrhage | journal = Progress in Neurobiology | volume = 92 | issue = 4 | pages = 463–77 | date = December 2010 | pmid = 20713126 | pmc = 2991407 | doi = 10.1016/j.pneurobio.2010.08.001 }}</ref> [[Inflammation]] contributes to the [[secondary brain injury]] after hemorrhage.<ref name="Wang 2010"/>
{{main|Transient ischemic attack}}
If the symptoms resolve within an hour, or maximum 24 hours, the diagnosis is [[transient ischemic attack]] (TIA), which is in essence a mini or brief stroke. This syndrome may be a warning sign, and a large proportion of patients develop strokes in the future. Recent data indicate that there is about a ten to fifteen percent chance of suffering a stroke in the year following a TIA, with half of that risk manifest in the first month, and, further, with much of that risk manifest in the first 48 hours. The chances of suffering an [[ischemic stroke]] can be reduced by using [[aspirin]] or related compounds such as clopidogrel, which inhibit platelets from aggregating and forming obstructive clots; but, for the same reason, such treatments (slightly) increase the likelihood and effects of [[hemorrhagic stroke]] since they impair clotting.
 
==Diagnosis==
<!-- Old File:StrokeMCA.png -->
Stroke is diagnosed through several techniques: a neurological examination, [[blood test]]s, [[CT scan]]s (without contrast enhancements) or [[MRI scan]]s, [[Doppler ultrasound]], and [[arteriography]].
[[File:StrokeMCA overlay.png|thumb|A CT showing early signs of a middle cerebral artery stroke with loss of definition of the gyri and grey white boundary]]
[[File:Dens media sign mit Mediainfarkt - CCT 001.jpg|thumb|Dense artery sign in a patient with [[middle cerebral artery]] infarction shown on the left. Right image after 7 hours.]]
Stroke is diagnosed through several techniques: a neurological examination (such as the [[NIHSS]]), CT scans (most often without contrast enhancements) or [[MRI scan]]s, [[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.<ref name="hill2005">{{cite journal | vauthors = Hill MD | title = Diagnostic biomarkers for stroke: a stroke neurologist's perspective | journal = Clinical Chemistry | volume = 51 | issue = 11 | pages = 2001–2 | date = November 2005 | pmid = 16244286 | doi = 10.1373/clinchem.2005.056382 | doi-access = free }}</ref> In deceased people, an [[autopsy of stroke]] may help establishing the time between stroke onset and death.
 
===Physical examination===
A [[physical examination]], including taking a [[medical history]] of the symptoms and a neurological status, helps giving an evaluation of the ___location and severity of stroke. It can give a standard score on e.g., the [[NIH stroke scale]].
A systematic review by the [http://www.sgim.org/clinexam-rce.cfm Rational Clinical Examination] found that acute facial paresis, arm drift, or abnormal speech are the best findings <ref name="pmid15900010">{{cite journal |author=Goldstein L, Simel D |title=Is this patient having a stroke? |journal=JAMA |volume=293 |issue=19 |pages=2391-402 |year=2005 |id=PMID 15900010 | doi=10.1001/jama.296.16.2012 | url=http://jama.ama-assn.org/cgi/content/full/296/16/2012}}</ref>.
 
===Imaging===
For diagnosing ischemic (blockage) stroke in the emergency setting :<ref name="pmid17258669">{{cite journal |author vauthors = Chalela JJA, Kidwell CCS, Nentwich LLM, Luby M, Butman JJA, Demchuk AAM, Hill MMD, Patronas N, Latour L, Warach S | title = Magnetic resonance imaging and computed tomography in emergency assessment of patients with suspected acute stroke: a prospective comparison | journal = Lancet | volume = 369 | issue = 9558 | pages =293-8 293–8 |year date = January 2007 |id pmid =PMID 17258669 | pmc = 1859855 | doi = 10.1016/S0140-6736(07)60151-2 }}</ref>:
* [[CT scan]]sscans (''without'' contrast enhancements)
:** [[sensitivity (tests)|sensitivity]]= 16% (less than 10% within first 3 hours of symptom onset)
:** [[specificity (tests)|specificity]]= 96%
* [[MRI scan]]
:** [[sensitivity]] = 83%
:** specificity = 98%
 
For diagnosing hemorrhagic stroke in the emergency setting:
* [[CT scan]]sscans (''without'' contrast enhancements)
:** [[sensitivity]]= 89%
:** specificity = 100%
* [[MRI scan]]
:** [[sensitivity]] = 81%
:** specificity = 100%
For detecting chronic hemorrhages, an MRI scan is more sensitive.<ref name="pmid15494579">{{cite journal | vauthors = Kidwell CS, Chalela JA, Saver JL, Starkman S, Hill MD, Demchuk AM, Butman JA, Patronas N, Alger JR, Latour LL, Luby ML, Baird AE, Leary MC, Tremwel M, Ovbiagele B, Fredieu A, Suzuki S, Villablanca JP, Davis S, Dunn B, Todd JW, Ezzeddine MA, Haymore J, Lynch JK, Davis L, Warach S | title = Comparison of MRI and CT for detection of acute intracerebral hemorrhage | journal = JAMA | volume = 292 | issue = 15 | pages = 1823–30 | date = October 2004 | pmid = 15494579 | doi = 10.1001/jama.292.15.1823 | doi-access = }}</ref>
 
For the assessment of stable stroke, nuclear medicine scans such as [[single-photon emission computed tomography]] (SPECT) and [[positron emission tomography–computed tomography]] (PET/CT) may be helpful. SPECT documents cerebral blood flow, whereas PET with an FDG isotope shows cerebral glucose metabolism.
For detecting chronic hemorrhages, [[MRI scan]] is better <ref name="pmid15494579">{{cite journal |author=Kidwell C, Chalela J, Saver J, Starkman S, Hill M, Demchuk A, Butman J, Patronas N, Alger J, Latour L, Luby M, Baird A, Leary M, Tremwel M, Ovbiagele B, Fredieu A, Suzuki S, Villablanca J, Davis S, Dunn B, Todd J, Ezzeddine M, Haymore J, Lynch J, Davis L, Warach S |title=Comparison of MRI and CT for detection of acute intracerebral hemorrhage |journal=JAMA |volume=292 |issue=15 |pages=1823-30 |year=2004 |id=PMID 15494579}}</ref>
 
CT scans may not detect ischemic stroke, especially if it is small, of recent onset,<ref name=AFP2009/> or in the brainstem or cerebellum areas ([[posterior circulation infarct]]). MRI is better at detecting a posterior circulation infarct with [[Diffusion MRI|diffusion-weighted imaging]].<ref name="pmid24778625">{{cite journal | vauthors = Nouh A, Remke J, Ruland S | title = Ischemic posterior circulation stroke: a review of anatomy, clinical presentations, diagnosis, and current management | journal = Frontiers in Neurology | volume = 5 | issue = | pages = 30 | date = 2014 | pmid = 24778625 | pmc = 3985033 | doi = 10.3389/fneur.2014.00030 | url = | doi-access = free }}</ref> A CT scan is used more to ''rule out'' certain stroke mimics and detect bleeding.<ref name=AFP2009/> The presence of [[leptomeningeal collateral circulation]] in the brain is associated with better clinical outcomes after recanalization treatment.<ref name="pmid28864854">{{cite journal |vauthors=Tong E, Patrie J, Tong S, Evans A, Michel P, Eskandari A, Wintermark M |title=Time-resolved CT assessment of collaterals as imaging biomarkers to predict clinical outcomes in acute ischemic stroke |journal=Neuroradiology |volume=59 |issue=11 |pages=1101–1109 |date=November 2017 |pmid=28864854 |doi=10.1007/s00234-017-1914-z |s2cid=19070631 |url=}}</ref> Cerebrovascular reserve capacity is another factor that affects stroke outcome {{ndash}} it is the amount of increase in cerebral blood flow after a purposeful stimulation of blood flow by the physician, such as by giving inhaled carbon dioxide or [[intravenous]] [[acetazolamide]]. The increase in blood flow can be measured by PET scan or transcranial doppler sonography.<ref name="pmid12242957">{{cite journal |vauthors=Stoll M, Hamann GF |title=[Cerebrovascular reserve capacity] |language=German |journal=Der Nervenarzt |volume=73 |issue=8 |pages=711–8 |date=August 2002 |pmid=12242957 |doi=10.1007/s00115-002-1313-4 |s2cid=34870086 |url=}}</ref> However, in people with obstruction of the [[internal carotid artery]] of one side, the presence of leptomeningeal collateral circulation is associated with reduced cerebral reserve capacity.<ref name="pmid34112002">{{cite journal |vauthors=Sebök M, Niftrik BV, Lohaus N, Esposito G, Amki ME, Winklhofer S, Wegener S, Regli L, Fierstra J |title=Leptomeningeal collateral activation indicates severely impaired cerebrovascular reserve capacity in patients with symptomatic unilateral carotid artery occlusion |journal=Journal of Cerebral Blood Flow and Metabolism |volume=41 |issue=11 |pages=3039–3051 |date=November 2021 |pmid=34112002 |pmc=8545056 |doi=10.1177/0271678X211024373 |url=}}</ref>
==Investigation of underlying etiology==
If a stroke is confirmed on imaging, various other studies may be performed to determine whether there is a peripheral source of [[embolus|emboli]]:
* an [[medical ultrasonography|ultrasound/doppler study]] of the [[carotid artery|carotid arteries]] (to detect [[carotid stenosis]])
* an [[electrocardiogram]] (ECG) and [[echocardiogram]] (to identify [[cardiac arrhythmia|arrhythmias]] and resultant clots in the heart which may spread to the brain vessels through the bloodstream)
* a [[Holter monitor]] study to identify intermittent arrhythmias
* an [[angiogram]] of the cerebral vasculature (if a bleed is thought to have originated from an [[aneurysm]] or [[arteriovenous malformation]])
 
===Underlying cause===
==Treatment==
[[File:Left MCA Stroke.png|thumb|12-lead ECG of a patient with stroke, showing large deeply inverted [[T wave|T-waves]]. ECG changes may occur in people with stroke and other brain disorders.]]
===Early assessment===
When stroke has been diagnosed, other studies may be performed to determine the underlying cause. With the 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. The following are commonly used techniques:{{Citation needed|date=April 2025}}
It is important to identify a stroke as early as possible because patients who are treated earlier are more likely to survive and have better recoveries. As many doctors note, "Time lost is brain lost."
* an [[medical ultrasonography|ultrasound/doppler study]] of the [[carotid artery|carotid arteries]] (to detect [[carotid stenosis]]) or dissection of the precerebral arteries;
* an [[electrocardiogram]] (ECG) and [[echocardiogram]] (to identify [[cardiac arrhythmia|arrhythmias]] and resultant clots in the heart which may spread to the brain vessels through the bloodstream);
* a [[Holter monitor]] study to identify intermittent [[Heart arrhythmia|abnormal heart rhythms]];
* an [[angiogram]] of the cerebral vasculature (if a bleed is thought to have originated from an [[aneurysm]] or [[arteriovenous malformation]]);
* blood tests to determine if [[hypercholesterolemia|blood cholesterol is high]], if there is an abnormal [[bleeding diathesis|tendency to bleed]], and if some rarer processes such as [[homocysteinuria|homocystinuria]] might be involved.
 
For hemorrhagic stroke, a [[Computed tomography angiography|CT]] or [[Magnetic resonance angiography|MRI scan with intravascular contrast]] may be able to identify abnormalities in the brain arteries (such as aneurysms) or other sources of bleeding, and structural MRI if this shows no cause. If this too does not identify an underlying reason for the bleeding, invasive [[cerebral angiography]] could be performed but this requires access to the bloodstream with an intravascular catheter and can cause further stroke as well as complications at the insertion site and this investigation is therefore reserved for specific situations.<ref name=Wilson2015>{{cite journal | vauthors = Wilson D, Adams ME, Robertson F, Murphy M, Werring DJ | title = Investigating intracerebral haemorrhage | journal = BMJ | volume = 350 | issue = may20 10 | pages = h2484 | date = May 2015 | pmid = 25994363 | doi = 10.1136/bmj.h2484 | s2cid = 26908106 }}</ref> If there are symptoms suggesting that the hemorrhage might have occurred as a result of [[cerebral venous sinus thrombosis|venous thrombosis]], CT or MRI venography can be used to examine the cerebral veins.<ref name=Wilson2015/>
If you feel you or someone you know has had a stroke, call the ambulance, even if the symptoms have dissipated or apparently resolved - speed of reaction time is critical, receiving hospital treatment within three hours of the attack to have a hope of avoiding irreversible brain damage.
 
===Misdiagnosis===
Some suggest that a simple set of tasks may help those without medical training help to identify someone who is having a stroke, but remember that, while many individuals with stroke may find the following tasks difficult, not all stroke symptoms can be encompassed in the following tasks:
 
Among people with ischemic stroke, misdiagnosis occurs 2 to 26% of the time.<ref name=Bak2018/> A "stroke chameleon" (SC) is stroke which is diagnosed as something else.<ref name=Bak2018>{{cite journal | vauthors = Bakradze E, Liberman AL | title = Diagnostic Error in Stroke-Reasons and Proposed Solutions | journal = Current Atherosclerosis Reports | volume = 20 | issue = 2 | article-number = 11 | date = February 2018 | pmid = 29441421 | doi = 10.1007/s11883-018-0712-3 | s2cid = 3335617 }}</ref><ref name="Stroke chameleons, Dupre et. al, 2013">{{cite journal | vauthors = Dupre CM, Libman R, Dupre SI, Katz JM, Rybinnik I, Kwiatkowski T | title = Stroke chameleons | journal = Journal of Stroke and Cerebrovascular Diseases | volume = 23 | issue = 2 | pages = 374–8 | date = February 2014 | pmid = 23954604 | doi = 10.1016/j.jstrokecerebrovasdis.2013.07.015 | orig-year = Available online 15 August 2013 }}</ref>
* Ask the individual to smile.
* Ask the individual to raise both arms and keep them raised.
* Ask the individual to speak a simple sentence (coherently). For example, "It is sunny out today."
 
People not having stroke may also be misdiagnosed with the condition. Giving thrombolytics (clot-busting) in such cases causes intracerebral bleeding 1 to 2% of the time, which is less than that of people with stroke. This unnecessary treatment adds to health care costs. Even so, the AHA/ASA guidelines state that starting intravenous tPA in possible mimics is preferred to delaying treatment for additional testing.<ref name=Bak2018/>
In addition, there are cases of individuals who exhibit none of the above, but suddenly experience imbalance while walking or veering to one side which also may be symptomatic of having a stroke.
 
Women, African-Americans, Hispanic-Americans, Asian and Pacific Islanders are more often misdiagnosed for a condition other than stroke when in fact having stroke. In addition, adults under 44 years of age are seven times more likely to have stroke missed than are adults over 75 years of age. This is especially the case for younger people with posterior circulation infarcts.<ref name=Bak2018/> Some medical centers have used hyperacute MRI in experimental studies for people initially thought to have a low likelihood of stroke, and in some of these people, stroke has been found which were then treated with thrombolytic medication.<ref name=Bak2018/>
Stroke can also manifest itself in a myriad of ways, including the transient loss of vision in one or both eyes.
 
==Prevention==
While the ideal hospital for stroke treatment would be a hospital with a dedicated stroke unit, any ER is better than no ER or a distant ER. The faster stroke therapies (aspirin) are started for hemorrhagic and ischemic stroke, the greater the chances for recovery from the stroke.
Given the disease burden of stroke, [[Prevention (medical)|prevention]] is an important [[public health]] concern.<ref name="pmid12234233">{{cite journal | vauthors = Straus SE, Majumdar SR, McAlister FA | title = New evidence for stroke prevention: scientific review | journal = JAMA | volume = 288 | issue = 11 | pages = 1388–95 | date = September 2002 | pmid = 12234233 | doi = 10.1001/jama.288.11.1388 | doi-access = }}</ref> [[Primary prevention]] is less effective than secondary prevention (as judged by the [[number needed to treat]] to prevent one stroke per year).<ref name="pmid12234233"/> Recent guidelines detail the evidence for primary prevention in stroke.<ref name="PreventionGuidelines">{{cite journal | vauthors = 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 | title = 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: the American Academy of Neurology affirms the value of this guideline | journal = Stroke | volume = 37 | issue = 6 | pages = 1583–633 | date = June 2006 | pmid = 16675728 | doi = 10.1161/01.STR.0000223048.70103.F1 | doi-access = free }}</ref> About the use of aspirin as a preventive medication for stroke, in healthy people aspirin does not appear beneficial and thus is not recommended,<ref>{{Cite web|title = Information for Consumers (Drugs) - Use of Aspirin for Primary Prevention of Heart Attack and Stroke|url = https://www.fda.gov/Drugs/ResourcesForYou/Consumers/ucm390574.htm|website = www.fda.gov|access-date = 2015-11-16| author = Center for Drug Evaluation and Research |url-status=dead|archive-url = https://web.archive.org/web/20151117063135/https://www.fda.gov/Drugs/ResourcesForYou/Consumers/ucm390574.htm|archive-date = 2015-11-17}}</ref> but in people with high cardiovascular risk, or those who have had a myocardial infarction, it provides some protection against a first stroke.<ref name="AP01">{{Cite web |date=2012-04-07 |title=Stroke prevention - Antiplatelets and anticoagulants: NPS - Better choices, Better health |url=https://www.nps.org.au/health_professionals/publications/prescribing_practice_review/current/nps_prescribing_practice_review_44 |access-date=2024-01-29 |archive-date=2012-04-07 |archive-url=https://web.archive.org/web/20120407044139/https://www.nps.org.au/health_professionals/publications/prescribing_practice_review/current/nps_prescribing_practice_review_44 |url-status=bot: unknown }}</ref><ref name="BMJ2002">{{cite journal | author = Antithrombotic Trialists' Collaboration | title = Collaborative meta-analysis of randomised trials of antiplatelet therapy for prevention of death, myocardial infarction, and stroke in high risk patients | journal = BMJ | volume = 324 | issue = 7329 | pages = 71–86 | date = January 2002 | pmid = 11786451 | pmc = 64503 | doi = 10.1136/bmj.324.7329.71 }}</ref> In those who have previously had stroke, treatment with medications such as [[aspirin]], [[clopidogrel]], and [[dipyridamole]] may be beneficial.<ref name="AP01" /> The [[U.S. Preventive Services Task Force]] (USPSTF) recommends against [[Screening (medicine)|screening]] for [[carotid artery stenosis]] in those without symptoms.<ref>{{cite journal | vauthors = Jonas DE, Feltner C, Amick HR, Sheridan S, Zheng ZJ, Watford DJ, Carter JL, Rowe CJ, Harris R | title = Screening for asymptomatic carotid artery stenosis: a systematic review and meta-analysis for the U.S. Preventive Services Task Force | journal = Annals of Internal Medicine | volume = 161 | issue = 5 | pages = 336–46 | date = September 2014 | pmid = 25004169 | doi = 10.7326/M14-0530 | s2cid = 8741746 }}</ref>
 
===Risk factors===
Only detailed [[physical examination]] and [[medical imaging]] provide information on the presence, type, and extent of stroke.
The most important modifiable risk factors for stroke are chronic uncontrolled [[hypertension]] and [[atrial fibrillation]], although the size of the effect is small; 833 people have to be treated for 1 year to prevent one stroke.<ref>{{cite journal | author = Medical Research Council Working Party | title = MRC trial of treatment of mild hypertension: principal results. Medical Research Council Working Party | journal = British Medical Journal | volume = 291 | issue = 6488 | pages = 97–104 | date = July 1985 | pmid = 2861880 | pmc = 1416260 | doi = 10.1136/bmj.291.6488.97 }}</ref><ref>{{cite journal | vauthors = Thomson R | title = Evidence based implementation of complex interventions | journal = BMJ | volume = 339 | pages = b3124 | date = August 2009 | pmid = 19675081 | doi = 10.1136/bmj.b3124 | s2cid = 692596 }}</ref> Other modifiable risk factors include high blood cholesterol levels, [[diabetes mellitus]], [[end-stage kidney disease]],<ref name="Hu2018"/> cigarette smoking<ref>{{cite journal | vauthors = Hankey GJ | title = Smoking and risk of stroke | journal = Journal of Cardiovascular Risk | volume = 6 | issue = 4 | pages = 207–11 | date = August 1999 | pmid = 10501270 | doi = 10.1177/204748739900600403 | s2cid = 43819614 | doi-access = free }}</ref><ref name="pmid7596004">{{cite journal | vauthors = Wannamethee SG, Shaper AG, Whincup PH, Walker M | title = Smoking cessation and the risk of stroke in middle-aged men | journal = JAMA | volume = 274 | issue = 2 | pages = 155–60 | date = July 1995 | pmid = 7596004 | doi = 10.1001/jama.274.2.155 }}</ref> (active and passive), heavy [[Alcohol consumption and health|alcohol]] use,<ref name="pmid12578491">{{cite journal | vauthors = Reynolds K, Lewis B, Nolen JD, Kinney GL, Sathya B, He J, Lewis BL | title = Alcohol consumption and risk of stroke: a meta-analysis | journal = JAMA | volume = 289 | issue = 5 | pages = 579–88 | date = February 2003 | pmid = 12578491 | doi = 10.1001/jama.289.5.579 | s2cid = 28076015 }}</ref> drug use,<ref name="pmid1891081">{{cite journal | vauthors = Sloan MA, Kittner SJ, Rigamonti D, Price TR | title = Occurrence of stroke associated with use/abuse of drugs | journal = Neurology | volume = 41 | issue = 9 | pages = 1358–64 | date = September 1991 | pmid = 1891081 | doi = 10.1212/WNL.41.9.1358 | s2cid = 26670239 }}</ref> lack of [[physical activity]], [[obesity]], processed [[red meat]] consumption,<ref>{{cite journal | vauthors = Larsson SC, Virtamo J, Wolk A | title = Red meat consumption and risk of stroke in Swedish men | journal = The American Journal of Clinical Nutrition | volume = 94 | issue = 2 | pages = 417–21 | date = August 2011 | pmid = 21653800 | doi = 10.3945/ajcn.111.015115 | doi-access = free }}</ref> and unhealthy diet.<ref name="American heart risk">{{cite web |url=http://www.AmericanHeart.org/presenter.jhtml?identifier=4716 |title= Stroke Risk Factors |publisher= [[American Heart Association]] |year=2007 |access-date=January 22, 2007}}</ref> Smoking just one cigarette per day increases the risk more than 30%.<ref>{{cite journal | vauthors = Hackshaw A, Morris JK, Boniface S, Tang JL, Milenković D | title = Low cigarette consumption and risk of coronary heart disease and stroke: meta-analysis of 141 cohort studies in 55 study reports | journal = BMJ | volume = 360 | pages = j5855 | date = January 2018 | pmid = 29367388 | pmc = 5781309 | doi = 10.1136/bmj.j5855 }}</ref> Alcohol use could predispose to ischemic stroke, as well as intracerebral and subarachnoid hemorrhage via multiple mechanisms (for example, via hypertension, atrial fibrillation, rebound [[thrombocytosis]] and [[platelet aggregation]] and [[clotting]] disturbances).<ref name="pmid3810763">{{cite journal | vauthors = Gorelick PB | title = Alcohol and stroke | journal = Stroke | volume = 18 | issue = 1 | pages = 268–71 | year = 1987 | pmid = 3810763 | doi = 10.1161/01.STR.18.1.268 | doi-access = free }}</ref> Drugs, most commonly amphetamines and cocaine, can induce stroke through damage to the blood vessels in the brain and acute hypertension.<ref name="Harrison's">{{cite book| vauthors = Smith WS, English JD, Johnston SC | chapter = Chapter 370: Cerebrovascular Diseases | pages = 3270–3299 | veditors = Longo DL, Fauci AS, Kasper DL, Hauser SL, Jameson JL, Loscalzo J |title=Harrison's principles of internal medicine. |year=2012 |publisher=McGraw-Hill |___location=New York |isbn=978-0-07-174889-6 |edition=18th}}</ref><ref name="pmid17404126">{{cite journal | vauthors = Westover AN, McBride S, Haley RW | title = Stroke in young adults who abuse amphetamines or cocaine: a population-based study of hospitalized patients | journal = Archives of General Psychiatry | volume = 64 | issue = 4 | pages = 495–502 | date = April 2007 | pmid = 17404126 | doi = 10.1001/archpsyc.64.4.495 | doi-access = }}</ref>{{quotation needed|reason=amphetamines do not normally cause any of this (hypertension or stroke) without pre-existing abnormalities, see DOI 10.1056/NEJMoa1110212 and related adult study, esp hazard ratio supplements|date=November 2024}} [[Migraine]] with [[aura (symptom)|aura]] doubles a person's risk for ischemic stroke.<ref name=Stroke2009>{{cite journal | vauthors = Schürks M, Rist PM, Bigal ME, Buring JE, Lipton RB, Kurth T | title = Migraine and cardiovascular disease: systematic review and meta-analysis | journal = BMJ | volume = 339 | issue = oct27 1 | pages = b3914 | date = October 2009 | pmid = 19861375 | pmc = 2768778 | doi = 10.1136/bmj.b3914 }}</ref><ref>{{cite journal | vauthors = Kurth T, Chabriat H, Bousser MG | title = Migraine and stroke: a complex association with clinical implications | journal = The Lancet. Neurology | volume = 11 | issue = 1 | pages = 92–100 | date = January 2012 | pmid = 22172624 | doi = 10.1016/S1474-4422(11)70266-6 | s2cid = 31939284 }}</ref> Untreated, [[celiac disease]] regardless of the presence of symptoms can be an underlying cause of stroke, both in children and adults.<ref name="CiaccioLewis2017">{{cite journal | vauthors = Ciaccio EJ, Lewis SK, Biviano AB, Iyer V, Garan H, Green PH | title = Cardiovascular involvement in celiac disease | journal = World Journal of Cardiology | volume = 9 | issue = 8 | pages = 652–666 | date = August 2017 | pmid = 28932354 | pmc = 5583538 | doi = 10.4330/wjc.v9.i8.652 | type = Review | doi-access = free }}</ref> According to a 2021 WHO study, working 55+ hours a week raises the risk of stroke by 35% and the risk of dying from heart conditions by 17%, when compared to a 35-40-hour week.<ref>{{cite journal | vauthors = Pega F, Náfrádi B, Momen NC, Ujita Y, Streicher KN, Prüss-Üstün AM, Descatha A, Driscoll T, Fischer FM, Godderis L, Kiiver HM, Li J, Magnusson Hanson LL, Rugulies R, Sørensen K, Woodruff TJ | title = Global, regional, and national burdens of ischemic heart disease and stroke attributable to exposure to long working hours for 194 countries, 2000-2016: A systematic analysis from the WHO/ILO Joint Estimates of the Work-related Burden of Disease and Injury | journal = Environment International | volume = 154 | article-number = 106595 | date = September 2021 | pmid = 34011457 | pmc = 8204267 | doi = 10.1016/j.envint.2021.106595 | doi-access = free | bibcode = 2021EnInt.15406595P }}</ref>
 
High levels of physical activity reduce the risk of stroke by about 26%.<ref name=BMJ2016>{{cite journal | vauthors = Kyu HH, Bachman VF, Alexander LT, Mumford JE, Afshin A, Estep K, Veerman JL, Delwiche K, Iannarone ML, Moyer ML, Cercy K, Vos T, Murray CJ, Forouzanfar MH | title = Physical activity and risk of breast cancer, colon cancer, diabetes, ischemic heart disease, and ischemic stroke events: systematic review and dose-response meta-analysis for the Global Burden of Disease Study 2013 | journal = BMJ | volume = 354 | pages = i3857 | date = August 2016 | pmid = 27510511 | pmc = 4979358 | doi = 10.1136/bmj.i3857 }}</ref> There is a lack of high quality studies looking at promotional efforts to improve lifestyle factors.<ref name="pmid14705756">{{cite journal | vauthors = Ezekowitz JA, Straus SE, Majumdar SR, McAlister FA | title = Stroke: strategies for primary prevention | journal = American Family Physician | volume = 68 | issue = 12 | pages = 2379–86 | date = December 2003 | pmid = 14705756 }}</ref> Nonetheless, given the large body of circumstantial evidence, best medical management for stroke includes advice on diet, exercise, smoking and alcohol use.<ref name="endart-review">{{cite journal | vauthors = Ederle J, Brown MM | title = The evidence for medicine versus surgery for carotid stenosis | journal = European Journal of Radiology | volume = 60 | issue = 1 | pages = 3–7 | date = October 2006 | pmid = 16920313 | doi = 10.1016/j.ejrad.2006.05.021 }}</ref> Medication is the most common method of stroke prevention; [[carotid endarterectomy]] can be a useful surgical method of preventing stroke.
Studies show that patients treated in hospitals with a dedicated Stroke Team or Stroke Unit and a specialized care program for stroke patients have improved odds of recovery. Again, however, the patient has to get to the ER promptly to get the immediate and appropriate care they need.
 
A recent 2025 reports that women under 50 with a history of [[Complications of pregnancy|pregnancy complications]] face a higher risk of ischemic stroke.<ref>{{Cite journal |last=Verburgt |first=Esmée |last2=Hilkens |first2=Nina A. |last3=Verhoeven |first3=Jamie I. |last4=Schellekens |first4=Mijntje M.I. |last5=Ekker |first5=Merel S. |last6=Boot |first6=Esther M. |last7=van Alebeek |first7=Mayte E. |last8=Brouwers |first8=Paul J.A.M. |last9=Arntz |first9=Renate M. |last10=Van Dijk |first10=Gert |last11=Gons |first11=Rob A.R. |last12=Van Uden |first12=Ingeborg W.M. |last13=Den Heijer |first13=Tom |last14=van Tuijl |first14=Julia |last15=de Laat |first15=Karlijn F. |date=2025-09-09 |title=History of Pregnancy Complications and the Risk of Ischemic Stroke in Young Women |url=https://www.neurology.org/doi/10.1212/WNL.0000000000214009 |journal=Neurology |volume=105 |issue=5 |pages=e214009 |doi=10.1212/WNL.0000000000214009|pmc=12334341 }}</ref> Conditions such as [[hypertensive disorders]] of pregnancy, [[gestational diabetes]], [[preterm birth]], [[Small for gestational age|small-for-gestational-age]] infants, stillbirth, and miscarriage were more common among stroke patients than those without [[Stroke|'''stroke''']].<ref>{{Cite web |date=2025-08-08 |title=History of Pregnancy Complications Associated With Increased Ischemic Stroke Risk |url=https://www.neurologyadvisor.com/news/history-pregnancy-complications-increased-ischemic-stroke-risk/ |access-date=2025-08-09 |website=Neurology Advisor |language=en-US}}</ref> The risk was especially elevated for strokes linked to large artery disease in women with prior [[hypertensive disorders]], [[Preterm birth|preterm births]] or [[Small for gestational age|small-for-gestational-age]] deliveries.<ref>{{Cite web |date=2025-08-08 |title=History of Pregnancy Complications Associated With Increased Ischemic Stroke Risk |url=https://www.endocrinologyadvisor.com/news/history-of-pregnancy-complications-associated-with-increased-ischemic-stroke-risk/ |access-date=2025-08-09 |website=Endocrinology Advisor |language=en-US}}</ref>
===Ischemic stroke===
As ischemic stroke is due to a [[thrombus]] (blood clot) occluding a cerebral artery, a patient is given [[antiplatelet drug|antiplatelet medication]] ([[aspirin]], [[clopidogrel]], [[dipyridamole]]), or [[anticoagulant]] medication ([[warfarin]]), dependent on the cause, when this type of stroke has been found. Hemorrhagic stroke must be ruled out with medical imaging, since this therapy would be harmful to patients with that type of stroke.
 
====Blood pressure====
Whether thrombolysis is performed or not, the following investigations are required:
[[Hypertension|High blood pressure]] accounts for 35–50% of stroke risk.<ref name="pmid8614485">{{cite journal | vauthors = Whisnant JP | title = Effectiveness versus efficacy of treatment of hypertension for stroke prevention | journal = Neurology | volume = 46 | issue = 2 | pages = 301–7 | date = February 1996 | pmid = 8614485 | doi = 10.1212/WNL.46.2.301 | s2cid = 28985425 }}</ref> Blood pressure reduction of 10 mmHg systolic or 5 mmHg diastolic reduces the risk of stroke by ~40%.<ref>{{cite journal | vauthors = Law MR, Morris JK, Wald NJ | title = 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 | journal = BMJ | volume = 338 | pages = b1665 | date = May 2009 | pmid = 19454737 | pmc = 2684577 | doi = 10.1136/bmj.b1665 }}</ref> Lowering blood pressure has been conclusively shown to prevent both ischemic and hemorrhagic stroke.<ref name="Psaty2003">{{cite journal | vauthors = Psaty BM, Lumley T, Furberg CD, Schellenbaum G, Pahor M, Alderman MH, Weiss NS | title = Health outcomes associated with various antihypertensive therapies used as first-line agents: a network meta-analysis | journal = JAMA | volume = 289 | issue = 19 | pages = 2534–44 | date = May 2003 | pmid = 12759325 | doi = 10.1001/jama.289.19.2534 | s2cid = 123289 }}</ref><ref name="pmid8551820">{{cite journal | vauthors = | title = Cholesterol, diastolic blood pressure, and stroke: 13,000 strokes in 450,000 people in 45 prospective cohorts. Prospective studies collaboration | journal = Lancet | volume = 346 | issue = 8991–8992 | pages = 1647–53 | year = 1995 | pmid = 8551820 | doi = 10.1016/S0140-6736(95)92836-7 | s2cid = 12043767 }}</ref> It is equally important in secondary prevention.<ref name="pmid9412649">{{cite journal | vauthors = 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 | title = 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 | journal = Stroke | volume = 28 | issue = 12 | pages = 2557–62 | date = December 1997 | pmid = 9412649 | doi = 10.1161/01.STR.28.12.2557 }}</ref> Even people older than 80 years and those with [[isolated systolic hypertension]] benefit from antihypertensive therapy.<ref name="INDANAsub">{{cite journal | vauthors = Gueyffier F, Bulpitt C, Boissel JP, Schron E, Ekbom T, Fagard R, Casiglia E, Kerlikowske K, Coope J | title = Antihypertensive drugs in very old people: a subgroup meta-analysis of randomised controlled trials. INDANA Group | journal = Lancet | volume = 353 | issue = 9155 | pages = 793–6 | date = March 1999 | pmid = 10459960 | doi = 10.1016/S0140-6736(98)08127-6 | url = https://zenodo.org/record/891425 | s2cid = 43858004 }}</ref><ref name="Staessen2000">{{cite journal | vauthors = 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 | title = Risks of untreated and treated isolated systolic hypertension in the elderly: meta-analysis of outcome trials | journal = Lancet | volume = 355 | issue = 9207 | pages = 865–72 | date = March 2000 | pmid = 10752701 | doi = 10.1016/S0140-6736(99)07330-4 | s2cid = 31403774 }}</ref><ref name="HYVET-NEJM2008">{{cite journal | vauthors = 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 | title = Treatment of hypertension in patients 80 years of age or older | journal = The New England Journal of Medicine | volume = 358 | issue = 18 | pages = 1887–98 | date = May 2008 | pmid = 18378519 | doi = 10.1056/NEJMoa0801369 | url = http://researchonline.lshtm.ac.uk/7818/1/nejmoa0801369.pdf | archive-url=https://web.archive.org/web/20231108002951/http://researchonline.lshtm.ac.uk/7818/1/nejmoa0801369.pdf | archive-date=November 8, 2023 | url-status=live }}</ref> 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.<ref name="BPLT">{{cite journal | vauthors = Neal B, MacMahon S, Chapman N | title = Effects of ACE inhibitors, calcium antagonists, and other blood-pressure-lowering drugs: results of prospectively designed overviews of randomised trials. Blood Pressure Lowering Treatment Trialists' Collaboration | journal = Lancet | volume = 356 | issue = 9246 | pages = 1955–64 | date = December 2000 | pmid = 11130523 | doi = 10.1016/S0140-6736(00)03307-9 | s2cid = 46148907 }}</ref><ref name="pmid12479763">{{cite journal | author = The Allhat Officers and Coordinators for the Allhat Collaborative Research Group | title = 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) | journal = JAMA | volume = 288 | issue = 23 | pages = 2981–97 | date = December 2002 | pmid = 12479763 | doi = 10.1001/jama.288.23.2981 | doi-access = }}</ref> The routine use of [[beta-blocker]]s following stroke or TIA has not been shown to result in benefits.<ref>{{cite journal | vauthors = De Lima LG, Saconato H, Atallah AN, da Silva EM | title = Beta-blockers for preventing stroke recurrence | journal = The Cochrane Database of Systematic Reviews | volume = 2014 | issue = 10 | pages = CD007890 | date = October 2014 | pmid = 25317988 | doi = 10.1002/14651858.CD007890.pub3 | pmc = 10590202 }}</ref>
* Stroke symptoms are documented, often using scoring systems such as the [[National Institutes of Health Stroke Scale]], the [[Cincinnati Stroke Scale]], and the [[Los Angeles Prehospital Stroke Screen]]. The latter is used by [[emergency medical technicians]] (EMTs) to determine whether a patient needs transport to a stroke center.
* A [[Computed axial tomography|CT scan]] is performed to rule out hemorrhagic stroke
* [[Blood test]]s, such as a [[full blood count]], [[coagulation]] studies ([[prothrombin time|PT/INR]] and [[Partial thromboplastin time|APTT]]), and tests of [[electrolyte]]s, [[renal function]], [[liver function tests]] and [[glucose]] levels are carried out.
 
====Blood lipids====
Other immediate strategies to protect the brain during stroke include ensuring that blood sugar is as normal as possible (such as commencement of an [[insulin sliding scale]] in known [[diabetes|diabetics]]), and that the stroke patient is receiving adequate [[oxygen]] and [[intravenous fluid]]s. The patient may be positioned so that his or her head is flat on the stretcher, rather than sitting up, since studies have shown that this increases blood flow to the brain. Additional therapies for ischemic stroke include [[aspirin]] (50 to 325 mg daily), [[clopidogrel]] (75 mg daily), and combined aspirin and [[dipyridamole]] extended release (25/200 mg twice daily).
High cholesterol levels have been inconsistently associated with (ischemic) stroke.<ref name="pmid8551820"/><ref name="NEJM1989">{{cite journal | vauthors = Iso H, Jacobs DR, Wentworth D, Neaton JD, Cohen JD | title = Serum cholesterol levels and six-year mortality from stroke in 350,977 men screened for the multiple risk factor intervention trial | journal = The New England Journal of Medicine | volume = 320 | issue = 14 | pages = 904–10 | date = April 1989 | pmid = 2619783 | doi = 10.1056/NEJM198904063201405 }}</ref> [[Statins]] have been shown to reduce the risk of stroke by about 15%.<ref name="Statins2008">{{cite journal | vauthors = O'Regan C, Wu P, Arora P, Perri D, Mills EJ | title = Statin therapy in stroke prevention: a meta-analysis involving 121,000 patients | journal = The American Journal of Medicine | volume = 121 | issue = 1 | pages = 24–33 | date = January 2008 | pmid = 18187070 | doi = 10.1016/j.amjmed.2007.06.033 }}</ref> Since earlier meta-analyses of other [[lipid-lowering drugs]] did not show a decreased risk,<ref name="pmid7802520">{{cite journal | vauthors = Hebert PR, Gaziano JM, Hennekens CH | title = An overview of trials of cholesterol lowering and risk of stroke | journal = Archives of Internal Medicine | volume = 155 | issue = 1 | pages = 50–5 | date = January 1995 | pmid = 7802520 | doi = 10.1001/archinte.155.1.50 }}</ref> statins might exert their effect through mechanisms other than their lipid-lowering effects.<ref name="Statins2008"/>
 
====Diabetes mellitus====
It is common for the [[blood pressure]] to be [[arterial hypertension|elevated]] immediately following a stroke. Studies indicated that while high blood pressure causes stroke, it is actually beneficial in the emergency period to allow better blood flow to the brain.
[[Diabetes mellitus]] increases the risk of stroke by 2 to 3 times.{{clarify|date=September 2021}}{{citation needed|date=September 2021}} While intensive blood sugar control has been shown to reduce small blood vessel complications such as [[Diabetic nephropathy|kidney damage]] and [[Diabetic retinopathy|damage to the retina of the eye]] it has not been shown to reduce large blood vessel complications such as stroke.<ref name="UKPDS">{{cite journal | vauthors = | title = Intensive blood-glucose control with sulphonylureas or insulin compared with conventional treatment and risk of complications in patients with type 2 diabetes (UKPDS 33). UK Prospective Diabetes Study (UKPDS) Group | journal = Lancet | volume = 352 | issue = 9131 | pages = 837–53 | date = September 1998 | pmid = 9742976 | doi = 10.1016/S0140-6736(98)07019-6 | s2cid = 7019505 }}</ref><ref name="ProACTIVE">{{cite journal | vauthors = Dormandy JA, Charbonnel B, Eckland DJ, Erdmann E, Massi-Benedetti M, Moules IK, Skene AM, Tan MH, Lefèbvre PJ, Murray GD, Standl E, Wilcox RG, Wilhelmsen L, Betteridge J, Birkeland K, Golay A, Heine RJ, Korányi L, Laakso M, Mokán M, Norkus A, Pirags V, Podar T, Scheen A, Scherbaum W, Schernthaner G, Schmitz O, Skrha J, Smith U, Taton J | title = Secondary prevention of macrovascular events in patients with type 2 diabetes in the PROactive Study (PROspective pioglitAzone Clinical Trial In macroVascular Events): a randomised controlled trial | journal = Lancet | volume = 366 | issue = 9493 | pages = 1279–89 | date = October 2005 | pmid = 16214598 | doi = 10.1016/S0140-6736(05)67528-9 | url = http://orbi.ulg.ac.be/handle/2268/6536 | s2cid = 11825315 | hdl = 2268/6536 | hdl-access = free }}</ref>
 
====Anticoagulant drugs====
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.
Oral anticoagulants such as [[warfarin]] have been the mainstay of stroke prevention for over 50 years. However, several studies have shown that aspirin and other [[antiplatelet drug|antiplatelets]] are highly effective in [[secondary prevention]] after stroke or transient ischemic attack.<ref name="AP01" /> Low doses of aspirin (for example 75–150&nbsp;mg) are as effective as high doses but have fewer side effects; the lowest effective dose remains unknown.<ref name="pmid10371234">{{cite journal | vauthors = Johnson ES, Lanes SF, Wentworth CE, Satterfield MH, Abebe BL, Dicker LW | title = A metaregression analysis of the dose-response effect of aspirin on stroke | journal = Archives of Internal Medicine | volume = 159 | issue = 11 | pages = 1248–53 | date = June 1999 | pmid = 10371234 | doi = 10.1001/archinte.159.11.1248 | doi-access = }}</ref> [[Thienopyridine]]s ([[clopidogrel]], [[ticlopidine]]) might be slightly more effective than aspirin and have a decreased risk of [[gastrointestinal bleeding]] but are more expensive.<ref name="CochraneThienopyridines">{{cite journal | vauthors = Sudlow CL, Mason G, Maurice JB, Wedderburn CJ, Hankey GJ | title = Thienopyridine derivatives versus aspirin for preventing stroke and other serious vascular events in high vascular risk patients | journal = The Cochrane Database of Systematic Reviews | issue = 4 | pages = CD001246 | date = October 2009 | volume = 2009 | pmid = 19821273 | pmc = 7055203 | doi = 10.1002/14651858.CD001246.pub2 | s2cid = 205162946 }}</ref> Both aspirin and clopidogrel may be useful in the first few weeks after a minor stroke or high-risk TIA.<ref>{{cite journal | vauthors = Hao Q, Tampi M, O'Donnell M, Foroutan F, Siemieniuk RA, Guyatt G | title = Clopidogrel plus aspirin versus aspirin alone for acute minor ischaemic stroke or high risk transient ischaemic attack: systematic review and meta-analysis | journal = BMJ | volume = 363 | pages = k5108 | date = December 2018 | pmid = 30563866 | pmc = 6298178 | doi = 10.1136/bmj.k5108 }}</ref> Clopidogrel has less side effects than ticlopidine.<ref name="CochraneThienopyridines"/> [[Dipyridamole]] can be added to aspirin therapy to provide a small additional benefit, even though headache is a common side effect.<ref name="ESPRIT">{{cite journal | vauthors = Halkes PH, van Gijn J, Kappelle LJ, Koudstaal PJ, Algra A | title = Aspirin plus dipyridamole versus aspirin alone after cerebral ischaemia of arterial origin (ESPRIT): randomised controlled trial | journal = Lancet | volume = 367 | issue = 9523 | pages = 1665–73 | date = May 2006 | pmid = 16714187 | doi = 10.1016/S0140-6736(06)68734-5 | s2cid = 10691264 }}</ref> Low-dose aspirin is also effective for stroke prevention after having a myocardial infarction.<ref name="BMJ2002"/>
 
Those with [[atrial fibrillation]] have a 5% a year risk of stroke, and those with valvular atrial fibrillation have an even higher risk.<ref name="AFIB">{{cite journal | vauthors = Wolf PA, Abbott RD, Kannel WB | title = Atrial fibrillation: a major contributor to stroke in the elderly. The Framingham Study | journal = Archives of Internal Medicine | volume = 147 | issue = 9 | pages = 1561–4 | date = September 1987 | pmid = 3632164 | doi = 10.1001/archinte.147.9.1561 }}</ref> Depending on the stroke risk, anticoagulation with medications such as [[warfarin]] or aspirin is useful for prevention with various levels of [[Comparative effectiveness research|comparative effectiveness]] depending on the type of treatment used.<ref name="AFib-guidelines">{{cite journal | vauthors = Fuster V, Rydén LE, Cannom DS, Crijns HJ, Curtis AB, Ellenbogen KA, Halperin JL, Le Heuzey JY, Kay GN, Lowe JE, Olsson SB, Prystowsky EN, Tamargo JL, Wann S, Smith SC, Jacobs AK, Adams CD, Anderson JL, Antman EM, Halperin JL, Hunt SA, Nishimura R, Ornato JP, Page RL, Riegel B, Priori SG, Blanc JJ, Budaj A, Camm AJ, Dean V, Deckers JW, Despres C, Dickstein K, Lekakis J, McGregor K, Metra M, Morais J, Osterspey A, Tamargo JL, Zamorano JL | title = ACC/AHA/ESC 2006 Guidelines for the Management of Patients with Atrial Fibrillation: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines and the European Society of Cardiology Committee for Practice Guidelines (Writing Committee to Revise the 2001 Guidelines for the Management of Patients With Atrial Fibrillation): developed in collaboration with the European Heart Rhythm Association and the Heart Rhythm Society | journal = Circulation | volume = 114 | issue = 7 | pages = e257-354 | date = August 2006 | pmid = 16908781 | doi = 10.1161/CIRCULATIONAHA.106.177292 | doi-access = free }}</ref><ref name=":1">{{Cite report | vauthors = Sanders GD, Lowenstern A, Borre E, Chatterjee R, Goode A, Sharan L, Lapointe NA, Raitz G, Shah B, Yapa R, Davis JK |url=https://effectivehealthcare.ahrq.gov/topics/stroke-afib-update/research-2018 |title=Stroke Prevention in Patients With Atrial Fibrillation: A Systematic Review Update |date=2018-10-30 |publisher=Agency for Healthcare Research and Quality (AHRQ) |doi=10.23970/ahrqepccer214 |doi-broken-date=1 July 2025 |doi-access=free |access-date=2023-08-20 |archive-date=2019-03-29 |archive-url=https://web.archive.org/web/20190329195137/https://effectivehealthcare.ahrq.gov/topics/stroke-afib-update/research-2018 |url-status=dead }}</ref>
If the stroke has been the result of [[cardiac arrhythmia]] (such as [[atrial fibrillation]]) with cardiogenic emboli, treatment of the arrhythmia and [[anticoagulation]] with [[warfarin]] or high-dose aspirin may decrease the risk of recurrence.
 
[[Oral anticoagulants]], especially Xa ([[apixaban]]) and thrombin ([[dabigatran]]) inhibitors, have been shown to be superior to warfarin in stroke reduction and have a lower or similar bleeding risk in patients with atrial fibrillation.<ref name=":1" /> Except in people with atrial fibrillation, [[oral anticoagulants]] are not advised for stroke prevention—any benefit is offset by bleeding risk.<ref name="pmid17239798">{{cite journal | vauthors = Halkes PH, van Gijn J, Kappelle LJ, Koudstaal PJ, Algra A | title = Medium intensity oral anticoagulants versus aspirin after cerebral ischaemia of arterial origin (ESPRIT): a randomised controlled trial | journal = The Lancet. Neurology | volume = 6 | issue = 2 | pages = 115–24 | date = February 2007 | pmid = 17239798 | doi = 10.1016/S1474-4422(06)70685-8 | s2cid = 21982861 }}</ref>
 
In primary prevention, however, antiplatelet drugs did not reduce the risk of ischemic stroke but increased the risk of major bleeding.<ref name="aspirin">{{cite journal | vauthors = Hart RG, Halperin JL, McBride R, Benavente O, Man-Son-Hing M, Kronmal RA | title = Aspirin for the primary prevention of stroke and other major vascular events: meta-analysis and hypotheses | journal = Archives of Neurology | volume = 57 | issue = 3 | pages = 326–32 | date = March 2000 | pmid = 10714657 | doi = 10.1001/archneur.57.3.326 | author-link2 = Jonathan L. Halperin | doi-access = }}</ref><ref name="aspirin-meta">{{cite journal | vauthors = Bartolucci AA, Howard G | title = Meta-analysis of data from the six primary prevention trials of cardiovascular events using aspirin | journal = The American Journal of Cardiology | volume = 98 | issue = 6 | pages = 746–50 | date = September 2006 | pmid = 16950176 | doi = 10.1016/j.amjcard.2006.04.012 | url = http://www.ajconline.org/article/S000291490601068X/pdf | doi-access = free }}</ref> Further studies are needed to investigate a possible protective effect of aspirin against ischemic stroke in women.<ref name="aspirin-women">{{cite journal | vauthors = Berger JS, Roncaglioni MC, Avanzini F, Pangrazzi I, Tognoni G, Brown DL | title = Aspirin for the primary prevention of cardiovascular events in women and men: a sex-specific meta-analysis of randomized controlled trials | journal = JAMA | volume = 295 | issue = 3 | pages = 306–13 | date = January 2006 | pmid = 16418466 | doi = 10.1001/jama.295.3.306 | s2cid = 11952921 }}</ref><ref name="gender">{{cite journal | vauthors = Yerman T, Gan WQ, Sin DD | title = The influence of gender on the effects of aspirin in preventing myocardial infarction | journal = BMC Medicine | volume = 5 | article-number = 29 | date = October 2007 | pmid = 17949479 | pmc = 2131749 | doi = 10.1186/1741-7015-5-29 | doi-access = free }}</ref>
 
====Surgery====
[[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.<ref name="endart-review"/> Endarterectomy for a significant stenosis has been shown to be useful in preventing further stroke in those who have already had the condition.<ref name="pmid12531577">{{cite journal | vauthors = Rothwell PM, Eliasziw M, Gutnikov SA, Fox AJ, Taylor DW, Mayberg MR, Warlow CP, Barnett HJ | title = Analysis of pooled data from the randomised controlled trials of endarterectomy for symptomatic carotid stenosis | journal = Lancet | volume = 361 | issue = 9352 | pages = 107–16 | date = January 2003 | pmid = 12531577 | doi = 10.1016/S0140-6736(03)12228-3 | s2cid = 2484664 }}</ref> Carotid artery stenting has not been shown to be equally useful.<ref name="endarterectomy-meta">{{cite journal | vauthors = Ringleb PA, Chatellier G, Hacke W, Favre JP, Bartoli JM, Eckstein HH, Mas JL | title = Safety of endovascular treatment of carotid artery stenosis compared with surgical treatment: a meta-analysis | journal = Journal of Vascular Surgery | volume = 47 | issue = 2 | pages = 350–5 | date = February 2008 | pmid = 18241759 | doi = 10.1016/j.jvs.2007.10.035 | doi-access = free }}</ref><ref>{{cite journal | vauthors = Müller MD, Lyrer P, Brown MM, Bonati LH | title = Carotid artery stenting versus endarterectomy for treatment of carotid artery stenosis | journal = The Cochrane Database of Systematic Reviews | volume = 2020 | pages = CD000515 | date = February 2020 | issue = 2 | pmid = 32096559 | pmc = 7041119 | doi = 10.1002/14651858.CD000515.pub5 }}</ref> People are selected for surgery based on age, gender, degree of stenosis, time since symptoms and the person's preferences.<ref name="endart-review"/> Surgery is most efficient when not delayed too long—the risk of recurrent stroke in a person 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 person was 5 for early surgery (within two weeks after the initial stroke), but 125 if delayed longer than 12 weeks.<ref name="pmid15043958">{{cite journal | vauthors = Rothwell PM, Eliasziw M, Gutnikov SA, Warlow CP, Barnett HJ | title = Endarterectomy for symptomatic carotid stenosis in relation to clinical subgroups and timing of surgery | journal = Lancet | volume = 363 | issue = 9413 | pages = 915–24 | date = March 2004 | pmid = 15043958 | doi = 10.1016/S0140-6736(04)15785-1 | s2cid = 3916408 }}</ref><ref name="pmid16087900">{{cite journal | vauthors = Fairhead JF, Mehta Z, Rothwell PM | title = Population-based study of delays in carotid imaging and surgery and the risk of recurrent stroke | journal = Neurology | volume = 65 | issue = 3 | pages = 371–5 | date = August 2005 | pmid = 16087900 | doi = 10.1212/01.wnl.0000170368.82460.b4 | s2cid = 24829283 }}</ref>
 
[[Screening (medicine)|Screening]] for carotid artery narrowing has not been shown to be a useful test in the general population.<ref name="USPSTF-carotidUS">{{cite journal | author = U.S. Preventive Services Task Force | title = Screening for carotid artery stenosis: U.S. Preventive Services Task Force recommendation statement | journal = Annals of Internal Medicine | volume = 147 | issue = 12 | pages = 854–9 | date = December 2007 | pmid = 18087056 | doi = 10.7326/0003-4819-147-12-200712180-00005 | doi-access = free }}</ref> Studies of surgical intervention for carotid artery stenosis without symptoms have shown only a small decrease in the risk of stroke.<ref name="pmid15135594">{{cite journal | vauthors = Halliday A, Mansfield A, Marro J, Peto C, Peto R, Potter J, Thomas D | title = Prevention of disabling and fatal strokes by successful carotid endarterectomy in patients without recent neurological symptoms: randomised controlled trial | journal = Lancet | volume = 363 | issue = 9420 | pages = 1491–502 | date = May 2004 | pmid = 15135594 | doi = 10.1016/S0140-6736(04)16146-1 | s2cid = 22814764 }}</ref><ref name="pmid16235289">{{cite journal | vauthors = Chambers BR, Donnan GA | title = Carotid endarterectomy for asymptomatic carotid stenosis | journal = The Cochrane Database of Systematic Reviews | issue = 4 | pages = CD001923 | date = October 2005 | volume = 2008 | pmid = 16235289 | pmc = 6669257 | doi = 10.1002/14651858.CD001923.pub2 }}</ref> To be beneficial, the complication rate of the surgery should be kept below 4%. Even then, for 100 surgeries, 5 people 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.<ref name="endart-review"/>
 
====Diet====
Nutrition, specifically the [[Mediterranean diet|Mediterranean-style diet]], has the potential to decrease the risk of having a stroke by more than half.<ref name=strokenutrition>{{cite journal | vauthors = Spence JD | title = Nutrition and stroke prevention | journal = Stroke | volume = 37 | issue = 9 | pages = 2430–5 | date = September 2006 | pmid = 16873712 | doi = 10.1161/01.STR.0000236633.40160.ee | doi-access = free | citeseerx = 10.1.1.326.6681 }}</ref> It does not appear that lowering levels of [[homocysteine]] with [[folic acid]] affects the risk of stroke.<ref>{{cite journal | vauthors = Zhou YH, Tang JY, Wu MJ, Lu J, Wei X, Qin YY, Wang C, Xu JF, He J | title = Effect of folic acid supplementation on cardiovascular outcomes: a systematic review and meta-analysis | journal = PLOS ONE | volume = 6 | issue = 9 | pages = e25142 | year = 2011 | pmid = 21980387 | pmc = 3182189 | doi = 10.1371/journal.pone.0025142 | bibcode = 2011PLoSO...625142Z | doi-access = free }}</ref><ref>{{cite journal | vauthors = 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 | title = 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 | journal = Archives of Internal Medicine | volume = 170 | issue = 18 | pages = 1622–31 | date = October 2010 | pmid = 20937919 | doi = 10.1001/archinternmed.2010.348 | doi-access = | s2cid = 204988253 }}</ref>
 
[[File:CDC video about stroke 2.ogg|thumb|A [[Centers for Disease Control and Prevention]] public service announcement about a woman who had stroke after pregnancy]]
 
===Women===
A number of specific recommendations have been made for women including taking aspirin after the 11th week of pregnancy if there is a history of previous chronic high blood pressure and taking blood pressure medications during pregnancy if the blood pressure is greater than 150&nbsp;mmHg systolic or greater than 100&nbsp;mmHg diastolic.<!-- <ref name=Bush2014/> --> In those who have previously had [[preeclampsia]], other risk factors should be treated more aggressively.<ref name=Bush2014>{{cite journal | vauthors = 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 | title = Guidelines for the prevention of stroke in women: a statement for healthcare professionals from the American Heart Association/American Stroke Association | journal = Stroke | volume = 45 | issue = 5 | pages = 1545–88 | date = May 2014 | pmid = 24503673 | doi = 10.1161/01.str.0000442009.06663.48 | pmc = 10152977 | author-link2 = Louise McCullough | doi-access = free }}</ref>
 
===Previous stroke or TIA===
Keeping blood pressure below 140/90 mmHg is recommended.<ref name=AHA2014>{{cite journal | vauthors = 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 | title = 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 | journal = Stroke | volume = 45 | issue = 7 | pages = 2160–236 | date = July 2014 | pmid = 24788967 | doi = 10.1161/STR.0000000000000024 | doi-access = free }}</ref> Anticoagulation can prevent recurrent ischemic stroke. Among people with nonvalvular atrial fibrillation, anticoagulation can reduce stroke by 60% while antiplatelet agents can reduce stroke by 20%.<ref name="pmid17577005">{{cite journal | vauthors = Hart RG, Pearce LA, Aguilar MI | title = Meta-analysis: antithrombotic therapy to prevent stroke in patients who have nonvalvular atrial fibrillation | journal = Annals of Internal Medicine | volume = 146 | issue = 12 | pages = 857–67 | date = June 2007 | pmid = 17577005 | doi = 10.7326/0003-4819-146-12-200706190-00007 | s2cid = 25505238 }}</ref> However, a recent meta-analysis suggests harm from anticoagulation started early after an embolic stroke.<ref name="pmid17204681">{{cite journal | vauthors = Paciaroni M, Agnelli G, Micheli S, Caso V | title = Efficacy and safety of anticoagulant treatment in acute cardioembolic stroke: a meta-analysis of randomized controlled trials | journal = Stroke | volume = 38 | issue = 2 | pages = 423–30 | date = February 2007 | pmid = 17204681 | doi = 10.1161/01.STR.0000254600.92975.1f | doi-access = free }}</ref><ref>{{cite journal | vauthors = Johnston SC | title = Review: anticoagulants increase intracerebral bleeding and do not reduce death or disability in acute cardioembolic stroke | journal = ACP Journal Club | volume = 147 | issue = 1 | pages = 17 | date = 1 July 2007 | pmid = 17608382 | doi = 10.7326/ACPJC-2007-147-1-017 }}</ref> Stroke prevention treatment for atrial fibrillation is determined according to the [[CHA2DS2–VASc score]]. The most widely used anticoagulant to prevent thromboembolic stroke in people 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.<ref name=AHA2014/>
 
Anticoagulants, when used following stroke, should not be stopped for dental procedures.<ref>{{cite journal | vauthors = Armstrong MJ, Gronseth G, Anderson DC, Biller J, Cucchiara B, Dafer R, Goldstein LB, Schneck M, Messé SR | title = 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 | journal = Neurology | volume = 80 | issue = 22 | pages = 2065–9 | date = May 2013 | pmid = 23713086 | pmc = 3716407 | doi = 10.1212/WNL.0b013e318294b32d }}</ref>
 
If studies show carotid artery stenosis, and the person has a degree of residual function on the affected side, carotid endarterectomy (surgical removal of the stenosis) may decrease the risk of recurrence if performed rapidly after stroke.
 
==Management==
Stroke, whether ischemic or hemorrhagic, is an emergency that warrants immediate medical attention.<ref name=HLB2014W/><ref name=HLB2023T>{{cite web|title=Stroke Treatment|url=https://www.nhlbi.nih.gov/health/stroke/treatment|website=www.nhlbi.nih.gov|access-date=18 March 2024|date=26 May 2023|url-status=live|archive-url=https://web.archive.org/web/20240229131247/https://www.nhlbi.nih.gov/health/stroke/treatment|archive-date=29 February 2024}}</ref> The specific treatment will depend on the type of stroke, the time elapsed since the onset of symptoms, and the underlying cause or presence of [[comorbidity|comorbidities]].<ref name=HLB2023T/>
 
===Ischemic stroke===
[[Aspirin]] reduces the overall risk of recurrence by 13% with greater benefit early on.<ref>{{cite journal | vauthors = Rothwell PM, Algra A, Chen Z, Diener HC, Norrving B, Mehta Z | title = Effects of aspirin on risk and severity of early recurrent stroke after transient ischaemic attack and ischaemic stroke: time-course analysis of randomised trials | journal = Lancet | volume = 388 | issue = 10042 | pages = 365–375 | date = July 2016 | pmid = 27209146 | pmc = 5321490 | doi = 10.1016/S0140-6736(16)30468-8 }}</ref> 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.<ref>{{cite journal | vauthors = Gomez CR | title = Editorial: Time is brain! | journal = Journal of Stroke and Cerebrovascular Diseases | volume = 3 | issue = 1 | pages = 1–2 | date = 1993 | pmid = 26487071 | doi = 10.1016/S1052-3057(10)80125-9 }}</ref> Years later, that same idea, that rapid cerebral blood flow restoration results in fewer brain cells dying, has been proved and quantified.<ref>{{cite journal | vauthors = Saver JL | title = Time is brain--quantified | journal = Stroke | volume = 37 | issue = 1 | pages = 263–6 | date = January 2006 | pmid = 16339467 | doi = 10.1161/01.STR.0000196957.55928.ab | doi-access = free }}</ref>
 
Tight blood sugar control in the first few hours does not improve outcomes and may cause harm.<ref>{{cite journal | vauthors = Bellolio MF, Gilmore RM, Ganti L | title = Insulin for glycaemic control in acute ischaemic stroke | journal = The Cochrane Database of Systematic Reviews | volume = 1 | issue = 1 | pages = CD005346 | date = January 2014 | pmid = 24453023 | doi = 10.1002/14651858.CD005346.pub4 | pmc = 10770823 }}</ref> High blood pressure is also not typically lowered as this has not been found to be helpful.<ref>{{cite journal | vauthors = Bath PM, Krishnan K | title = Interventions for deliberately altering blood pressure in acute stroke | journal = The Cochrane Database of Systematic Reviews | volume = 2014 | issue = 10 | pages = CD000039 | date = October 2014 | pmid = 25353321 | pmc = 7052738 | doi = 10.1002/14651858.CD000039.pub3 }}</ref><ref>{{cite journal | vauthors = Lee M, Ovbiagele B, Hong KS, Wu YL, Lee JE, Rao NM, Feng W, Saver JL | title = Effect of Blood Pressure Lowering in Early Ischemic Stroke: Meta-Analysis | journal = Stroke | volume = 46 | issue = 7 | pages = 1883–9 | date = July 2015 | pmid = 26022636 | doi = 10.1161/STROKEAHA.115.009552 | doi-access = | s2cid = 16136213 }}</ref> [[Cerebrolysin]], a mixture of pig brain-derived [[neurotrophic factors]] used widely to treat acute ischemic stroke in China, Eastern Europe, Russia, post-Soviet countries, and other Asian countries, does not improve outcomes or prevent death and may increase the risk of severe adverse events.<ref name=":0">{{cite journal | vauthors = Ziganshina LE, Abakumova T, Nurkhametova D, Ivanchenko K | title = Cerebrolysin for acute ischaemic stroke | journal = The Cochrane Database of Systematic Reviews | volume = 2023 | issue = 10 | pages = CD007026 | date = October 2023 | pmid = 37818733 | pmc = 10565895 | doi = 10.1002/14651858.CD007026.pub7 | collaboration = Cochrane Stroke Group }}</ref> There is also no evidence that cerebrolysin‐like peptide mixtures which are extracted from cattle brain is helpful in treating acute ischemic stroke.<ref name=":0" />
 
====Thrombolysis====
[[File:CDC video about stroke emergency treatment.ogg|thumb|A [[Centers for Disease Control and Prevention]] public service announcement on emergency medical treatment after or during stroke from 2021]]
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 (eg, abnormal lab values, high blood pressure, recent surgery...). This position for tPA is based upon the findings of one study (NINDS; N Engl J Med 1995;333:1581-1587.[http://content.nejm.org/cgi/content/abstract/333/24/1581]) which showed that tPA improves the chances for a good neurological outcome. When administered within the first 3 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. However, 55% of patients with large strokes developed substantial brain hemorrhage as a complication from being given tPA. tPA is often misconstrued in the news 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.<ref name="Dubinsky06">{{cite journal | last =Dubinsky | first = R| authorlink = | coauthors =Lai SM | title =Mortality of stroke patients treated with thrombolysis: analysis of nationwide inpatient sample | journal =Neurology | volume =66 | issue =11 | pages =1742-1744 | publisher = | date =2006 | url = | doi = | id =PMID 16769953 | accessdate =2007-01-22 }} </ref> 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. (http://www.aaem.org/positionstatements/thrombolytictherapy.shtml) Until additional evidence clarifies such controversies, physicians are advised to use their discretion when considering its use. Given the cited absence of definitive evidence, AAEM believes it is inappropriate to claim that either use or non-use of intravenous thrombolytic therapy constitutes a standard of care issue in the treatment of stroke.
 
[[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.<ref name=Ward2014>{{cite journal | vauthors = Wardlaw JM, Murray V, Berge E, del Zoppo GJ | title = Thrombolysis for acute ischaemic stroke | journal = The Cochrane Database of Systematic Reviews | volume = 7 | issue = 7 | pages = CD000213 | date = July 2014 | pmid = 25072528 | pmc = 4153726 | doi = 10.1002/14651858.CD000213.pub3 | author1-link = Joanna Wardlaw }}</ref><ref name="Lancet2014">{{cite journal | vauthors = 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 | title = 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 | journal = Lancet | volume = 384 | issue = 9958 | pages = 1929–35 | date = November 2014 | pmid = 25106063 | pmc = 4441266 | doi = 10.1016/S0140-6736(14)60584-5 }}</ref> It does not, however, improve chances of survival.<ref name=Ward2014/> Benefit is greater the earlier it is used.<ref name=Ward2014 /> Between three and four and a half hours the effects are less clear.<ref name=Dyna2014>{{cite journal |title=Thrombolytics for acute stroke |journal=Dynamed |date=Sep 15, 2014 |quote=at 3–4.5 hours after stroke onset t-PA increases risk of symptomatic intracranial hemorrhage but effect on functional outcomes is inconsistent }}{{verify source|date=September 2022}}</ref><ref>{{cite journal | vauthors = Alper BS, Malone-Moses M, McLellan JS, Prasad K, Manheimer E | title = Thrombolysis in acute ischaemic stroke: time for a rethink? | journal = BMJ | volume = 350 | issue = h1075 | pages = h1075 | date = March 2015 | pmid = 25786912 | doi = 10.1136/bmj.h1075 | s2cid = 38909467 }}</ref><ref>{{cite web|title=Canadian Association of Emergency Physicians Position Statement on Acute Ischemic Stroke|url=http://caep.ca/sites/caep.ca/files/caep/PositionStatments/caep_ps_stroke_2015_eng.pdf|website=caep.ca|access-date=7 April 2015|date=March 2015|url-status=dead|archive-url=https://web.archive.org/web/20150918203805/http://www.caep.ca/sites/caep.ca/files/caep/PositionStatments/caep_ps_stroke_2015_eng.pdf|archive-date=2015-09-18}}</ref> The AHA/ASA recommend it for certain people in this time frame.<ref>{{Cite web|url=https://www.acc.org/latest-in-cardiology/ten-points-to-remember/2018/01/29/12/45/2018-guidelines-for-the-early-management-of-stroke|title=10 points to remember|date=2018|website=American College of Cardiology|access-date=March 27, 2020}}</ref> 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.<ref name=Lancet2014/> After four and a half hours thrombolysis worsens outcomes.<ref name=Dyna2014/> These benefits or lack of benefits occurred regardless of the age of the person treated.<ref name=Lancet2012>{{cite journal | vauthors = Wardlaw JM, Murray V, Berge E, del Zoppo G, Sandercock P, Lindley RL, Cohen G | title = Recombinant tissue plasminogen activator for acute ischaemic stroke: an updated systematic review and meta-analysis | journal = Lancet | volume = 379 | issue = 9834 | pages = 2364–72 | date = June 2012 | pmid = 22632907 | pmc = 3386494 | doi = 10.1016/S0140-6736(12)60738-7 }}</ref> There is no reliable way to determine who will have an intracranial bleed post-treatment versus who will not.<ref>{{cite journal | vauthors = Whiteley WN, Slot KB, Fernandes P, Sandercock P, Wardlaw J | title = 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 | journal = Stroke | volume = 43 | issue = 11 | pages = 2904–9 | date = November 2012 | pmid = 22996959 | doi = 10.1161/STROKEAHA.112.665331 | doi-access = free }}</ref> In those with findings of savable tissue on medical imaging between 4.5 hours and 9 hours or who wake up with stroke, [[alteplase]] results in some benefit.<ref>{{cite journal | vauthors = Campbell BC, Ma H, Ringleb PA, Parsons MW, Churilov L, Bendszus M, Levi CR, Hsu C, Kleinig TJ, Fatar M, Leys D, Molina C, Wijeratne T, Curtze S, Dewey HM, Barber PA, Butcher KS, De Silva DA, Bladin CF, Yassi N, Pfaff JA, Sharma G, Bivard A, Desmond PM, Schwab S, Schellinger PD, Yan B, Mitchell PJ, Serena J, Toni D, Thijs V, Hacke W, Davis SM, Donnan GA | title = Extending thrombolysis to 4·5-9 h and wake-up stroke using perfusion imaging: a systematic review and meta-analysis of individual patient data | journal = Lancet | volume = 394 | issue = 10193 | pages = 139–147 | date = July 2019 | pmid = 31128925 | doi = 10.1016/S0140-6736(19)31053-0 | hdl-access = free | s2cid = 205990717 | hdl = 10138/312914 }}</ref>
 
Its use is endorsed by the [[American Heart Association]], the [[American College of Emergency Physicians]] 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 no 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<ref>{{cite journal | author = The National Institute Of Neurological Disorders And Stroke Rt-Pa Stroke Study Group | title = Tissue plasminogen activator for acute ischemic stroke | journal = The New England Journal of Medicine | volume = 333 | issue = 24 | pages = 1581–7 | date = December 1995 | pmid = 7477192 | doi = 10.1056/NEJM199512143332401 | doi-access = free }}</ref> 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.<ref>{{cite journal | vauthors = Wardlaw JM, Murray V, Berge E, del Zoppo GJ | title = Thrombolysis for acute ischaemic stroke | journal = The Cochrane Database of Systematic Reviews | volume = 7 | issue = 7 | pages = CD000213 | date = July 2014 | pmid = 25072528 | pmc = 4153726 | doi = 10.1002/14651858.CD000213.pub3 }}</ref> 6.4% of people with large stroke developed substantial brain bleeding as a complication from being given tPA thus part of the reason for increased short term mortality.<ref name="Dubinsky06">{{cite journal | vauthors = Dubinsky R, Lai SM | title = Mortality of stroke patients treated with thrombolysis: analysis of nationwide inpatient sample | journal = Neurology | volume = 66 | issue = 11 | pages = 1742–4 | date = June 2006 | pmid = 16769953 | doi = 10.1212/01.wnl.0000218306.35681.38 | s2cid = 13610719 }}</ref> The [[American Academy of Emergency Medicine]] had previously stated that objective evidence regarding the applicability of tPA for acute ischemic stroke was insufficient.<ref>{{cite web |url=http://www.aaem.org/positionstatements/thrombolytictherapy.shtml |title=Position Statement on the Use of Intravenous Thrombolytic Therapy in the Treatment of Stroke |publisher=American Academy of Emergency Medicine |access-date=2008-01-25 |url-status=live |archive-url=https://web.archive.org/web/20061004184429/http://www.aaem.org/positionstatements/thrombolytictherapy.shtml |archive-date=2006-10-04 }}</ref> In 2013 the American College of Emergency Medicine refuted this position,<ref>{{cite journal | vauthors = Chapman SN, Mehndiratta P, Johansen MC, McMurry TL, Johnston KC, Southerland AM | title = Current perspectives on the use of intravenous recombinant tissue plasminogen activator (tPA) for treatment of acute ischemic stroke | journal = Vascular Health and Risk Management | volume = 10 | pages = 75–87 | date = 2014-02-24 | pmid = 24591838 | pmc = 3938499 | doi = 10.2147/VHRM.S39213 | doi-access = free }}</ref> acknowledging the body of evidence for the use of tPA in ischemic stroke;<ref>{{cite journal | title = Clinical Policy: Use of intravenous tPA for the management of acute ischemic stroke in the emergency department | journal = Annals of Emergency Medicine | volume = 61 | issue = 2 | pages = 225–43 | date = February 2013 | pmid = 23331647 | doi = 10.1016/j.annemergmed.2012.11.005 | author1 = American College of Emergency Physicians }}</ref> but debate continues.<ref>{{cite news | vauthors = Kolata G |title=For Many Strokes, There's an Effective Treatment. Why Aren't Some Doctors Offering It? |url=https://www.nytimes.com/2018/03/26/health/stroke-clot-buster.html |work=The New York Times |date=26 March 2018 }}</ref><ref>{{cite news | vauthors = Mandrola JM |title=The Case Against Thrombolytic Therapy in Stroke |url=https://www.medscape.com/viewarticle/895159 |work=Medscape |date=13 April 2018 |url-access=subscription }}</ref> [[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.<ref>{{cite journal | vauthors = Lee M, Hong KS, Saver JL | title = Efficacy of intra-arterial fibrinolysis for acute ischemic stroke: meta-analysis of randomized controlled trials | journal = Stroke | volume = 41 | issue = 5 | pages = 932–7 | date = May 2010 | pmid = 20360549 | doi = 10.1161/STROKEAHA.109.574335 | doi-access = free }}</ref>
 
====Endovascular treatment====
Mechanical removal of the blood clot causing the ischemic stroke, called [[Thrombectomy|mechanical thrombectomy]], is a potential treatment for occlusion of a large artery, such as the [[middle cerebral artery]]. In 2015, one review demonstrated the safety and efficacy of this procedure if performed within 12 hours of the onset of symptoms.<ref>{{cite journal | vauthors = Sardar P, Chatterjee S, Giri J, Kundu A, Tandar A, Sen P, Nairooz R, Huston J, Ryan JJ, Bashir R, Parikh SA, White CJ, Meyers PM, Mukherjee D, Majersik JJ, Gray WA | title = Endovascular therapy for acute ischaemic stroke: a systematic review and meta-analysis of randomized trials | journal = European Heart Journal | volume = 36 | issue = 35 | pages = 2373–80 | date = September 2015 | pmid = 26071599 | doi = 10.1093/eurheartj/ehv270 | doi-access = free }}</ref><ref>{{cite journal | vauthors = Saver JL, Goyal M, van der Lugt A, Menon BK, Majoie CB, Dippel DW, Campbell BC, Nogueira RG, Demchuk AM, Tomasello A, Cardona P, Devlin TG, Frei DF, du Mesnil de Rochemont R, Berkhemer OA, Jovin TG, Siddiqui AH, van Zwam WH, Davis SM, Castaño C, Sapkota BL, Fransen PS, Molina C, van Oostenbrugge RJ, Chamorro Á, Lingsma H, Silver FL, Donnan GA, Shuaib A, Brown S, Stouch B, Mitchell PJ, Davalos A, Roos YB, Hill MD | title = Time to Treatment With Endovascular Thrombectomy and Outcomes From Ischemic Stroke: A Meta-analysis | journal = JAMA | volume = 316 | issue = 12 | pages = 1279–88 | date = September 2016 | pmid = 27673305 | doi = 10.1001/jama.2016.13647 }}</ref> It did not change the risk of death but did reduce disability compared to the use of intravenous thrombolysis, which is generally used in people evaluated for mechanical thrombectomy.<ref>{{cite journal | vauthors = Goyal M, Menon BK, van Zwam WH, Dippel DW, Mitchell PJ, Demchuk AM, Dávalos A, Majoie CB, van der Lugt A, de Miquel MA, Donnan GA, Roos YB, Bonafe A, Jahan R, Diener HC, van den Berg LA, Levy EI, Berkhemer OA, Pereira VM, Rempel J, Millán M, Davis SM, Roy D, Thornton J, Román LS, Ribó M, Beumer D, Stouch B, Brown S, Campbell BC, van Oostenbrugge RJ, Saver JL, Hill MD, Jovin TG | title = Endovascular thrombectomy after large-vessel ischaemic stroke: a meta-analysis of individual patient data from five randomised trials | journal = Lancet | volume = 387 | issue = 10029 | pages = 1723–31 | date = April 2016 | pmid = 26898852 | doi = 10.1016/s0140-6736(16)00163-x | s2cid = 34799180 }}</ref><ref>{{cite journal | vauthors = Mistry EA, Mistry AM, Nakawah MO, Chitale RV, James RF, Volpi JJ, Fusco MR | title = Mechanical Thrombectomy Outcomes With and Without Intravenous Thrombolysis in Stroke Patients: A Meta-Analysis | journal = Stroke | volume = 48 | issue = 9 | pages = 2450–2456 | date = September 2017 | pmid = 28747462 | doi = 10.1161/STROKEAHA.117.017320 | s2cid = 3751956 | doi-access = free }}</ref> Certain cases may benefit from thrombectomy up to 24 hours after the onset of symptoms.<ref>{{cite journal | vauthors = Powers WJ, Rabinstein AA, Ackerson T, Adeoye OM, Bambakidis NC, Becker K, Biller J, Brown M, Demaerschalk BM, Hoh B, Jauch EC, Kidwell CS, Leslie-Mazwi TM, Ovbiagele B, Scott PA, Sheth KN, Southerland AM, Summers DV, Tirschwell DL | title = 2018 Guidelines for the Early Management of Patients With Acute Ischemic Stroke: A Guideline for Healthcare Professionals From the American Heart Association/American Stroke Association | journal = Stroke | volume = 49 | issue = 3 | pages = e46–e110 | date = March 2018 | pmid = 29367334 | doi = 10.1161/STR.0000000000000158 | s2cid = 4972922 | doi-access = free }}</ref>
 
====Mechanical ThrombectomyCraniectomy ====
Stroke affecting large portions of the brain can cause significant brain swelling with secondary brain injury in surrounding tissue. This phenomenon is mainly encountered in stroke affecting brain tissue dependent upon the middle cerebral artery for blood supply 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 people – who would otherwise have died – survive with disability.<ref name="pmid21190097">{{cite journal | vauthors = Simard JM, Sahuquillo J, Sheth KN, Kahle KT, Walcott BP | title = Managing malignant cerebral infarction | journal = Current Treatment Options in Neurology | volume = 13 | issue = 2 | pages = 217–229 | date = April 2011 | pmid = 21190097 | pmc = 3243953 | doi = 10.1007/s11940-010-0110-9 }}</ref><ref>{{cite journal | vauthors = Jüttler E, Unterberg A, Woitzik J, Bösel J, Amiri H, Sakowitz OW, Gondan M, Schiller P, Limprecht R, Luntz S, Schneider H, Pinzer T, Hobohm C, Meixensberger J, Hacke W | title = Hemicraniectomy in older patients with extensive middle-cerebral-artery stroke | journal = The New England Journal of Medicine | volume = 370 | issue = 12 | pages = 1091–1100 | date = March 2014 | pmid = 24645942 | doi = 10.1056/NEJMoa1311367 | doi-access = free }}</ref>
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 up into the cerebral circulation, and deploying a corkscrew-like device to ensnare the clot, which is then withdrawn from the body. In August 2004, based on data from the MERCI (Mechanical Embolus Removal in Cerebral Ischemia) Trial, the FDA cleared one such device, called the Merci Retriever.<ref>{{cite web | author= Smith WS, Sung G, Starkman S, Saver JL, Kidwell CS, Gobin YP, Lutsep HL, Nesbit GM, Grobelny T, Rymer MM, Silverman IE, Higashida RT, Budzik RF, Marks MP; MERCI Trial Investigators| year=2005 | title= Safety and efficacy of mechanical embolectomy in acute ischemic stroke: results of the MERCI trial| publisher=Stroke. 2005 Jul;36(7):1432-8| url=http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed&cmd=Retrieve&dopt=AbstractPlus&list_uids=15961709&query_hl=6&itool=pubmed_docsum}}</ref><!--
--><ref name="FDA2004-MerciRetriever">{{cite web | author=Celia Witten | year=2004 | title=Concentric Merci Retriever product licence |url=http://www.fda.gov/cdrh/pdf3/k033736.pdf | format=PDF | publisher=FDA}}</ref>
Already newer generation devices are being tested in the Multi MERCI trial.<ref>{{cite web | author= W. Smith | year=2006 | title= 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| publisher=AJNR Am J Neuroradiol. 2006 Jun-Jul;27(6):1177-82 | url=http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed&cmd=Retrieve&dopt=AbstractPlus&list_uids=16775259&query_hl=2&itool=pubmed_docsum}}</ref><ref>{{cite web | author= W. Smith | year=2006 | title= Mechanical Intervention for Ischemic Stroke | publisher=Touch Briefings | url=http://www.touchneurology.com/articles.cfm?article_id=5734&level=2}}</ref> Both the MERCI and Multi MERCI trials evaluated the use of mechanical thrombectomy up to 8 hours after onset of symptoms.
 
===Hemorrhagic stroke===
People with [[intracerebral hemorrhage]] require supportive care, including blood pressure control if required. People are monitored for changes in the level of consciousness, and their blood sugar and oxygenation are kept at optimum levels. Anticoagulants and antithrombotics can make bleeding worse and are generally discontinued (and reversed if possible).{{citation needed|date=June 2016}} A proportion may benefit from [[neurosurgery|neurosurgical]] intervention to remove the blood and treat the underlying cause, but this depends on the ___location and the size of the hemorrhage as well as patient-related factors, and ongoing research is being conducted into the question as to which people with intracerebral hemorrhage may benefit.<ref>{{cite journal | vauthors = Vespa PM, Martin N, Zuccarello M, Awad I, Hanley DF | title = Surgical trials in intracerebral hemorrhage | journal = Stroke | volume = 44 | issue = 6 Suppl 1 | pages = S79-82 | date = June 2013 | pmid = 23709739 | pmc = 6778724 | doi = 10.1161/STROKEAHA.113.001494 }}</ref>
Patients with bleeding into ([[intracerebral hemorrhage]]) or around the brain ([[subarachnoid hemorrhage]]), require [[neurosurgery|neurosurgical]] evaluation to detect and treat the cause of the bleeding. 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.
 
In [[subarachnoid hemorrhage]], early treatment for underlying cerebral aneurysms may reduce the risk of further hemorrhages. Depending on the site of the aneurysm this may be by [[craniotomy|surgery that involves opening the skull]] or [[Interventional neuroradiology|endovascularly]] (through the blood vessels).<ref>{{cite journal | vauthors = Steiner T, Juvela S, Unterberg A, Jung C, Forsting M, Rinkel G | title = European Stroke Organization guidelines for the management of intracranial aneurysms and subarachnoid haemorrhage | journal = Cerebrovascular Diseases | volume = 35 | issue = 2 | pages = 93–112 | date = 2013 | pmid = 23406828 | doi = 10.1159/000346087 | s2cid = 3526670 | doi-access = free | url = http://archiv.ub.uni-heidelberg.de/volltextserver/27044/1/346087.pdf }}</ref>
===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.
 
===Stroke unit===
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 work]]ers, and [[pharmacist]]s since at least one third of the patients manifest [[post stroke depression]].
Ideally, people who have had stroke are admitted to a "stroke unit", a ward or dedicated area in a hospital staffed by nurses and therapists with experience in stroke treatment. It has been shown that people admitted to stroke units have a higher chance of surviving than those admitted elsewhere in hospital, even if they are being cared for by doctors without experience in stroke.<ref name=Donnan2008/><ref>{{cite journal | vauthors = Langhorne P, Ramachandra S | title = Organised inpatient (stroke unit) care for stroke: network meta-analysis | journal = The Cochrane Database of Systematic Reviews | volume = 2020 | pages = CD000197 | date = April 2020 | issue = 4 | pmid = 32324916 | pmc = 7197653 | doi = 10.1002/14651858.CD000197.pub4 }}</ref> [[Nursing care]] is fundamental in maintaining [[Skin|skin care]], feeding, hydration, positioning, and monitoring [[vital signs]] such as temperature, pulse, and blood pressure.<ref>{{cite journal | vauthors = Clarke DJ | title = Nursing practice in stroke rehabilitation: systematic review and meta-ethnography | journal = Journal of Clinical Nursing | volume = 23 | issue = 9–10 | pages = 1201–26 | date = May 2014 | pmid = 24102924 | doi = 10.1111/jocn.12334 }}</ref>
 
== Rehabilitation ==
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.
[[Stroke rehabilitation]] is the process by which those with disabling stroke 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. Stroke rehabilitation should begin almost immediately with a multidisciplinary approach. The rehabilitation team may involve physicians trained in rehabilitation medicine, [[neurologist]]s, [[clinical pharmacist]]s, nursing staff, [[physiotherapist]]s, [[occupational therapist]]s, [[Speech-language pathology|speech-language pathologist]]s, and [[orthotist]]s. Some teams may also include [[psychologists]] and [[social work]]ers, since at least one-third of affected people manifests [[post stroke depression]]. Validated instruments such as the [[Barthel scale]] may be used to assess the likelihood of a person who has had stroke being able to manage at home with or without support subsequent to discharge from a hospital.<ref>{{cite journal | vauthors = Duffy L, Gajree S, Langhorne P, Stott DJ, Quinn TJ | title = Reliability (inter-rater agreement) of the Barthel Index for assessment of stroke survivors: systematic review and meta-analysis | journal = Stroke | volume = 44 | issue = 2 | pages = 462–8 | date = February 2013 | pmid = 23299497 | doi = 10.1161/STROKEAHA.112.678615 | s2cid = 9499113 | doi-access = free }}</ref>
 
[[Stroke rehabilitation]] should be started as quickly as possible and can last anywhere from a few days to over a year. Most return of function is seen in the first few months, 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.{{Medical citation needed|date=August 2020}} However, some people have reported that they continue to improve for years, regaining and strengthening abilities like writing, walking, running, and talking.{{Medical citation needed|date=August 2020}} Daily rehabilitation exercises should continue to be part of the daily routine for people who have had stroke. Complete recovery is unusual but not impossible and most people will improve to some extent: proper diet and exercise are known to help the brain to recover.
For most stroke patients, [[physical therapy]] is the cornerstone of the rehabilitation process. Often, [[assistive technology]] such as a [[wheelchair]] and [[standing frame]] may be beneficial. Another type of therapy involving relearning daily activities is [[occupational therapy]] (OT). OT involves exercise and training to help the stroke patient relearn everyday activities sometimes called the [[Activities of daily living]] (ADLs) such as eating, drinking and swallowing, dressing, bathing, cooking, reading and writing, and toileting. [[Speech and language therapy]] is appropriate for patients with problems understanding speech or written words, or problems forming speech.
 
=== Spatial neglect ===
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.
 
The body of evidence is uncertain on the efficacy of cognitive rehabilitation for reducing the disabling effects of neglect and increasing independence remains unproven.<ref name="Longley Hazelton Heal et al 2021">{{cite journal | vauthors = Longley V, Hazelton C, Heal C, Pollock A, Woodward-Nutt K, Mitchell C, Pobric G, Vail A, Bowen A | title = Non-pharmacological interventions for spatial neglect or inattention following stroke and other non-progressive brain injury | journal = The Cochrane Database of Systematic Reviews | volume = 2021 | issue = 7 | pages = CD003586 | date = July 2021 | pmid = 34196963 | pmc = 8247630 | doi = 10.1002/14651858.CD003586.pub4 }}</ref> However, there is limited evidence that cognitive rehabilitation may have an immediate beneficial effect on tests of neglect.<ref name="Longley Hazelton Heal et al 2021"/> Overall, no rehabilitation approach can be supported by evidence for spatial neglect.
Stroke rehabilitation should be started as immediately as possible and can last anywhere from a few days to several months. 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 in its process of self-recovery.
 
=== Automobile driving ===
Stem-cell research in the coming years may provide new concepts as to how the "plasticity" of the brain may help it to repair itself.
 
The body of evidence is uncertain whether the use of rehabilitation can improve on-road driving skills following stroke.<ref name="George-2014">{{cite journal | vauthors = George S, Crotty M, Gelinas I, Devos H | title = Rehabilitation for improving automobile driving after stroke | journal = The Cochrane Database of Systematic Reviews | volume = 2014 | issue = 2 | pages = CD008357 | date = February 2014 | pmid = 24567028 | pmc = 6464773 | doi = 10.1002/14651858.CD008357.pub2 }}</ref> There is limited evidence that training on a driving simulator will improve performance on recognizing road signs after training.<ref name="George-2014" /> The findings are based on low-quality evidence as further research is needed involving large numbers of participants.
==Prognosis==
Disability affects 75% of stroke survivors enough to decrease their employability.<!--
--><ref name="Coffey2000">{{cite book | author=Coffey C. Edward, Cummings Jeffrey L, Starkstein Sergio, Robinson Robert | title=Stroke - The American Psychiatric Press Textbook of Geriatric Neuropsychiatry | year=2000 | edition=Second Edition | pages=601-617 | ___location=Washington DC | publisher=American Psychiatric Press}}</ref>
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.<!--
--><ref name="Stanford2005">{{cite web | author=Stanford Hospital & Clinics | title=Cardiovascular Diseases: Effects of Stroke | url=http://www.stanfordhospital.com/healthLib/atoz/cardiac/effects.html | accessyear=2005}}</ref>
Dysfunctions correspond to areas in the brain that have been damaged.
 
=== Yoga ===
Some of the physical disabilities that can result from stroke include [[paralysis]], numbness, [[pressure sore]]s, [[pneumonia]], [[incontinence]], [[apraxia]] (inability to perform learned movements), difficulties carrying out daily activities, appetite loss, vision loss, and [[Pain and nociception|pain]]. If the stroke is severe enough, [[coma]] or [[death]] can result.
 
Based on low quality evidence, it is uncertain whether yoga has a significant benefit for stroke rehabilitation on measures of quality of life, balance, strength, endurance, pain, and disability scores.<ref name="Lawrence-2017">{{cite journal | vauthors = Lawrence M, Celestino Junior FT, Matozinho HH, Govan L, Booth J, Beecher J | title = Yoga for stroke rehabilitation | journal = The Cochrane Database of Systematic Reviews | volume = 2017 | issue = 12 | pages = CD011483 | date = December 2017 | pmid = 29220541 | pmc = 6486003 | doi = 10.1002/14651858.CD011483.pub2 }}</ref> Yoga may reduce anxiety and could be included as part of patient-centred stroke rehabilitation.<ref name="Lawrence-2017" /> Further research is needed assessing the benefits and safety of yoga in stroke rehabilitation.
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 attack]]s, [[flat affect]] (failure to express emotions), [[mania]], apathy, and [[psychosis]].
 
=== Action observation physical therapy for upper limbs ===
30 to 50% of stroke survivors suffer post stroke [[Clinical depression|depression]] ([[Post stroke depression]]), which is characterized by lethargy, irritability, sleep disturbances, lowered self esteem, and withdrawal.<!--
--><ref name="Senelick1994">{{cite book | author=Senelick Richard C., Rossi, Peter W., Dougherty, Karla | title=Living with Stroke: A Guide For Families | year=1994 | publisher=Contemporary Books, Chicago}}</ref>
Depression can reduce motivation and worsen outcome, but can be treated with [[antidepressant]]s.
 
Low-quality evidence suggests that action observation (a type of physiotherapy that is meant to improve neural plasticity through the mirror-neuronal system) may be of some benefit and has no significant adverse effects, however this benefit may not be clinically significant and further research is suggested.<ref>{{cite journal | vauthors = Borges LR, Fernandes AB, Oliveira Dos Passos J, Rego IA, Campos TF | title = Action observation for upper limb rehabilitation after stroke | journal = The Cochrane Database of Systematic Reviews | volume = 2022 | issue = 8 | pages = CD011887 | date = August 2022 | pmid = 35930301 | pmc = 9354942 | doi = 10.1002/14651858.CD011887.pub3 }}</ref>
[[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.<!--
--><ref name="Coffey2000"/>
Some patients show the opposite of what they feel, for example crying when they are happy.<!--
--><ref name="Villarosa1993">{{cite book | author=Villarosa, Linda, Ed., Singleton, LaFayette, MD, Johnson, Kirk A. | title=Black Health Library Guide to Stroke | year=1993 | publisher=Henry Holt and Company, New York}}</ref>
Emotional lability occurs in about 20% of stroke patients.
 
=== Cognitive rehabilitation for attention deficits ===
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.
 
The body of scientific evidence is uncertain on the effectiveness of cognitive rehabilitation for attention deficits in patients following stroke.<ref name="Loetscher-2019">{{cite journal | vauthors = Loetscher T, Potter KJ, Wong D, das Nair R | title = Cognitive rehabilitation for attention deficits following stroke | journal = The Cochrane Database of Systematic Reviews | volume = 2019 | issue = 11 | date = November 2019 | pmid = 31706263 | pmc = 6953353 | doi = 10.1002/14651858.CD002842.pub3 }}</ref> While there may be an immediate effect after treatment on attention, the findings are based on low to moderate quality and small number of studies.<ref name="Loetscher-2019" /> Further research is needed to assess whether the effect can be sustained in day-to-day tasks requiring attention.
Up to 10% of all stroke patients develop [[seizure]]s, most commonly in the week subsequent to the event; the severity of the stroke increases the likelihood of a seizure<ref name=Reith1997>Reith J, Jorgensen HS, Nakayama H, Raaschou HO, Olsen TS. Seizures in acute stroke: predictors and prognostic significance. The Copenhagen Stroke Study. ''Stroke'' 1997;28:1585-9. PMID 9259753.</ref><ref name=Burn1997>Burn J, Dennis M, Bamford J, Sandercock P, Wade D, Warlow C. Epileptic seizures after a first stroke: the Oxfordshire Community Stroke Project. ''BMJ'' 1997;315:1582-7. PMID 9437276.</ref>.
 
=== Motor imagery for gait rehabilitation ===
==Risk factors and prevention==
[[Prevention (medical)|Prevention]] of stroke can work at various levels including:
#''primary prevention'' - the reduction of risk factors across the board, by public health measures such as reducing smoking and the other behaviours that increase risk;
#''secondary prevention'' - actions taken to reduce the risk in those who already have disease or risk factors that may have been identified through [[Screening (medicine)|screening]]; and
#''tertiary prevention'' - actions taken to reduce the risk of complications (including further strokes) in people who have already had a stroke.
 
The latest evidence supports the short-term benefits of motor imagery (MI) on walking speed in individuals who have had stroke, in comparison to other therapies.<ref name="Silva-2020">{{cite journal | vauthors = Silva S, Borges LR, Santiago L, Lucena L, Lindquist AR, Ribeiro T | title = Motor imagery for gait rehabilitation after stroke | journal = The Cochrane Database of Systematic Reviews | volume = 2020 | issue = 9 | pages = CD013019 | date = September 2020 | pmid = 32970328 | pmc = 8094749 | doi = 10.1002/14651858.CD013019.pub2 | collaboration = Cochrane Stroke Group }}</ref> MI does not improve motor function after stroke and does not seem to cause significant adverse events.<ref name="Silva-2020" /> The findings are based on low-quality evidence as further research is needed to estimate the effect of MI on walking endurance and the dependence on personal assistance.
The most important modifiable risk factors for stroke are hypertension, heart disease, diabetes, and cigarette smoking. Other risks include heavy alcohol consumption (see [[Alcohol consumption and health]]), high blood cholesterol levels, illicit drug use,{{Fact|date=February 2007}} and genetic or congenital conditions. 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.<ref>{{cite journal | author = Bongers T, de Maat M, van Goor M, et. al | title = High von Willebrand factor levels increase the risk of first ischemic stroke: influence of ADAMTS13, inflammation, and genetic variability. | journal = Stroke | volume = 37 | issue = 11 | pages = 2672-7 | year = 2006 | id = PMID 16990571}}</ref><!--
--> 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.
 
=== Physical and occupational therapy ===
One of the most significant stroke risk factors is advanced age. 95% of strokes occur in people age 45 and older, and two-thirds of strokes occur in those over the age of 65.<ref name="Senelick1994"/><!--
Physical and occupational therapy have overlapping areas of expertise; however, physical therapy 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 people who have had stroke 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 people's goals. One example physiotherapists employ to promote [[motor learning]] involves [[constraint-induced movement therapy]]. Through continuous practice the person relearns to use and adapt the hemiplegic limb during functional activities to create lasting permanent changes.<ref>{{harvnb|O'Sullivan|2007|pp=471, 484, 737, 740}}</ref> Physical therapy is effective for recovery of function and mobility after stroke.<ref name="CD001920">{{cite journal | vauthors = Pollock A, Baer G, Campbell P, Choo PL, Forster A, Morris J, Pomeroy VM, Langhorne P | title = Physical rehabilitation approaches for the recovery of function and mobility following stroke | journal = The Cochrane Database of Systematic Reviews | issue = 4 | pages = CD001920 | date = April 2014 | volume = 2014 | pmid = 24756870 | pmc = 6465059 | doi = 10.1002/14651858.CD001920.pub3 | collaboration = Cochrane Stroke Group }}</ref>{{Update inline|reason=Updated version https://www.ncbi.nlm.nih.gov/pubmed/39932103|date = March 2025}} Occupational therapy is involved in training to help relearn everyday activities known as the [[activities of daily living]] (ADLs) such as eating, drinking, dressing, bathing, cooking, [[Alexia (condition)|reading]] and [[agraphia|writing]], and toileting. Approaches to helping people with urinary incontinence include physical therapy, cognitive therapy, and specialized interventions with experienced medical professionals, however, it is not clear how effective these approaches are at improving urinary incontinence following stroke.<ref name="Thomas-2019">{{cite journal | vauthors = Thomas LH, Coupe J, Cross LD, Tan AL, Watkins CL | title = Interventions for treating urinary incontinence after stroke in adults | journal = The Cochrane Database of Systematic Reviews | volume = 2019 | issue = 2 | pages = CD004462 | date = February 2019 | pmid = 30706461 | pmc = 6355973 | doi = 10.1002/14651858.CD004462.pub4 }}</ref>
--><ref name="NINDS1999">{{cite web | author=National Institute of Neurological Disorders and Stroke (NINDS) | authorlink= National Institute of Neurological Disorders and Stroke | year=1999 | title=Stroke: Hope Through Research | url=http://www.ninds.nih.gov/disorders/stroke/detail_stroke.htm | publisher=National Institutes of Health}}</ref> 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.
 
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 different positions.<ref name="OSul07_719" /> Gaining initial improvement in range of motion is often achieved through rhythmic rotational patterns associated with the affected limb.<ref name="OSul07_719" /> 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.<ref name="OSul07_719" /> Cold ice wraps or ice packs may briefly relieve spasticity by temporarily reducing neural firing rates.<ref name="OSul07_719" /> [[Sensory stimulation therapy#Coactivation|Electrical stimulation]] to the antagonist muscles or vibrations has also been used with some success.<ref name="OSul07_719" /> Physical therapy is sometimes suggested for people who experience sexual dysfunction following stroke.<ref name="Stratton-2020">{{cite journal | vauthors = Stratton H, Sansom J, Brown-Major A, Anderson P, Ng L | title = Interventions for sexual dysfunction following stroke | journal = The Cochrane Database of Systematic Reviews | volume = 2020 | issue = 5 | pages = CD011189 | date = May 2020 | pmid = 32356377 | pmc = 7197697 | doi = 10.1002/14651858.CD011189.pub2 }}</ref>
Sickle cell anemia, which can cause blood cells to clump up and block blood vessels, also increases stroke risk. Stroke is the second leading killer of people under 20 who suffer from sickle-cell anemia.<!--
--><ref name="NINDS1999"/>
 
==== Interventions for age-related visual problems in patients with stroke ====
Men are 1.25 times more likely to suffer CVAs than women,<!--
With the prevalence of vision problems increasing with age in stroke patients, the overall effect of interventions for age-related visual problems is uncertain. It is also not sure whether people with stroke respond differently from the general population when treating eye problems.<ref>{{cite journal | vauthors = Pollock A, Hazelton C, Henderson CA, Angilley J, Dhillon B, Langhorne P, Livingstone K, Munro FA, Orr H, Rowe FJ, Shahani U | title = Interventions for age-related visual problems in patients with stroke | journal = The Cochrane Database of Systematic Reviews | issue = 3 | pages = CD008390 | date = March 2012 | pmid = 22419333 | doi = 10.1002/14651858.cd008390.pub2 | pmc = 11569885 }}</ref> Further research in this area is needed as the body of evidence is very low quality.
--><ref name="NINDS1999"/> yet 60% of deaths from stroke occur in women.<!--
--><ref name="Villarosa1993"/> Since women live longer, they are older on average when they have their strokes and thus more often killed (NIMH 2002).<!--
--><ref name="NINDS1999"/> Some risk factors for stroke apply only to women. Primary among these are pregnancy, childbirth, menopause and the treatment thereof ([[Hormone replacement therapy|HRT]]). Stroke seems to run in some families.
 
=== Speech and language therapy ===
Prevention is an important public health concern. Identification of patients with treatable risk factors for stroke is paramount. Treatment of risk factors in patients who have already had strokes (secondary prevention) is also very important as they are at high risk of subsequent events compared with those who have never had a stroke. Medication or drug therapy is the most common method of stroke prevention. Aspirin (usually at a low dose of 75 mg) is recommended for the primary and secondary prevention of stroke. Also see [[Antiplatelet drug]] treatment. Treating [[hypertension]], [[diabetes mellitus]], smoking cessation, control of [[hypercholesterolemia]], physical exercise, and avoidance of illicit drugs and excessive alcohol consumption are all recommended ways of reducing the risk of stroke.<ref name="americanheart risk">American Heart Association. (2007). [http://www.americanheart.org/presenter.jhtml?identifier=4716 Stroke Risk Factors] Americanheart.org. Retrieved on [[January 22]], [[2007]].</ref>
[[Speech and language therapy]] is appropriate for people with the speech production disorders: [[dysarthria]]<ref name="Mackenzie 2011">{{cite journal | vauthors = Mackenzie C | title = Dysarthria in stroke: a narrative review of its description and the outcome of intervention | journal = International Journal of Speech-Language Pathology | volume = 13 | issue = 2 | pages = 125–36 | date = April 2011 | pmid = 21480809 | doi = 10.3109/17549507.2011.524940 | s2cid = 39377646 | url = https://strathprints.strath.ac.uk/28413/1/Mackenzie---IJSLP---penultimate1.doc }}</ref> and [[apraxia of speech]],<ref name="West 2005">{{cite journal | vauthors = West C, Hesketh A, Vail A, Bowen A | title = Interventions for apraxia of speech following stroke | journal = The Cochrane Database of Systematic Reviews | issue = 4 | pages = CD004298 | date = October 2005 | volume = 2010 | pmid = 16235357 | doi = 10.1002/14651858.CD004298.pub2 | pmc = 8769681 }}</ref> [[aphasia]],<ref name="Brady2016"/> cognitive-communication impairments, and [[dysphagia|problems with swallowing]].
 
Speech and language therapy for aphasia following stroke improves functional communication, reading, writing and expressive language. Speech and language therapy that is higher intensity, higher dose or provided over a long duration of time leads to significantly better functional communication but people might be more likely to drop out of high intensity treatment (up to 15 hours per week).<ref name="Brady2016">{{cite journal | vauthors = Brady MC, Kelly H, Godwin J, Enderby P, Campbell P | title = Speech and language therapy for aphasia following stroke | journal = The Cochrane Database of Systematic Reviews | volume = 2016 | issue = 6 | pages = CD000425 | date = June 2016 | pmid = 27245310 | pmc = 8078645 | doi = 10.1002/14651858.CD000425.pub4 | hdl-access = free | hdl = 1893/26112 }}</ref> A total of 20–50 hours of speech and language therapy is necessary for the best recovery. The most improvement happens when 2–5 hours of therapy is provided each week over 4–5 days. Recovery is further improved when besides the therapy people practice tasks at home.<ref name="Brady-2022a">{{cite journal | title = Complex speech-language therapy interventions for stroke-related aphasia: the RELEASE study incorporating a systematic review and individual participant data network meta-analysis | journal = Health and Social Care Delivery Research | volume = 10 | issue = 28 | pages = 1–272 | date = October 2022 | pmid = 36223438 | doi = 10.3310/RTLH7522 | hdl-access = free | s2cid = 252707680 | doi-access = free | hdl = 10072/419101 | vauthors = Brady MC, Ali M, Vandenberg K, Williams LJ, Williams LR, Abo M, Becker F, Bowen A, Brandenburg C, Breitenstein C, Bruehl S, Copland DA, Cranfill TB, Di Pietro-Bachmann M, Enderby P, Fillingham J, Galli FL, Gandolfi M, Glize B, Godecke E, Hawkins N, Hilari K, Hinckley J, Horton S, Howard D, Jaecks P, Jefferies E, Jesus LM, Kambanaros M, Kang EK }}</ref><ref name="NIHR-2023a">{{Cite journal |date=2023-09-01 |title=Speech and language therapy for aphasia after a stroke |url=https://evidence.nihr.ac.uk/alert/therapy-for-language-problems-after-a-stroke-is-most-effective-when-given-early-and-intensively/ |access-date=2023-09-08 |website=NIHR Evidence |publisher=National Institute for Health and Care Research |language=en-GB |type=Plain English summary |doi=10.3310/nihrevidence_59653|s2cid= 261470072|url-access=subscription }}</ref> Speech and language therapy is also effective if it is [[Telerehabilitation|delivered online through video]] or by a family member who has been trained by a professional therapist.<ref name="Brady-2022a" /><ref name="NIHR-2023a" />
In patients who have strokes due to abnormalities of the heart, such as [[atrial fibrillation]], [[anticoagulation]] with medications such as warfarin is often necessary for stroke prevention.<ref>American Heart Association. (2007). [http://www.americanheart.org/presenter.jhtml?identifier=4451 Atrial Fibrillation] Americanheart.org. Retrieved on [[January 22]], [[2007]].</ref>
 
Recovery with therapy for aphasia is also dependent on the recency of stroke and the age of the person. Receiving therapy within a month after the stroke leads to the greatest improvements. 3 or 6 months after the stroke more therapy will be needed but symptoms can still be improved. People with aphasia who are younger than 55 years are the most likely to improve but people older than 75 years can still get better with therapy.<ref name="Brady-2022a"/><ref name="NIHR-2023a"/>
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. These procedures have been shown to prevent stroke in certain patients, especially where carotid stenosis leads to [[ischemic]] events such as [[transient ischemic attack]]. (The value and role of carotid artery ultrasound scanning in [[Screening (medicine)|screening]] has yet to be established.)
 
People who have had stroke may have particular problems, such as [[dysphagia]], 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 intubation|nasogastric tube]] may be inserted, enabling liquid food to be given directly into the stomach. If swallowing is still deemed unsafe, then a [[percutaneous endoscopic gastrostomy]] (PEG) tube is passed and this can remain indefinitely. Swallowing therapy has mixed results as of 2018.<ref>{{cite journal | vauthors = Bath PM, Lee HS, Everton LF | title = Swallowing therapy for dysphagia in acute and subacute stroke | journal = The Cochrane Database of Systematic Reviews | volume = 2018 | pages = CD000323 | date = October 2018 | issue = 10 | pmid = 30376602 | pmc = 6516809 | doi = 10.1002/14651858.CD000323.pub3 }}</ref>
==Pathophysiology==
Ischemic stroke occurs due to a loss of blood supply to part of the brain, initiating the [[Ischemic cascade]]. Brain tissue ceases to function if deprived of oxygen for more than 60 to 90 seconds and after a few hours will suffer irreversible injury possibly leading to death of the tissue, i.e., [[infarction]]. [[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 atria fibriliation, or in the carotid arteries. These break off, enter the cerebral circulation, then lodge in and occlude brain blood vessels.
 
=== Devices ===
Due to collateral circulation, within the region of brain tissue affected by ischemia there is a spectrum of severity. Thus, part of the tissue may immediately die while other parts may only be injured and could potentially recover. The ischemia area where tissue might recover is referred to as the ''ischemic penumbra''.
Often, [[assistive technology]] such as [[wheelchairs]], walkers and canes may be beneficial. Many mobility problems can be improved by the use of [[Orthotics|ankle foot orthoses]].<ref>{{cite web|title=NHS Scotland – SHOW|url=http://www.stroke.scot.nhs.uk/docs/UseOfAnkle-FootOrthosesFollowingStroke.pdf|url-status=dead|archive-url=https://web.archive.org/web/20130516181844/http://www.stroke.scot.nhs.uk/docs/UseOfAnkle-FootOrthosesFollowingStroke.pdf|archive-date=2013-05-16|access-date=2012-11-09}}</ref>
 
=== Physical fitness ===
As oxygen or glucose becomes depleted in ischemic brain tissue, the production of high energy phosphate compounds such as adenine triphosphate (ATP) fails leading to failure of energy dependent processes necessary for tissue cell survival. This sets off a series of interrelated events that result in cellular injury and death. These include the failure of [[mitochondria]], which can lead further toward energy depletion and may trigger cell death due to [[apoptosis]]. Other processes include the loss of membrane ion pump function leading to electrolyte imbalances in brain cells. There is also the release of excitatory neurotransmitters, which have toxic effects in excessive concentrations.
Stroke can also reduce people's general fitness.<ref name="Saunders-2020">{{cite journal | vauthors = Saunders DH, Sanderson M, Hayes S, Johnson L, Kramer S, Carter DD, Jarvis H, Brazzelli M, Mead GE | title = Physical fitness training for stroke patients | journal = The Cochrane Database of Systematic Reviews | volume = 2020 | pages = CD003316 | date = March 2020 | issue = 3 | pmid = 32196635 | pmc = 7083515 | doi = 10.1002/14651858.CD003316.pub7 }}</ref> Reduced fitness can reduce capacity for rehabilitation as well as general health.<ref name="IQWiG-Fitness">{{cite web|last=Institute for Quality and Efficiency in Health Care (IQWiG)|title=After a stroke: Does fitness training improve overall health and mobility?|url=https://www.ncbi.nlm.nih.gov/books/NBK279215/|access-date=20 June 2013|work=Informed Health Online|publisher=Institute for Quality and Efficiency in Health Care (IQWiG)}}</ref> Physical exercises as part of a rehabilitation program following stroke appear safe.<ref name="Saunders-2020" /> Cardiorespiratory fitness training that involves walking in rehabilitation can improve speed, tolerance and independence during walking, and may improve balance.<ref name="Saunders-2020" /> There are inadequate long-term data about the effects of exercise and training on death, dependence and disability after stroke.<ref name="Saunders-2020" /> The future areas of research may concentrate on the optimal exercise prescription and long-term health benefits of exercise. The effect of physical training on cognition also may be studied further.
 
The ability to walk independently in their community, indoors or outdoors, is important following stroke. Although no negative effects have been reported, it is unclear if outcomes can improve with these walking programs when compared to usual treatment.<ref>{{cite journal | vauthors = Barclay RE, Stevenson TJ, Poluha W, Ripat J, Nett C, Srikesavan CS | title = Interventions for improving community ambulation in individuals with stroke | journal = The Cochrane Database of Systematic Reviews | volume = 2015 | issue = 3 | pages = CD010200 | date = March 2015 | pmid = 25767912 | pmc = 6465042 | doi = 10.1002/14651858.CD010200.pub2 }}</ref>
Ischaemia 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]] .<!--
--><ref name="NINDS1999"/>
 
=== Other therapy methods ===
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.
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 people to perform specific therapy tasks that many other forms do not.<ref name="Lange">{{cite journal| vauthors = Lange B, Flynn S, Rizzo A |title=Initial usability assessment of off-the-shelf video game consoles for clinical game-based motor rehabilitation|journal=Physical Therapy Reviews|year=2009|volume=14|issue=5|pages=355–62|doi=10.1179/108331909X12488667117258 |s2cid=14767181 }}</ref> While virtual reality and interactive video gaming are not more effective than conventional therapy for improving upper limb function, when used in conjunction with usual care these approaches may improve upper limb function and ADL function.<ref name="Laver-2017" /> There are inadequate data on the effect of virtual reality and interactive video gaming on gait speed, balance, participation and quality of life.<ref name="Laver-2017">{{cite journal | vauthors = Laver KE, Lange B, George S, Deutsch JE, Saposnik G, Crotty M | title = Virtual reality for stroke rehabilitation | journal = The Cochrane Database of Systematic Reviews | volume = 11 | pages = CD008349 | date = November 2017 | issue = 11 | pmid = 29156493 | pmc = 6485957 | doi = 10.1002/14651858.CD008349.pub4 | collaboration = Cochrane Stroke Group }}</ref>{{Update inline|reason=Updated version https://www.ncbi.nlm.nih.gov/pubmed/40537150|date = August 2025}} 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.<ref name="Lange" />
 
[[Mirror therapy]] is associated with improved motor function of the upper extremity in people who have had stroke.<ref>{{cite journal | vauthors = Thieme H, Mehrholz J, Pohl M, Behrens J, Dohle C | title = Mirror therapy for improving motor function after stroke | journal = Stroke | volume = 44 | issue = 1 | pages = e1-2 | date = January 2013 | pmid = 23390640 | doi = 10.1161/strokeaha.112.673087 | doi-access = free }}</ref>
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 [http://content.nejm.org/cgi/content/short/354/6/588 reported] be neuroprotective in stroke. This agent appears to work at the level of the blood vessel lining or [[endothelium]]. Unfortunately, after producing favorable results in one large-scale clinical trial, a second trial failed to show favorable results. <!--
--><ref name="NINDS1999"/>
 
Other non-invasive rehabilitation methods used to augment physical therapy of motor function in people recovering from stroke include [[neurotherapy]] as [[transcranial magnetic stimulation]] and [[transcranial direct-current stimulation]].<ref>{{cite journal | vauthors = Fregni F, Pascual-Leone A | title = Technology insight: noninvasive brain stimulation in neurology-perspectives on the therapeutic potential of rTMS and tDCS | journal = Nature Clinical Practice. Neurology | volume = 3 | issue = 7 | pages = 383–93 | date = July 2007 | pmid = 17611487 | doi = 10.1038/ncpneuro0530 | s2cid = 11365968 }}</ref> and [[Rehabilitation robotics|robotic therapies]].<ref>{{cite journal | vauthors = Balasubramanian S, Klein J, Burdet E | title = Robot-assisted rehabilitation of hand function | journal = Current Opinion in Neurology | volume = 23 | issue = 6 | pages = 661–70 | date = December 2010 | pmid = 20852421 | doi = 10.1097/WCO.0b013e32833e99a4 }}</ref> Constraint‐induced movement therapy (CIMT), mental practice, mirror therapy, interventions for sensory impairment, virtual reality and a relatively high dose of repetitive task practice may be effective in improving upper limb function. However, further primary research, specifically of CIMT, mental practice, mirror therapy and virtual reality is needed.<ref>{{cite journal | vauthors = Pollock A, Farmer SE, Brady MC, Langhorne P, Mead GE, Mehrholz J, van Wijck F | title = Interventions for improving upper limb function after stroke | journal = The Cochrane Database of Systematic Reviews | issue = 11 | pages = CD010820 | date = November 2014 | volume = 2014 | pmid = 25387001 | pmc = 6469541 | doi = 10.1002/14651858.CD010820.pub2 | collaboration = Cochrane Stroke Group }}</ref>
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.
 
=== Orthotics ===
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.
[[File:Gehen mit Orthese nach Schlaganfall 220.jpg|thumb|Walking with an [[Orthotics#Stroke|orthosis after stroke]]]]
Clinical studies confirm the importance of [[Orthotics|orthoses]] in stroke rehabilitation.<ref>{{cite journal | vauthors = Falso M, Cattaneo E, Foglia E, Zucchini M, Zucchini F |title=How does a Personalized Rehabilitative Model influence the Functional Response of Different Ankle Foot Orthoses in a Cohort of Patients Affected by Neurological Gait Pattern? |journal=Journal of Novel Physiotherapy and Rehabilitation |date=2017 |volume=1 |issue=2 |pages=072–092 |doi=10.29328/journal.jnpr.1001010 |doi-access=free }}</ref><ref>{{cite book |vauthors=Bowers R |date=2004 |title=Report of a Consensus Conference on the Orthotic Management of Stroke Patients, Non-Articulated Ankle-Foot Ortheses |url= https://pure.strath.ac.uk/ws/portalfiles/portal/35599006/Consensus_Conference_On_The_Orthotic_Management_Of_Stroke_Patients_Netherlands_2003.pdf |publisher=International Society for Prosthetics and Orthotics|pages=87–94}}</ref><ref>{{Cite book| vauthors = Condie E, Bowers RJ |url=https://musculoskeletalkey.com/lower-limb-orthoses-for-persons-who-have-had-a-stroke/|title=Lower limb orthoses for persons who have had a stroke| veditors = Hsu JD, Michael JW, Fisk JR |year=2008|isbn=978-0-323-03931-4|series=AAOS Atlas of Orthoses and Assistive Devices|___location=Philadelphia | publisher = Elsevier Health Sciences |pages=433–440}}</ref> The orthosis supports the therapeutic applications and also helps to mobilize the patient at an early stage. With the help of an orthosis, physiological standing and walking can be learned again, and late health consequences caused by a wrong gait pattern can be prevented. A treatment with an orthosis can therefore be used to support the therapy.
 
=== Self-management ===
Hemorrhagic strokes result in tissue injury by causing compression of tissue from an expanding [[hematoma]] or hematomas. This can distort and injure tissue. In addition, the pressure may lead to a loss of blood supply to affected tissue with resulting infarction, and the blood released by brain hemorrhage appears to have direct toxic effects on brain tissue and vasculature.<!--
Stroke can affect the ability to live independently and with quality.<!-- <ref name="Fryer-2016"/> --> Self-management programs are a special training that educates stroke survivors about stroke and its consequences, helps them acquire skills to cope with their challenges, and helps them set and meet their own goals during their recovery process.<!-- <ref name="Fryer-2016"/> --> These programs are tailored to the target audience, and led by someone trained and expert in stroke and its consequences (most commonly professionals, but also stroke survivors and peers).<!-- <ref name="Fryer-2016"/> --> A 2016 review reported that these programs improve the quality of life after stroke, without negative effects.<!-- <ref name="Fryer-2016"/> --> People with stroke felt more empowered, happy and satisfied with life after participating in this training.<ref name="Fryer-2016">{{cite journal | vauthors = Fryer CE, Luker JA, McDonnell MN, Hillier SL | title = Self management programmes for quality of life in people with stroke | journal = The Cochrane Database of Systematic Reviews | volume = 2016 | issue = 8 | pages = CD010442 | date = August 2016 | pmid = 27545611 | pmc = 6450423 | doi = 10.1002/14651858.CD010442.pub2 }}</ref>
--><ref name="NINDS1999"/>
 
==Prognosis==
Disability affects 75% of stroke survivors enough to decrease their ability to work.<ref name="Coffey2000">{{cite book | vauthors = Coffey CE, Cummings JL, Starkstein S, Robinson R | title=Stroke – the American Psychiatric Press Textbook of Geriatric Neuropsychiatry | url = https://archive.org/details/americanpsychiat00coff | url-access = limited | year=2000 | edition=Second | pages=[https://archive.org/details/americanpsychiat00coff/page/n619 601]–17 | ___location=Washington DC | publisher=American Psychiatric Press| isbn = 9780880488419 }}</ref>
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.<ref name="Stanford2005">{{cite web|author=Stanford Hospital & Clinics |title=Cardiovascular Diseases: Effects of Stroke |url= http://www.stanfordhospital.com/healthLib/atoz/cardiac/effects.html |url-status=dead |archive-url=https://web.archive.org/web/20090210050456/http://www.stanfordhospital.com/healthLib/atoz/cardiac/effects.html |archive-date=2009-02-10 }}</ref>
 
=== Physical effects ===
Some of the physical disabilities that can result from stroke include muscle weakness, numbness, [[pressure sore]]s, [[pneumonia]], [[Urinary incontinence|incontinence]], [[apraxia]] (inability to perform learned movements), difficulties carrying out [[activities of daily living|daily activities]], appetite loss, [[aphasia|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. Up to 10% of people following stroke develop [[seizure]]s, most commonly in the week subsequent to the event; the severity of the stroke increases the likelihood of a seizure.<ref name="Reith1997">{{cite journal | vauthors = Reith J, Jørgensen HS, Nakayama H, Raaschou HO, Olsen TS | title = Seizures in acute stroke: predictors and prognostic significance. The Copenhagen Stroke Study | journal = Stroke | volume = 28 | issue = 8 | pages = 1585–9 | date = August 1997 | pmid = 9259753 | doi = 10.1161/01.STR.28.8.1585 }}</ref><ref name="Burn1997">{{cite journal | vauthors = Burn J, Dennis M, Bamford J, Sandercock P, Wade D, Warlow C | title = Epileptic seizures after a first stroke: the Oxfordshire Community Stroke Project | journal = BMJ | volume = 315 | issue = 7122 | pages = 1582–7 | date = December 1997 | pmid = 9437276 | pmc = 2127973 | doi = 10.1136/bmj.315.7122.1582 }}</ref> An estimated 15% of people experience urinary incontinence for more than a year following stroke.<ref name="Thomas-2019" /> 50% of people have a decline in sexual function ([[sexual dysfunction]]) following stroke.<ref name="Stratton-2020" />
 
=== Emotional and mental effects ===
Emotional and mental dysfunctions correspond to areas in the brain that have been damaged. Emotional problems following stroke can be due to direct damage to emotional centers in the brain or from frustration and difficulty adapting to new limitations. Post-stroke emotional difficulties include [[anxiety]], [[panic attack]]s, [[flat affect]] (failure to express emotions), [[mania]], [[apathy]] and [[psychosis]]. Other difficulties may include a decreased ability to communicate emotions through facial expression, body language and voice.<ref>{{cite book | vauthors = Heilman KM | title = The Behavioral Consequences of Stroke | chapter = Disorders of Emotional Communication After Stroke | veditors = Schweizer TA, Macdonald RL |date=2014 |publisher=Springer |___location=New York [u.a.] | doi = 10.1007/978-1-4614-7672-6_7 |isbn=978-1-4614-7671-9 |pages=119–33 }}</ref>
 
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 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 stroke.<ref name="Mackenzie 2011"/> Those who experience a stroke are at risk of [[paralysis]], which could result in a self-disturbed body image, which may also lead to other social issues.<ref>{{cite book| vauthors = Ackley B, Ladwig GB, Kelley H |title=Nursing diagnosis handbook: an evidence-based guide to planning care|date=2010|publisher=Mosby|___location=Maryland Heights, MO.|edition=9th}}</ref>
 
30 to 50% of stroke survivors develop [[post-stroke depression]], which is characterized by lethargy, irritability, [[Sleep disorder|sleep disturbances]], lowered [[self-esteem]] and withdrawal.<ref name="Senelick1994">{{cite book | vauthors = Senelick RC, Rossi PW, Dougherty K | title=Living with Stroke: A Guide for Families | year=1994 | publisher=Contemporary Books, Chicago | isbn=978-0-8092-2607-8 | oclc=40856888 | url-access=registration | url=https://archive.org/details/livingwithstroke00sene }}</ref> It is most common in those with a stroke affecting the anterior parts of the brain or the [[basal ganglia]], particularly on the left side.<ref>{{Cite book |last1=Ropper |first1=Allan H. |title=Adams and Victor's principles of neurology |last2=Samuels |first2=Martin A. |last3=Klein |first3=Joshua P. |last4=Prasad |first4=Sashank |date=2023 |publisher=McGraw Hill |isbn=978-1-264-26452-0 |edition=12th |___location=New York Chicago San Francisco Athens London}}</ref> [[Clinical depression|Depression]] can reduce motivation and worsen outcome, but can be treated with social and family support, [[psychotherapy]] and, in severe cases, [[antidepressant]]s. Psychotherapy sessions may have a small effect on improving mood and preventing depression after stroke.<ref name=":2">{{cite journal | vauthors = Allida SM, Hsieh CF, Cox KL, Patel K, Rouncefield-Swales A, Lightbody CE, House A, Hackett ML | title = Pharmacological, non-invasive brain stimulation and psychological interventions, and their combination, for treating depression after stroke | journal = The Cochrane Database of Systematic Reviews | volume = 2023 | issue = 7 | pages = CD003437 | date = July 2023 | pmid = 37417452 | pmc = 10327406 | doi = 10.1002/14651858.CD003437.pub5 }}</ref> Antidepressant medications may be useful for treating depression after stroke but are associated with central nervous system and gastrointestinal adverse events.<ref name=":2" />
 
[[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.<ref name="Coffey2000"/> Some people show the opposite of what they feel, for example crying when they are happy.<ref name="Villarosa1993">{{cite book | vauthors = Villarosa L, Singleton L, Johnson KA | title = The Black health library guide to stroke | publisher = Henry Holt and Co | ___location = New York | year = 1993 | isbn = 978-0-8050-2289-6 | oclc = 26929500 | url-access = registration | url = https://archive.org/details/blackhealthlibra00sing }}</ref> Emotional lability occurs in about 20% of those who have had stroke. Those with a right hemisphere stroke are more likely to have empathy problems which can make communication harder.<ref>{{cite journal | vauthors = Leigh R, Oishi K, Hsu J, Lindquist M, Gottesman RF, Jarso S, Crainiceanu C, Mori S, Hillis AE | title = Acute lesions that impair affective empathy | journal = Brain | volume = 136 | issue = Pt 8 | pages = 2539–49 | date = August 2013 | pmid = 23824490 | pmc = 3722353 | doi = 10.1093/brain/awt177 }}</ref>
 
Cognitive deficits resulting from stroke include perceptual disorders, [[aphasia]],<ref name="Hamilton 2011">{{cite journal | vauthors = Hamilton RH, Chrysikou EG, Coslett B | title = Mechanisms of aphasia recovery after stroke and the role of noninvasive brain stimulation | journal = Brain and Language | volume = 118 | issue = 1–2 | pages = 40–50 | date = July 2011 | pmid = 21459427 | pmc = 3109088 | doi = 10.1016/j.bandl.2011.02.005 }}</ref> [[dementia]],<ref name="Leys 2005">{{cite journal | vauthors = Leys D, Hénon H, Mackowiak-Cordoliani MA, Pasquier F | title = Poststroke dementia | journal = The Lancet. Neurology | volume = 4 | issue = 11 | pages = 752–9 | date = November 2005 | pmid = 16239182 | doi = 10.1016/S1474-4422(05)70221-0 | s2cid = 1129308 }}</ref><ref>{{cite journal | vauthors = Kuźma E, Lourida I, Moore SF, Levine DA, Ukoumunne OC, Llewellyn DJ | title = Stroke and dementia risk: A systematic review and meta-analysis | journal = Alzheimer's & Dementia | volume = 14 | issue = 11 | pages = 1416–1426 | date = November 2018 | pmid = 30177276 | pmc = 6231970 | doi = 10.1016/j.jalz.2018.06.3061 }}</ref> and problems with attention<ref name="Coulthard 2006">{{cite journal | vauthors = Coulthard E, Singh-Curry V, Husain M | title = Treatment of attention deficits in neurological disorders | journal = Current Opinion in Neurology | volume = 19 | issue = 6 | pages = 613–8 | date = December 2006 | pmid = 17102702 | doi = 10.1097/01.wco.0000247605.57567.9a | s2cid = 24315173 }}</ref> and memory.<ref name="Lim 2009">{{cite journal | vauthors = Lim C, Alexander MP | title = Stroke and episodic memory disorders | journal = Neuropsychologia | volume = 47 | issue = 14 | pages = 3045–58 | date = December 2009 | pmid = 19666037 | doi = 10.1016/j.neuropsychologia.2009.08.002 | s2cid = 9056952 }}</ref> Stroke survivors may be unaware of their 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. Cognitive and psychological outcome after stroke can be affected by the age at which the stroke happened, pre-stroke baseline intellectual functioning, psychiatric history and whether there is pre-existing brain pathology.<ref>{{cite book|title=Bradley's neurology in clinical practice.|year=2012|publisher=Elsevier/Saunders|___location=Philadelphia|isbn=978-1-4377-0434-1|vauthors=Murray ED, Buttner N, Price BH |volume=1|edition=6th|pages=100–01|veditors=Bradley WG, Daroff RB, Fenichel GM, Jankovic J |chapter=Depression and Psychosis in Neurological Practice}}</ref>
 
==Epidemiology==
[[File:Stroke world map-Deaths per million persons-WHO2012.svg|thumb|Stroke deaths per million persons in 2012:
<!-- References in this section are disrupted -->
{{Div col|small=yes|colwidth=10em}}{{legend|#ffff20|58–316}}{{legend|#ffe820|317–417}}{{legend|#ffd820|418–466}}{{legend|#ffc020|467–518}}{{legend|#ffa020|519–575}}{{legend|#ff9a20|576–640}}{{legend|#f08015|641–771}}{{legend|#e06815|772–974}}{{legend|#d85010|975-1,683}}{{legend|#d02010|1,684–3,477}}{{div col end}}]]
Stroke will soon be the most common cause of death worldwide<!--<ref name=globalburden_lancet1997/> The reference this once referred to has been deleted at some stage. -->. Stroke is the third leading cause of death in the Western world, after heart disease and cancer<ref name="feigin2005">{{cite journal
[[File:Cerebrovascular disease world map - DALY - WHO2004.svg|thumb|[[Disability-adjusted life year]] for cerebral vascular disease per 100,000&nbsp;inhabitants in 2004:<ref>{{cite web|url=https://www.who.int/healthinfo/global_burden_disease/estimates_country/en/index.html |title=WHO Disease and injury country estimates |year=2009 |work=World Health Organization |access-date=November 11, 2009| archive-url=https://web.archive.org/web/20091111101009/http://www.who.int/healthinfo/global_burden_disease/estimates_country/en/index.html|archive-date= 11 November 2009 <!--DASHBot-->| url-status=live}}</ref>
| last = Feigin
{{Col-begin}}
| first = VL
{{Col-break}}
| title = Stroke epidemiology in the developing world
{{legend|#b3b3b3|no data}}
| journal = The Lancet
{{legend|#ffff65|<250}}
| volume = 365
{{legend|#fff200|250–425}}
| issue =
{{legend|#ffdc00|425–600}}
| pages = 2160-2161
{{legend|#ffc600|600–775}}
| publisher =
{{legend|#ffb000|775–950}}
| date = 2005
{{legend|#ff9a00|950–1125}}
| url = http://linkinghub.elsevier.com/retrieve/pii/S0140-6736(05)66755-4
{{Col-break}}
}}</ref>, and causes 10% of world-wide deaths <ref name="worldhealth2004_app2">{{cite book
{{legend|#ff8400|1125–1300}}
| last =
{{legend|#ff6e00|1300–1475}}
| first =
{{legend|#ff5800|1475–1650}}
| authorlink =
{{legend|#ff4200|1650–1825}}
| coauthors =
{{legend|#ff2c00|1825–2000}}
| title = The World health report 2004. Annex Table 2: Deaths by cause, sex and mortality stratum in WHO regions, estimates for 2002.
{{legend|#cb0000|>2000}}
| publisher = World Health Organization
{{col-end}}]]
| date = 2004
 
| ___location = Geneva
Stroke was the second most frequent cause of death worldwide in 2011, accounting for 6.2&nbsp;million deaths (~11% of the total).<ref name="The top 10 causes of death">{{cite web|title=The top 10 causes of death|url=http://who.int/mediacentre/factsheets/fs310/en/|publisher=WHO|url-status=live|archive-url=https://web.archive.org/web/20131202221848/http://who.int/mediacentre/factsheets/fs310/en/|archive-date=2013-12-02}}</ref> Approximately 17&nbsp;million people had stroke in 2010 and 33&nbsp;million people have previously had stroke and were still alive.<ref name=Fei2013/> Between 1990 and 2010 the incidence of stroke decreased by approximately 10% in the developed world and increased by 10% in the developing world.<ref name=Fei2013/> Overall, two-thirds of stroke occurred in those over 65 years old.<ref name=Fei2013 /> South Asians are at particularly high risk of stroke, accounting for 40% of global stroke deaths.<ref name="Indian Stroke Association">{{cite web |work=Indian Heart Association |title=Why South Asians Facts |access-date=May 8, 2015 |url=http://indianheartassociation.org/why-indians-why-south-asians/overview/ |url-status=live |archive-url=https://web.archive.org/web/20150518111218/http://indianheartassociation.org/why-indians-why-south-asians/overview/ |archive-date=May 18, 2015 }}</ref> Incidence of ischemic stroke is ten times more frequent than haemorrhagic stroke.<ref>{{cite journal | vauthors = Andersen KK, Olsen TS, Dehlendorff C, Kammersgaard LP | title = Hemorrhagic and ischemic strokes compared: stroke severity, mortality, and risk factors | journal = Stroke | volume = 40 | issue = 6 | pages = 2068–2072 | date = June 2009 | pmid = 19359645 | doi = 10.1161/STROKEAHA.108.540112 | s2cid = 1506706 | doi-access = free }}</ref>
| url = http://www.who.int/entity/whr/2004/en/report04_en.pdf
 
}}</ref>
It is ranked after heart disease and before cancer.<ref name=Donnan2008/> 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.<ref name="pmid21778445">{{cite journal | vauthors = Towfighi A, Saver JL | title = Stroke declines from third to fourth leading cause of death in the United States: historical perspective and challenges ahead | journal = Stroke | volume = 42 | issue = 8 | pages = 2351–5 | date = August 2011 | pmid = 21778445 | doi = 10.1161/STROKEAHA.111.621904 | doi-access = free }}</ref> 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 <ref name="ellekjaer1997">{{cite journal
The risk of stroke [[Exponential growth|increases exponentially]] from 30 years of age, and the cause varies by age.<ref name="ellekjaer1997">{{cite journal | vauthors = Ellekjaer H, Holmen J, Indredavik B, Terent A | title = Epidemiology of stroke in Innherred, Norway, 1994 to 1996. Incidence and 30-day case-fatality rate | journal = Stroke | volume = 28 | issue = 11 | pages = 2180–4 | date = November 1997 | pmid = 9368561 | doi = 10.1161/01.STR.28.11.2180 }}</ref> Advanced age is one of the most significant stroke risk factors. 95% of stroke occurs in people age 45 and older, and two-thirds of stroke occurs in those over the age of 65.<ref name="NINDS1999">{{cite web | author=National Institute of Neurological Disorders and Stroke (NINDS) | author-link=National Institute of Neurological Disorders and Stroke | year=1999 | title=Stroke: Hope Through Research | url=http://www.ninds.nih.gov/disorders/stroke/detail_stroke.htm | publisher=National Institutes of Health | url-status=dead | archive-url=https://web.archive.org/web/20151004193735/http://www.ninds.nih.gov/disorders/stroke/detail_stroke.htm | archive-date=2015-10-04 }}</ref><ref name="Senelick1994"/>
| last = Ellekjær
 
| first = H
A person's risk of dying with stroke also increases with age. However, stroke can occur at any age, including in childhood.{{citation needed|date=March 2022}}
| coauthors = J Holmen, B Indredavik, A Terent
 
| title = Epidemiology of Stroke in Innherred, Norway, 1994 to 1996 : Incidence and 30-Day Case-Fatality Rate
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.<ref>{{cite journal | vauthors = Bongers TN, de Maat MP, van Goor ML, Bhagwanbali V, van Vliet HH, Gómez García EB, Dippel DW, Leebeek FW | title = High von Willebrand factor levels increase the risk of first ischemic stroke: influence of ADAMTS13, inflammation, and genetic variability | journal = Stroke | volume = 37 | issue = 11 | pages = 2672–7 | date = November 2006 | pmid = 16990571 | doi = 10.1161/01.STR.0000244767.39962.f7 | doi-access = free }}</ref><!--
| journal = Stroke
--> The results of this study found that the only significant genetic factor was the person's [[blood type]]. Having stroke in the past greatly increases one's risk of future stroke.
| volume = 28
 
| pages = 2180-2184
Men are 25% more likely to develop stroke than women,<ref name="NINDS1999"/> yet 60% of deaths from stroke occur in women.<ref name="Villarosa1993"/> Since women live longer, they are older on average when they have stroke and thus more often killed.<ref name="NINDS1999"/> Some risk factors for stroke apply only to women. Primary among these are pregnancy, childbirth, [[menopause]], and the treatment thereof ([[Hormone replacement therapy (menopause)|HRT]]).
| date = 1997
| url = http://stroke.ahajournals.org/cgi/content/abstract/strokeaha%3B28/11/2180
}}</ref>.
 
==History==
[[File:Hippocrates.jpg|thumb|upright|left|[[Hippocrates]] first described the sudden paralysis that is often associated with stroke.]]
Over 2,400 years ago, [[Hippocrates]] (460 to 370 BC) was first to describe the phenomenon of sudden [[paralysis]], which we now know is caused by stroke. [[Apoplexy]], from the [[Greek language|Greek]] word meaning "struck down with violence,” first appeared in Hippocratic writings to describe stroke symptoms.<!--
--><ref name="Stroke1996-Thompson">{{cite journal | author=Thompson JE | title=The evolution of surgery for the treatment and prevention of stroke. The Willis Lecture | journal=Stroke | year=1996 | pages=1427-34 | volume=27 | issue=8 | id=PMID 8711815 | url=http://stroke.ahajournals.org/cgi/content/full/27/8/1427}}</ref><!--
--><ref name="Merginet2001-Kopito">{{cite journal | author=Kopito, Jeff | title=A Stroke in Time | url=http://www.webasx.com/articles/strokeintime.html | journal=MERGINET.com | year=2001 | month=September | Volume=6 | issue=Number 9}}</ref>
 
Episodes of stroke and familial stroke have been reported from the 2nd millennium BC onward in ancient Mesopotamia and Persia.<ref>{{cite journal | vauthors = Ashrafian H | title = Familial stroke 2700 years ago | journal = Stroke | volume = 41 | issue = 4 | pages = e187; author reply e188 | date = April 2010 | pmid = 20185778 | doi = 10.1161/STROKEAHA.109.573170 | doi-access = }}</ref> [[Hippocrates]] (460 to 370 BC) was first to describe the phenomenon of sudden [[paralysis]] that is often associated with [[ischemia]]. [[Apoplexy]], from the [[Greek language|Greek]] word meaning "struck down with violence", first appeared in Hippocratic writings to describe this phenomenon.<!--
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.<!--
The Hippocratic dictum that "It is impossible to cure a severe attack of apoplexy and difficult to cure a mild one"
--><ref name="Stroke1996-Thompson"/><!--
--><ref name="Stroke1996-Thompson">{{cite journal | vauthors = Thompson JE | title = The evolution of surgery for the treatment and prevention of stroke. The Willis Lecture | journal = Stroke | volume = 27 | issue = 8 | pages = 1427–34 | date = August 1996 | pmid = 8711815 | doi = 10.1161/01.STR.27.8.1427 }}</ref><!--
--><ref name="NINDS1999"/>
--><ref name="Merginet2001-Kopito">{{cite journal | vauthors=Kopito J | title=A Stroke in Time | url=http://www.webasx.com/articles/strokeintime.html | archive-url=https://web.archive.org/web/20050829110720/http://www.webasx.com/articles/strokeintime.html | url-status=dead | archive-date=2005-08-29 | website=MERGINET.com | date=September 2001 | volume=6 | issue=9 | access-date=2005-10-28 }}</ref>
Wepfer also identified the main arteries supplying the brain, the [[vertebral artery|vertebral]] and [[carotid artery|carotid arteries]], and identified the cause of ischemic stroke when he suggested that apoplexy might be caused by a blockage to those vessels.<!--
The word ''stroke'' was used as a synonym for apoplectic [[seizure]] as early as 1599,<ref>{{cite book | veditors = Barnhart RK |title=The Barnhart Concise Dictionary of Etymology |date=1995 |publisher=HarperCollins Publishers |___location=New York |isbn=978-0-06-270084-1 |edition=1st}}</ref> and is a fairly literal translation of the Greek term. The term ''apoplectic stroke'' is an archaic, nonspecific term, for a cerebrovascular accident accompanied by haemorrhage or haemorrhagic stroke.<ref>{{cite web |title=Apoplectic Stroke |url=https://medical-dictionary.thefreedictionary.com/apoplectic+stroke |website=TheFreeDictionary.com |access-date=13 December 2020}}</ref> [[Martin Luther]] was described as having an ''apoplectic stroke'' that deprived him of his speech shortly before his death in 1546.<ref>{{cite book | vauthors = Brecht M | author-link1 = Martin Brecht | translator = Schaaf JL |title=Martin Luther: The Preservation of the Church, 1532-1546 | volume = 3 | pages = 369–79 |date=1999 |___location=Minneapolis | publisher = Fortress Press |isbn=978-0-8006-2815-4}}</ref>
--><ref name="NINDS1999"/>
 
In 1658, in his ''Apoplexia'', [[Johann Jakob Wepfer|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.<ref name="NINDS1999"/><ref name="Stroke1996-Thompson"/>
==See also==
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.<!--
* [[Transient ischemic attack]]
--><ref name="NINDS1999"/> [[Rudolf Virchow]] first described the mechanism of [[thromboembolism]] as a major factor.<ref name="pmid4914683">{{cite journal | vauthors = Schiller F | title = Concepts of stroke before and after Virchow | journal = Medical History | volume = 14 | issue = 2 | pages = 115–31 | date = April 1970 | pmid = 4914683 | pmc = 1034034 | doi = 10.1017/S0025727300015325 }}</ref>
* [[Apoplexy]]
* [[Subclavian steal syndrome]]
 
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".<ref name="FingerBoller2010">{{cite book| vauthors = Finger S, Boller F, Tyler KL |title=Handbook of Clinical Neurology|url=https://books.google.com/books?id=bggTAQAAMAAJ|access-date=1 October 2013|year=2010|publisher=North-Holland Publishing Company|isbn=978-0-444-52009-8|page=401|url-status=live|archive-url=https://web.archive.org/web/20131012220445/http://books.google.com/books?id=bggTAQAAMAAJ|archive-date=12 October 2013}}</ref> 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.<ref name="Scadding2011">{{cite book | vauthors = Scadding JW |title=Clinical Neurology|url=https://books.google.com/books?id=PdkIPE-xpYYC&pg=PA488|access-date=1 October 2013|date=2011|publisher=CRC Press|isbn=978-0-340-99070-4|page=488|url-status=live|archive-url=https://web.archive.org/web/20131012213853/http://books.google.com/books?id=PdkIPE-xpYYC&pg=PA488|archive-date=12 October 2013}}</ref><ref name="SirvenMalamut2008">{{cite book| vauthors = Sirven JI, Malamut BL |title=Clinical Neurology of the Older Adult|url=https://books.google.com/books?id=c1tL8C9ryMQC&pg=PA243|access-date=1 October 2013|year=2008|publisher=Lippincott Williams & Wilkins|isbn=978-0-7817-6947-1|page=243|url-status=live|archive-url=https://web.archive.org/web/20131012213727/http://books.google.com/books?id=c1tL8C9ryMQC&pg=PA243|archive-date=12 October 2013}}</ref><ref name="KaufmanMilstein2012">{{cite book| vauthors = Kaufman DM, Milstein MJ |title=Kaufman's Clinical Neurology for Psychiatrists|url=https://books.google.com/books?id=7fXzaAT_pwkC&pg=PT892|access-date=1 October 2013|date=5 December 2012|publisher=Elsevier Health Sciences|isbn=978-1-4557-4004-8|page=892|url-status=live|archive-url=https://web.archive.org/web/20131012220403/http://books.google.com/books?id=7fXzaAT_pwkC&pg=PT892|archive-date=12 October 2013}}</ref> ''Cerebrovascular insult'' may be used interchangeably.<ref name=Mosby>{{cite book|title=Mosby's Medical Dictionary, 8th edition|year=2009|publisher=Elsevier}}</ref>
==References==
<references />
 
The term ''brain attack'' was introduced for use to underline the acute nature of stroke according to the [[American Stroke Association]],<ref name=Mosby/> which has used the term since 1990,<ref name="NSA Brain Attack">{{cite web|title=What is a Stroke/Brain Attack?|url=http://www.stroke.org/site/DocServer/NSA_complete_guide.pdf|work=National Stroke Association|access-date=27 February 2014|archive-url=https://web.archive.org/web/20131019161334/http://www.stroke.org/site/DocServer/NSA_complete_guide.pdf|archive-date=19 October 2013|url-status=dead}}</ref> and is used colloquially to refer to both ischemic as well as hemorrhagic stroke.<ref>{{cite book|title=Segen's Medical Dictionary.|year=2010|publisher=Farlex, Inc}}</ref>
* {{cite book | author=Perry, Thomas and Miller Frank | title='Pathology: A Dynamic Introduction to Medicine and Surgery | year=1961 | ___location=Boston | publisher=Little, Brown and Company}}
 
==Further readingResearch==
As of 2017, [[angioplasty]] and [[stent]]s were under preliminary [[clinical research]] to determine the possible therapeutic advantages of these procedures in comparison to therapy with [[statin]]s, [[antithrombotic]]s, or [[antihypertensive drug]]s.<ref name="Morris">{{cite journal | vauthors = Morris DR, Ayabe K, Inoue T, Sakai N, Bulbulia R, Halliday A, Goto S | title = Evidence-Based Carotid Interventions for Stroke Prevention: State-of-the-art Review | journal = Journal of Atherosclerosis and Thrombosis | volume = 24 | issue = 4 | pages = 373–387 | date = April 2017 | pmid = 28260723 | pmc = 5392474 | doi = 10.5551/jat.38745 }}</ref>
* {{cite book | author = J. P. Mohr, Dennis Choi, James Grotta, Philip Wolf | title = Stroke: Pathophysiology, Diagnosis, and Management | publisher = Churchill Livingstone | ___location = New York | year = 2004 | id = ISBN 0-443-06600-0}}
 
Animal models indicate that administration of low-dose [[amphetamine]] facilitates behavioural recovery following ischemic stroke, when administered several days after the ischemic event.<ref>{{Cite journal |last1=Liu |first1=Hua-Shan |last2=Shen |first2=Hui |last3=Harvey |first3=Brandon K. |last4=Castillo |first4=Priscila |last5=Lu |first5=Hanbing |last6=Yang |first6=Yihong |last7=Wang |first7=Yun |date=2011-05-01 |title=Post-treatment with amphetamine enhances reinnervation of the ipsilateral side cortex in stroke rats |journal=NeuroImage |volume=56 |issue=1 |pages=280–289 |doi=10.1016/j.neuroimage.2011.02.049 |issn=1095-9572 |pmc=3070415 |pmid=21349337}}</ref> This is accompanied by reductions in volumes of tissue lost, increases in fractional anisotropy ratio on the affected side, and increases in [[Brain-derived neurotrophic factor|BDNF]] expression, [[matrix metalloproteinase]] activity, and expression of [[synaptophysin]].
==External links==
{{clear|left}}
* ''The original text for this article was taken from the [[National Institute of Neurological Disorders and Stroke]] [[public ___domain resource]] at [http://www.ninds.nih.gov/health_and_medical/disorders/stroke.htm this page]''
* [http://www.brainhelp.co.uk (Addressing the Challenges Faced as a Result of Brain Haemorrhage or Brain Injury for Sufferers Families and Carers)
* [http://www.canadianstrokenetwork.ca Canadian Stroke Network]
* [http://www.medicine.mcgill.ca/strokengine/ StrokEngine] (McGill University, Montreal, Quebec, Canada) Focuses on stroke rehabilitation and interventions
* [http://www.medlink.com/PublicCIP.ASP?access=public&UID=MLT00064&code= Ischemic stroke] - ''MedLink Neurology'' Clinical Summary
* [http://www.doctorslounge.com/primary/articles/stroke_risk/index.htm Cerebrovascular disease and risk of stroke]
* [http://www.strokecenter.org/ Stroke Center] of the Washington University School of Medicine
* [http://www.medicine.mcgill.ca/strokengine/ Stroke Engine.] [[Heart and Stroke Foundation]] of Canada
* [http://www.strokeassociation.org/presenter.jhtml?identifier=1200037 American Stroke Association]
* [http://www.stroke.org/home National Stroke Association]
* [http://www.stroke.org.uk The Stroke Association] UK
* [http://www.biaq.com.au/ The Brain Injury Association of Queensland] Australia
* [http://www.nasam.org National Stroke Association of Malaysia]
* [http://www.americanheart.org/presenter.jhtml?identifier=3053 "Heart Attack, Stroke and Cardiac Arrest Warning Signs," from the American Heart Association]
* [http://diabetes.niddk.nih.gov/ National Diabetes Information Clearinghouse]
[[Category:Neurology]]
[[Category:Medical emergencies]]
[[Category:Cardiovascular diseases]]
[[Category:Neurological disorders]]
[[Category:Causes of death]]
 
== See also ==
[[ar:سكتة]]
{{col div|colwidth=30em}}
[[zh-min-nan:Tiòng-hong]]
* [[Anoxic depolarization in the brain]]
[[ca:Accident vascular cerebral]]
* [[CADASIL]]
[[de:Schlaganfall]]
* [[Cerebrovascular disease]]
[[es:Accidente cerebrovascular]]
* [[Cerebral palsy]]
[[eo:Apopleksio]]
* [[Dejerine–Roussy syndrome]]
[[fr:Accident vasculaire cérébral]]
* [[Functional Independence Measure]]
[[ko:뇌경색]]
* [[Lipoprotein(a)]]
[[hr:Moždani udar]]
* [[Mobile Stroke Unit]]
[[io:Vaskulala cerebrala stroko]]
* [[Spinal cord stroke]], a rare type of stroke that doesn't typically affect blood flow to the brain
[[id:Stroke]]
* [[Ultrasound-enhanced systemic thrombolysis]]
[[it:Infarto cerebrale]]
* [[he:שבץWeber's מוחיsyndrome]]
* [[World Stroke Day]]
[[mk:Мозочен удар]]
{{colend}}
[[ms:Angin ahmar]]
 
[[nl:Beroerte]]
== References ==
[[ja:脳梗塞]]
{{Reflist}}
[[no:Hjerneslag]]
 
[[pl:Udar mózgu]]
== Further reading ==
[[pt:AVC]]
{{refbegin}}
[[ru:Инсульт]]
* {{cite journal |last1=Bushnell |first1=Cheryl |last2=Kernan |first2=Walter N. |last3=Sharrief |first3=Anjail Z. |last4=Chaturvedi |first4=Seemant |last5=Cole |first5=John W. |last6=Cornwell |first6=William K. |last7=Cosby-Gaither |first7=Christine |last8=Doyle |first8=Sarah |last9=Goldstein |first9=Larry B. |last10=Lennon |first10=Olive |last11=Levine |first11=Deborah A. |last12=Love |first12=Mary |last13=Miller |first13=Eliza |last14=Nguyen-Huynh |first14=Mai |last15=Rasmussen-Winkler |first15=Jennifer |last16=Rexrode |first16=Kathryn M. |last17=Rosendale |first17=Nicole |last18=Sarma |first18=Satyam |last19=Shimbo |first19=Daichi |last20=Simpkins |first20=Alexis N. |last21=Spatz |first21=Erica S. |last22=Sun |first22=Lisa R. |last23=Tangpricha |first23=Vin |last24=Turnage |first24=Dawn |last25=Velazquez |first25=Gabriela |last26=Whelton |first26=Paul |display-authors=3 |title=2024 Guideline for the Primary Prevention of Stroke: A Guideline From the American Heart Association/American Stroke Association |date=21 October 2024 |journal=Stroke |volume=55 |issue=12 |pages=e344–e424 |doi=10.1161/STR.0000000000000475|pmid=39429201 }}
[[sv:Slaganfall]]
* Gijn, Jan van (2023). Stroke: A History of Ideas. ''Cambridge University Press''. ISBN 978-1-108-83254-0.
[[vi:Tai biến mạch máu não]]
* {{cite book | vauthors = Mohr JP, Choi D, Grotta J, Wolf P | title = Stroke: Pathophysiology, Diagnosis, and Management | publisher = Churchill Livingstone | ___location = New York | year = 2004 | isbn=978-0-443-06600-9 | oclc = 50477349}}
[[zh:中風]]
* {{cite book | vauthors = Warlow CP, van Gijn J, Dennis MS, Wardlaw JM, Bamford JM, Hankey GJ, Sandercock PA, Rinkel G, Langhorne P, Sudlow C, Rothwell P |title=Stroke: Practical Management |publisher=Wiley-Blackwell |year=2008 |edition=3rd|isbn=978-1-4051-2766-0}}
{{refend}}
 
== External links ==
{{Commons category|Stroke}}
* [http://www.mdcalc.com/dragon-score-post-tpa-stroke-outcome/ DRAGON Score for Post-Thrombolysis] {{Webarchive|url=https://web.archive.org/web/20201027101249/https://www.mdcalc.com/dragon-score-post-tpa-stroke-outcome |date=2020-10-27 }}
* [http://www.mdcalc.com/thrive-score-for-stroke-outcome/ THRIVE score for stroke outcome] {{Webarchive|url=https://web.archive.org/web/20160913041433/http://www.mdcalc.com/thrive-score-for-stroke-outcome/ |date=2016-09-13 }}
* [https://web.archive.org/web/20161221102343/https://www.ninds.nih.gov/Disorders/all-disorders National Institute of Neurological Disorders and Stroke]
 
{{Medical condition classification and resources
| DiseasesDB = 2247
| ICD10 = {{ICD10|I|61||i|60}}-{{ICD10|I|64||i|60}}
| ICD9 = {{ICD9|434.91}}
| OMIM = 601367
| MedlinePlus = 000726
| eMedicineSubj = neuro
| eMedicineTopic = 9
| eMedicine_mult = {{eMedicine2|emerg|558}} {{eMedicine2|emerg|557}} {{eMedicine2|pmr|187}}
| MeshID = D020521
}}
{{Cerebrovascular diseases}}
{{CNS diseases of the nervous system}}
{{Authority control}}
 
[[Category:Stroke| ]]
[[Category:Causes of death]]
[[Category:Wikipedia medicine articles ready to translate]]
[[Category:Wikipedia emergency medicine articles ready to translate]]