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Stroke
Stroke (also known as a cerebrovascular accident
(CVA) or brain attack) is a medical condition in Stroke
which poor blood flow to the brain causes cell death.[5] Other names Cerebrovascular accident
There are two main types of stroke: (CVA), cerebrovascular insult
(CVI), brain attack
ischemic, due to lack of blood flow, and
hemorrhagic, due to bleeding.[5]
Both cause parts of the brain to stop functioning
properly.[5]

Signs and symptoms of stroke may include an inability

to move or feel on one side of the body, problems
understanding or speaking, dizziness, or loss of vision
to one side.[2][3] Signs and symptoms often appear soon
after the stroke has occurred.[3] If symptoms last less
than one or two hours, the stroke is a transient ischemic
attack (TIA), also called a mini-stroke.[3] Hemorrhagic
stroke may also be associated with a severe headache.[3]
The symptoms of stroke can be permanent.[5] Long- CT scan of the brain showing a massive, prior
term complications may include pneumonia and loss of right-sided ischemic stroke from blockage of
bladder control.[3] an artery. Changes on a CT may not be visible
early on.[1]
The biggest risk factor for stroke is high blood
Specialty Neurology, stroke medicine
pressure.[7] Other risk factors include high blood
cholesterol, tobacco smoking, obesity, diabetes mellitus, Symptoms Inability to move or feel on
a previous TIA, end-stage kidney disease, and atrial one side of the body,
fibrillation.[2][7][8] Ischemic stroke is typically caused by problems understanding or
blockage of a blood vessel, though there are also less speaking, dizziness, loss of
common causes.[13][14][15] Hemorrhagic stroke is caused vision to one side[2][3]
by either bleeding directly into the brain or into the Complications Persistent vegetative state[4]
space between the brain's membranes.[13][16] Bleeding Causes Ischemic (blockage) and
may occur due to a ruptured brain aneurysm.[13] hemorrhagic (bleeding)[5]
Diagnosis is typically based on a physical exam and
Risk factors Age,[6] high blood pressure,
supported by medical imaging such as a CT scan or MRI
tobacco smoking, obesity,
scan.[9] A CT scan can rule out bleeding, but may not
high blood cholesterol,
necessarily rule out ischemia, which early on typically
diabetes mellitus, previous
does not show up on a CT scan.[10] Other tests such as TIA, end-stage kidney

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an electrocardiogram (ECG) and blood tests are done to disease, atrial

determine risk factors and rule out other possible fibrillation[2][7][8]
causes.[9] Low blood sugar may cause similar Diagnostic Based on symptoms with
symptoms.[9] method medical imaging typically
used to rule out bleeding[9][10]
Prevention includes decreasing risk factors, surgery to
Differential Low blood sugar[9]
open up the arteries to the brain in those with
diagnosis
problematic carotid narrowing, and warfarin in people
with atrial fibrillation.[2] Aspirin or statins may be Treatment Based on the type[2]
recommended by physicians for prevention.[2] Stroke is Prognosis Average life expectancy 1
a medical emergency. [5] Ischemic strokes, if detected year[2]
within three to four-and-a-half hours, may be treatable Frequency 42.4 million (2015)[11]
[2]
with medication that can break down the clot, while
Deaths 6.3 million (2015)[12]
hemorrhagic strokes sometimes benefit from surgery.[2]
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.[2]

In 2023, 15 million people worldwide had a stroke.[17] In 2021, stroke was the third biggest cause of
death, responsible for approximately 10% of total deaths.[18] In 2015, there were about 42.4 million
people who had previously had stroke and were still alive.[11] 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.[19] In 2015, stroke was the second most frequent cause of death after coronary
artery disease, accounting for 6.3 million deaths (11% of the total).[12] About 3.0 million deaths
resulted from ischemic stroke while 3.3 million deaths resulted from hemorrhagic stroke.[12] About
half of people who have had stroke live less than one year.[2] Overall, two thirds of cases of stroke
occurred in those over 65 years old.[19]

Classification
Stroke can be classified into two major categories: ischemic and hemorrhagic.[20] Ischemic stroke is
caused by interruption of the blood supply to the brain, while hemorrhagic stroke results from the
rupture of a blood vessel or an abnormal vascular structure.

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.[2]

Definition
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",[21]
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

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syndrome of stroke symptoms that resolve completely within 24

hours.[2] 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 heart attack and acute
coronary syndrome, respectively), to reflect the urgency of stroke
symptoms and the need to act swiftly.[22]

There are two main categories of

Ischemic stroke. Ischemic (top), typically
caused by a blood clot in an artery
During ischemic stroke, blood supply to part of the brain is
(1a) resulting in brain death to the
decreased, leading to dysfunction of the brain tissue in that area.
affected area (2a). Hemorrhagic
There are four reasons why this might happen: (bottom), caused by blood leaking
into or around the brain from a
1. Thrombosis (obstruction of a blood vessel by a blood clot ruptured blood vessel (1b) allowing
forming locally) blood to pool in the affected area
2. Embolism (obstruction due to an embolus from elsewhere in (2b) thus increasing the pressure on
the body),[2] the brain.
3. Systemic hypoperfusion (general decrease in blood supply,
e.g., in shock)[23]
4. Cerebral venous sinus thrombosis.[24]
Stroke without an obvious explanation is termed cryptogenic
stroke (idiopathic); this constitutes 30–40% of all cases of
ischemic stroke.[2][25]

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
A slice of brain from the autopsy of a
the initial symptoms; based on the extent of the symptoms, the
person who had an acute middle
stroke episode is classified as total anterior circulation infarct cerebral artery (MCA) stroke
(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.[26][27]

The TOAST (Trial of Org 10172 in Acute Stroke Treatment) classification is based on clinical
symptoms as well as results of further investigations; on this basis, 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).[28]

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Users of stimulants such as cocaine and methamphetamine are at a high risk for ischemic stroke.[29]

Hemorrhagic
There are two main types of hemorrhagic stroke:[30][31]

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 CT scan of an intraparenchymal
accumulation of blood anywhere within the cranial vault; but the bleed (bottom arrow) with
surrounding edema (top arrow)
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".[32]

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.[33]

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.[34]

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

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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.[33]

Early recognition
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 ratio of 0.39).[35] 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

(facial droop, arm weakness, speech difficulty, and time to call
emergency services),[36] 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.[37] The revised mnemonic BE FAST, which A Centers for Disease Control and
adds balance (sudden trouble keeping balance while walking or Prevention infographic describing
standing) and eyesight (new onset of blurry or double vision or the FAST mnemonic for early
sudden, painless loss of sight) to the assessment, has been recognition of stroke
proposed to address this shortcoming and improve early detection
of stroke even further.[38][39] Other scales for prehospital
detection of stroke include the Los Angeles Prehospital Stroke Screen (LAPSS)[40] and the Cincinnati
Prehospital Stroke Scale (CPSS),[41] on which the FAST method was based.[42] Use of these scales is
recommended by professional guidelines.[43]

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.[43][44]

Associated symptoms
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.

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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 central nervous system pathways
—the spinothalamic tract, corticospinal tract, and the dorsal column–medial lemniscus pathway,
symptoms may include:

hemiplegia and muscle weakness of the face

numbness
reduction in sensory or vibratory sensation
initial flaccidity (reduced muscle tone), replaced by spasticity (increased muscle tone), excessive
reflexes, and obligatory synergies.[45]
In most cases, the symptoms affect only one side of the body (unilateral). The defect in the brain is
usually on the opposite side of the body. 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 affecting the brainstem
and brain, therefore, can produce symptoms relating to deficits in these cranial nerves:

altered smell, taste, hearing, or vision (total or partial)

drooping of eyelid (ptosis) and weakness of ocular muscles
decreased reflexes: gag, swallow, pupil reactivity to light
decreased sensation and muscle weakness of the face
balance problems and nystagmus
altered breathing and heart rate
weakness in sternocleidomastoid muscle with inability to turn head to one side
weakness in tongue (inability to stick out the tongue or move it from side to side)
If the cerebral cortex is involved, the central nervous system pathways can again be affected, but can
also produce the following symptoms:

aphasia (difficulty with verbal expression, auditory comprehension, reading and writing; Broca's or
Wernicke's area typically involved)
dysarthria (motor speech disorder resulting from neurological injury)
apraxia (altered voluntary movements)
visual field defect
memory deficits (involvement of temporal lobe)
hemineglect (involvement of parietal lobe)
disorganized thinking, confusion, hypersexual gestures (with involvement of frontal lobe)
lack of insight of his or her, usually stroke-related, disability
If the cerebellum is involved, ataxia might be present and this includes:

altered walking gait

altered movement coordination

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vertigo and or disequilibrium

Preceding signs and symptoms

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.[46] Its appearance makes it advisable to seek medical review and to consider prevention
against stroke.

Causes

Thrombotic stroke
In thrombotic stroke, a thrombus[47] (blood clot) usually forms
around 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 and internal

carotid arteries, the vertebral artery, and the Circle of Willis.[48]
Diseases that may form thrombi in the large vessels include (in
descending incidence): atherosclerosis, vasoconstriction
(tightening of the artery), aortic, 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 Illustration of an embolic stroke,
are in the strictest sense not always caused by a 'defined showing a blockage lodged in a
disease state', such events can occur in very young people blood vessel
and can be caused by physical injury such as hyperextension
of the neck area or often by other forms of trauma.[49]
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.[50]
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).[51]

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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.[52] Sickle-cell anemia, which can cause blood cells 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.[53] Air pollution may also increase stroke risk.[54]

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 (e.g., from bone
marrow in a broken bone), air, cancer cells or clumps of bacteria (usually from infectious
endocarditis).[55]

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 or ventricular septal defect in the heart into the brain.[55]

Causes of stroke related to the heart can be distinguished between high- and low-risk:[56]

High risk: atrial fibrillation and paroxysmal atrial fibrillation, rheumatic disease of the mitral or aortic
valve disease, artificial heart valves, 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, 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.[57]

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.[58]

Cerebral hypoperfusion
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 arrhythmias, or from reduced cardiac output as a result of myocardial infarction,
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pulmonary embolism, pericardial effusion, or bleeding. Hypoxemia (low blood oxygen content) may
precipitate the hypoperfusion. Because the reduction in blood flow is global, all parts of the brain may
be affected, especially 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.[24]

Intracerebral hemorrhage
It generally occurs in small arteries or arterioles and is commonly due to hypertension,[59]
intracranial vascular malformations (including cavernous angiomas or arteriovenous malformations),
cerebral amyloid angiopathy, or infarcts into which secondary hemorrhage has occurred.[2] Other
potential causes are trauma, bleeding disorders, amyloid angiopathy, illicit drug use (e.g.,
amphetamines or cocaine). The hematoma enlarges until pressure from surrounding tissue limits its
growth, or until it decompresses by emptying into the ventricular system, CSF or the pial surface. A
third of intracerebral bleed is into the brain's ventricles. ICH has a mortality rate of 44 percent after
30 days, higher than ischemic stroke or subarachnoid hemorrhage (which technically may also be
classified as a type of stroke[2]).

Other
Other causes may include spasm of an artery. This may occur due to cocaine.[60] 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 hypercoagulability.[61]

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.[62]
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 hemorrhages. Silent stroke typically causes lesions which are detected via the

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use of neuroimaging such as MRI. Silent stroke is estimated to occur at five times the rate of
symptomatic stroke.[63][64] The risk of silent stroke increases with age, but they may also affect
younger adults and children, especially those with acute anemia.[63][65]

Pathophysiology

Ischemic
Ischemic stroke occurs because of a loss of blood supply to part of
the brain, initiating the ischemic cascade.[66] 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.[67]
Embolic infarction occurs when emboli formed elsewhere in the Histopathology at high magnification
circulatory system, typically in the heart as a consequence of atrial of a normal neuron, and ischemic
fibrillation, or in the carotid arteries, break off, enter the cerebral stroke at approximately 24 hours on
H&E stain: The neurons become
circulation, then lodge in and block brain blood vessels. Since
hypereosinophilic and there is an
blood vessels in the brain are now blocked, the brain becomes low
infiltrate of neutrophils. There is
in energy, and thus it resorts to using anaerobic metabolism slight edema and loss of normal
within the region of brain tissue affected by ischemia. Anaerobic architecture in the surrounding
metabolism produces less adenosine triphosphate (ATP) but neuropil.
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".[68] After the initial ischemic event the penumbra transitions from a tissue remodeling
characterized by damage to a remodeling characterized by repair.[69]

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 Molecular pathways outlining the role of
glutamate excitoxicity following stroke
are powered by the concentration gradients of ions
(mainly Na+) across the cell membrane. However,
stroke cuts off the supply of oxygen and glucose which powers the ion pumps maintaining these
gradients. As a result, the transmembrane ion gradients run down, and glutamate transporters
reverse their direction, releasing glutamate into the extracellular space. Glutamate acts on receptors

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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
programmed cell death.[70]

Ischemia also induces production of oxygen free radicals and other reactive oxygen species. These
react with and damage a number of cellular and extracellular elements. Damage to the blood vessel
lining or endothelium 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
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 hemispheres. However, variations in the circle of
Willis, caliber of collateral vessels, and acquired arterial lesions
Impact of collateral flow on clot lysis
such as atherosclerosis can disrupt this compensatory mechanism,
and reperfusion
increasing the risk of brain ischemia resulting from artery
blockage.[71]

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.[71][72][73]

Hemorrhagic
Hemorrhagic stroke is classified based on their underlying pathology. Some causes of hemorrhagic
stroke are hypertensive hemorrhage, ruptured aneurysm, ruptured AV fistula, transformation of prior
ischemic infarction, and drug-induced bleeding.[74] They result in tissue injury by causing
compression of tissue from an expanding hematoma or hematomas. In addition, the pressure may

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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.[53][75]
Inflammation contributes to the secondary brain injury after hemorrhage.[75]

Diagnosis
Stroke is diagnosed through several techniques: a neurological
examination (such as the NIHSS), CT scans (most often without
contrast enhancements) or MRI scans, Doppler ultrasound, and
arteriography. The diagnosis of stroke itself is clinical, with
assistance from the imaging techniques. Imaging techniques also
assist in determining the subtypes and cause of stroke. There is yet
no commonly used blood test for the stroke diagnosis itself,
though blood tests may be of help in finding out the likely cause of
stroke.[76] 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 A CT showing early signs of a
middle cerebral artery stroke with
symptoms and a neurological status, helps giving an evaluation of
loss of definition of the gyri and grey
the location and severity of stroke. It can give a standard score on
white boundary
e.g., the NIH stroke scale.

Imaging
For diagnosing ischemic (blockage) stroke in the emergency
setting:[77]

CT scans (without contrast enhancements)

sensitivity= 16% (less than 10% within first 3 hours of
symptom onset) Dense artery sign in a patient with
specificity= 96% middle cerebral artery infarction
shown on the left. Right image after
MRI scan 7 hours.
sensitivity= 83%
specificity= 98%
For diagnosing hemorrhagic stroke in the emergency setting:

CT scans (without contrast enhancements)

sensitivity= 89%
specificity= 100%
MRI scan
sensitivity= 81%
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specificity= 100%
For detecting chronic hemorrhages, an MRI scan is more sensitive.[78]

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.

CT scans may not detect ischemic stroke, especially if it is small, of recent onset,[10] or in the
brainstem or cerebellum areas (posterior circulation infarct). MRI is better at detecting a posterior
circulation infarct with diffusion-weighted imaging.[79] A CT scan is used more to rule out certain
stroke mimics and detect bleeding.[10] The presence of leptomeningeal collateral circulation in the
brain is associated with better clinical outcomes after recanalization treatment.[80] Cerebrovascular
reserve capacity is another factor that affects stroke outcome – 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.[81] 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.[82]

Underlying cause
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:
12-lead ECG of a patient with
an ultrasound/doppler study of the carotid arteries (to detect stroke, showing large deeply
carotid stenosis) or dissection of the precerebral arteries; inverted T-waves. ECG changes
may occur in people with stroke and
an electrocardiogram (ECG) and echocardiogram (to identify
other brain disorders.
arrhythmias and resultant clots in the heart which may spread
to the brain vessels through the bloodstream);
a Holter monitor study to identify intermittent 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 blood cholesterol is high, if there is an abnormal tendency to bleed, and
if some rarer processes such as homocystinuria might be involved.
For hemorrhagic stroke, a CT or 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

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this investigation is therefore reserved for specific situations.[83] If there are symptoms suggesting
that the hemorrhage might have occurred as a result of venous thrombosis, CT or MRI venography
can be used to examine the cerebral veins.[83]

Misdiagnosis
Among people with ischemic stroke, misdiagnosis occurs 2 to 26% of the time.[84] A "stroke
chameleon" (SC) is stroke which is diagnosed as something else.[84][85]

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.[84]

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.[84] 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.[84]

Prevention
Given the disease burden of stroke, prevention is an important public health concern.[86] Primary
prevention is less effective than secondary prevention (as judged by the number needed to treat to
prevent one stroke per year).[86] Recent guidelines detail the evidence for primary prevention in
stroke.[87] About the use of aspirin as a preventive medication for stroke, in healthy people aspirin
does not appear beneficial and thus is not recommended,[88] but in people with high cardiovascular
risk, or those who have had a myocardial infarction, it provides some protection against a first
stroke.[89][90] In those who have previously had stroke, treatment with medications such as aspirin,
clopidogrel, and dipyridamole may be beneficial.[89] The U.S. Preventive Services Task Force
(USPSTF) recommends against screening for carotid artery stenosis in those without symptoms.[91]

Risk factors
The most important modifiable risk factors for stroke are high blood pressure and atrial fibrillation,
although the size of the effect is small; 833 people have to be treated for 1 year to prevent one
stroke.[92][93] Other modifiable risk factors include high blood cholesterol levels, diabetes mellitus,
end-stage kidney disease,[8] cigarette smoking[94][95] (active and passive), heavy alcohol use,[96] drug
use,[97] lack of physical activity, obesity, processed red meat consumption,[98] and unhealthy diet.[99]
Smoking just one cigarette per day increases the risk more than 30%.[100] 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
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aggregation and clotting disturbances).[101]

Drugs, most commonly amphetamines and cocaine, can
induce stroke through damage to the blood vessels in the brain and acute hypertension.[74][102]
Migraine with aura doubles a person's risk for ischemic stroke.[103][104] Untreated, celiac disease
regardless of the presence of symptoms can be an underlying cause of stroke, both in children and
adults.[105] 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.[106]

High levels of physical activity reduce the risk of stroke by about 26%.[107] There is a lack of high
quality studies looking at promotional efforts to improve lifestyle factors.[108] Nonetheless, given the
large body of circumstantial evidence, best medical management for stroke includes advice on diet,
exercise, smoking and alcohol use.[109] Medication is the most common method of stroke prevention;
carotid endarterectomy can be a useful surgical method of preventing stroke.

Blood pressure
High blood pressure accounts for 35–50% of stroke risk.[110] Blood pressure reduction of 10 mmHg
systolic or 5 mmHg diastolic reduces the risk of stroke by ~40%.[111] Lowering blood pressure has
been conclusively shown to prevent both ischemic and hemorrhagic stroke.[112][113] It is equally
important in secondary prevention.[114] Even people older than 80 years and those with isolated
systolic hypertension benefit from antihypertensive therapy.[115][116][117] 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.[118][119] The routine use of beta-blockers following stroke or TIA has not been shown to
result in benefits.[120]

Blood lipids
High cholesterol levels have been inconsistently associated with (ischemic) stroke.[113][121] Statins
have been shown to reduce the risk of stroke by about 15%.[122] Since earlier meta-analyses of other
lipid-lowering drugs did not show a decreased risk,[123] statins might exert their effect through
mechanisms other than their lipid-lowering effects.[122]

Diabetes mellitus
Diabetes mellitus increases the risk of stroke by 2 to 3 times. While intensive blood sugar control has
been shown to reduce small blood vessel complications such as kidney damage and damage to the
retina of the eye it has not been shown to reduce large blood vessel complications such as
stroke.[124][125]

Anticoagulant drugs
Oral anticoagulants such as warfarin have been the mainstay of stroke prevention for over 50 years.
However, several studies have shown that aspirin and other antiplatelets are highly effective in
secondary prevention after stroke or transient ischemic attack.[89] Low doses of aspirin (for example
75–150 mg) are as effective as high doses but have fewer side effects; the lowest effective dose remains
unknown.[126] Thienopyridines (clopidogrel, ticlopidine) might be slightly more effective than aspirin
and have a decreased risk of gastrointestinal bleeding but are more expensive.[127] Both aspirin and
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clopidogrel may be useful in the first few weeks after a minor stroke or high-risk TIA.[128] Clopidogrel
has less side effects than ticlopidine.[127] Dipyridamole can be added to aspirin therapy to provide a
small additional benefit, even though headache is a common side effect.[129] Low-dose aspirin is also
effective for stroke prevention after having a myocardial infarction.[90]

Those with atrial fibrillation have a 5% a year risk of stroke, and those with valvular atrial fibrillation
have an even higher risk.[130] Depending on the stroke risk, anticoagulation with medications such as
warfarin or aspirin is useful for prevention with various levels of comparative effectiveness depending
on the type of treatment used.[131][132]

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.[132] Except in people with atrial fibrillation, oral anticoagulants are not advised
for stroke prevention—any benefit is offset by bleeding risk.[133]

In primary prevention, however, antiplatelet drugs did not reduce the risk of ischemic stroke but
increased the risk of major bleeding.[134][135] Further studies are needed to investigate a possible
protective effect of aspirin against ischemic stroke in women.[136][137]

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.[109] Endarterectomy for
a significant stenosis has been shown to be useful in preventing further stroke in those who have
already had the condition.[138] Carotid artery stenting has not been shown to be equally
useful.[139][140] People are selected for surgery based on age, gender, degree of stenosis, time since
symptoms and the person's preferences.[109] 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.[141][142]

Screening for carotid artery narrowing has not been shown to be a useful test in the general
population.[143] Studies of surgical intervention for carotid artery stenosis without symptoms have
shown only a small decrease in the risk of stroke.[144][145] 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.[109]

Diet
Nutrition, specifically the Mediterranean-style diet, has the potential to decrease the risk of having a
stroke by more than half.[146] It does not appear that lowering levels of homocysteine with folic acid
affects the risk of stroke.[147][148]

Women

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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 mmHg systolic or greater than
100 mmHg diastolic. In those who have previously had
preeclampsia, other risk factors should be treated more
A Centers for Disease Control and
aggressively.[149] Prevention public service
announcement about a woman who
had stroke after pregnancy
Previous stroke or TIA
Keeping blood pressure below 140/90 mmHg is
recommended. [150] 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%.[151] However, a recent meta-analysis suggests harm from anticoagulation
started early after an embolic stroke.[152][153] 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.[150]

Anticoagulants, when used following stroke, should not be stopped for dental procedures.[154]

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.[5][155] 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 comorbidities.[155]

Ischemic stroke
Aspirin reduces the overall risk of recurrence by 13% with greater benefit early on.[156] 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.[157] Years later, that same idea, that rapid cerebral blood flow restoration results in fewer brain
cells dying, has been proved and quantified.[158]

Tight blood sugar control in the first few hours does not improve outcomes and may cause harm.[159]
High blood pressure is also not typically lowered as this has not been found to be helpful.[160][161]
Cerebrolysin, a mixture of pig brain-derived neurotrophic factors used widely to treat acute ischemic

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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.[162] There is
also no evidence that cerebrolysin‐like peptide mixtures which are extracted from cattle brain is
helpful in treating acute ischemic stroke.[162]

Thrombolysis
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.[163][164] It does not, however,
improve chances of survival.[163] Benefit is greater the earlier it is
used.[163] Between three and four and a half hours the effects are
less clear.[165][166][167] The AHA/ASA recommend it for certain A Centers for Disease Control and
Prevention public service
people in this time frame.[168] A 2014 review found a 5% increase
announcement on emergency
in the number of people living without disability at three to six medical treatment after or during
months; however, there was a 2% increased risk of death in the stroke from 2021
short term.[164] After four and a half hours thrombolysis worsens
outcomes.[165] These benefits or lack of benefits occurred
regardless of the age of the person treated.[169] There is no reliable way to determine who will have an
intracranial bleed post-treatment versus who will not.[170] 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.[171]

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[172] 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.[173] 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.[174] The American Academy of Emergency Medicine had previously
stated that objective evidence regarding the applicability of tPA for acute ischemic stroke was
insufficient.[175] In 2013 the American College of Emergency Medicine refuted this position,[176]
acknowledging the body of evidence for the use of tPA in ischemic stroke;[177] but debate
continues.[178][179] 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.[180]

Endovascular treatment
Mechanical removal of the blood clot causing the ischemic stroke, called 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.[181][182] It did not change the risk of death but did reduce disability compared to

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the use of intravenous thrombolysis, which is generally used in people evaluated for mechanical
thrombectomy.[183][184] Certain cases may benefit from thrombectomy up to 24 hours after the onset
of symptoms.[185]

Craniectomy
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.[186][187]

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). A proportion may benefit from
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.[188]

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 surgery that involves
opening the skull or endovascularly (through the blood vessels).[189]

Stroke unit
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.[2][190] Nursing care
is fundamental in maintaining skin care, feeding, hydration, positioning, and monitoring vital signs
such as temperature, pulse, and blood pressure.[191]

Rehabilitation
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, neurologists, clinical pharmacists, nursing staff,

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physiotherapists, occupational therapists, speech-language pathologists, and orthotists. Some teams

may also include psychologists and social workers, 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.[192]

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. However, some people have reported that they
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 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.

Spatial neglect
The body of evidence is uncertain on the efficacy of cognitive rehabilitation for reducing the disabling
effects of neglect and increasing independence remains unproven.[193] However, there is limited
evidence that cognitive rehabilitation may have an immediate beneficial effect on tests of neglect.[193]
Overall, no rehabilitation approach can be supported by evidence for spatial neglect.

Automobile driving
The body of evidence is uncertain whether the use of rehabilitation can improve on-road driving skills
following stroke.[194] There is limited evidence that training on a driving simulator will improve
performance on recognizing road signs after training.[194] The findings are based on low-quality
evidence as further research is needed involving large numbers of participants.

Yoga
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.[195] Yoga may reduce anxiety and could be included as part of patient-centred stroke
rehabilitation.[195] Further research is needed assessing the benefits and safety of yoga in stroke
rehabilitation.

Action observation physical therapy for upper limbs

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.[196]

Cognitive rehabilitation for attention deficits

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The body of scientific evidence is uncertain on the effectiveness of cognitive rehabilitation for
attention deficits in patients following stroke.[197] 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.[197] Further research is needed to assess whether the effect can be sustained in day-to-day
tasks requiring attention.

Motor imagery for gait rehabilitation

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.[198] MI does not improve motor
function after stroke and does not seem to cause significant adverse events.[198] 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.

Physical and occupational therapy

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.[199] Physical therapy is effective
for recovery of function and mobility after stroke.[200] 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, reading and 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.[201]

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.[45] Gaining initial improvement in range of motion is often achieved through
rhythmic rotational patterns associated with the affected limb.[45] 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.[45] Cold ice wraps or ice packs may briefly relieve spasticity by temporarily reducing neural
firing rates.[45] Electrical stimulation to the antagonist muscles or vibrations has also been used with
some success.[45] Physical therapy is sometimes suggested for people who experience sexual
dysfunction following stroke.[202]

Interventions for age-related visual problems in patients with stroke

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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.[203] Further
research in this area is needed as the body of evidence is very low quality.

Speech and language therapy

Speech and language therapy is appropriate for people with the speech production disorders:
dysarthria[204] and apraxia of speech,[205] aphasia,[206] cognitive-communication impairments, and
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).[206]
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.[207][208] Speech and
language therapy is also effective if it is delivered online through video or by a family member who has
been trained by a professional therapist.[207][208]

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.[207][208]

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 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.[209]

Devices
Often, assistive technology such as wheelchairs, walkers and canes may be beneficial. Many mobility
problems can be improved by the use of ankle foot orthoses.[210]

Physical fitness
Stroke can also reduce people's general fitness.[211] Reduced fitness can reduce capacity for
rehabilitation as well as general health.[212] Physical exercises as part of a rehabilitation program
following stroke appear safe.[211] Cardiorespiratory fitness training that involves walking in
rehabilitation can improve speed, tolerance and independence during walking, and may improve
balance.[211] There are inadequate long-term data about the effects of exercise and training on death,

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dependence and disability after stroke.[211]

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.[213]

Other therapy methods

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.[214] 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.[215] There are inadequate data on the effect of virtual reality and interactive video gaming on
gait speed, balance, participation and quality of life.[215] 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.[214]

Mirror therapy is associated with improved motor function of the upper extremity in people who have
had stroke.[216]

Other non-invasive rehabilitation methods used to augment physical therapy of motor function in
people recovering from stroke include transcranial magnetic stimulation and transcranial direct-
current stimulation.[217] and robotic therapies.[218] 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.[219]

Orthotics
Clinical studies confirm the importance of orthoses in stroke rehabilitation.[220][221][222] 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
Stroke can affect the ability to live independently and with quality. 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. 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). A

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2016 review reported that these programs improve the quality of

life after stroke, without negative effects. People with stroke felt
more empowered, happy and satisfied with life after participating
in this training.[223]

Prognosis
Disability affects 75% of stroke survivors enough to decrease their
ability to work.[224] 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.[225]

Physical effects
Some of the physical disabilities that can result from stroke
include muscle weakness, numbness, pressure sores, pneumonia,
incontinence, apraxia (inability to perform learned movements),
difficulties carrying out daily activities, appetite loss, speech loss,
vision loss and pain. If the stroke is severe enough, or in a certain
location such as parts of the brainstem, coma or death can result.
Up to 10% of people following stroke develop seizures, most
commonly in the week subsequent to the event; the severity of the Walking with an orthosis after stroke
stroke increases the likelihood of a seizure.[226][227] An estimated
15% of people experience urinary incontinence for more than a
year following stroke.[201] 50% of people have a decline in sexual function (sexual dysfunction)
following stroke.[202]

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 attacks, 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.[228]

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.[204] 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.[229]

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30 to 50% of stroke survivors develop post-stroke depression, which is characterized by lethargy,

irritability, sleep disturbances, lowered self-esteem and withdrawal.[230] Depression can reduce
motivation and worsen outcome, but can be treated with social and family support, psychotherapy
and, in severe cases, antidepressants. Psychotherapy sessions may have a small effect on improving
mood and preventing depression after stroke.[231] Antidepressant medications may be useful for
treating depression after stroke but are associated with central nervous system and gastrointestinal
adverse events.[231]

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.[224] Some
people show the opposite of what they feel, for example crying when they are happy.[232] 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.[233]

Cognitive deficits resulting from stroke include perceptual disorders, aphasia,[234] dementia,[235][236]
and problems with attention[237] and memory.[238] 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.[239]

Epidemiology
Stroke was the second most frequent cause of death worldwide in
2011, accounting for 6.2 million deaths (~11% of the total).[241]
Approximately 17 million people had stroke in 2010 and
33 million people have previously had stroke and were still
alive.[19] Between 1990 and 2010 the incidence of stroke decreased
by approximately 10% in the developed world and increased by Stroke deaths per million persons in
10% in the developing world.[19] Overall, two-thirds of stroke 2012:
occurred in those over 65 years old.[19] South Asians are at 58–316
particularly high risk of stroke, accounting for 40% of global 317–417
stroke deaths.[242] Incidence of ischemic stroke is ten times more 418–466
467–518
frequent than haemorrhagic stroke.[243]
519–575
576–640
It is ranked after heart disease and before cancer.[2] In the United
641–771
States stroke is a leading cause of disability, and recently declined
772–974
from the third leading to the fourth leading cause of death.[244] 975-1,683
Geographic disparities in stroke incidence have been observed, 1,684–3,477

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including the existence of a "stroke belt" in the southeastern

United States, but causes of these disparities have not been
explained.

The risk of stroke increases exponentially from 30 years of age,

and the cause varies by age.[245] Advanced age is one of the most
Disability-adjusted life year for
significant stroke risk factors. 95% of stroke occurs in people age cerebral vascular disease per
45 and older, and two-thirds of stroke occurs in those over the age 100,000 inhabitants in 2004:[240]
of 65.[53][230] no data 1125–1300
<250 1300–1475
A person's risk of dying if he or she does have stroke also increases 250–425 1475–1650
with age. However, stroke can occur at any age, including in 425–600 1650–1825
childhood. 600–775 1825–2000
775–950 >2000
Family members may have a genetic tendency for stroke or share a
950–1125
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.[246] 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.

Men are 25% more likely to develop stroke than women,[53] yet 60% of deaths from stroke occur in
women.[232] Since women live longer, they are older on average when they have stroke and thus more
often killed.[53] Some risk factors for stroke apply only to women. Primary among these are
pregnancy, childbirth, menopause, and the treatment thereof (HRT).

History
Episodes of stroke and familial stroke have been reported from the 2nd
millennium BC onward in ancient Mesopotamia and Persia.[247]
Hippocrates (460 to 370 BC) was first to describe the phenomenon of
sudden paralysis that is often associated with ischemia. Apoplexy, from
the Greek word meaning "struck down with violence", first appeared in
Hippocratic writings to describe this phenomenon.[248][249] The word
stroke was used as a synonym for apoplectic seizure as early as 1599,[250]
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.[251] Martin Luther
was described as having an apoplectic stroke that deprived him of his
speech shortly before his death in 1546.[252]
Hippocrates first described
In 1658, in his Apoplexia, Johann Jacob Wepfer (1620–1695) identified
the sudden paralysis that is
often associated with the cause of hemorrhagic stroke when he suggested that people who had
stroke. died of apoplexy had bleeding in their brains.[53][248] Wepfer also
identified the main arteries supplying the brain, the vertebral and carotid

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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.[53] Rudolf Virchow first
described the mechanism of thromboembolism as a major factor.[253]

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".[254] 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.[255][256][257] Cerebrovascular insult may be used
interchangeably.[258]

The term brain attack was introduced for use to underline the acute nature of stroke according to the
American Stroke Association,[258] which has used the term since 1990,[259] and is used colloquially to
refer to both ischemic as well as hemorrhagic stroke.[260]

Research
As of 2017, angioplasty and stents were under preliminary clinical research to determine the possible
therapeutic advantages of these procedures in comparison to therapy with statins, antithrombotics, or
antihypertensive drugs.[261]

See also
Anoxic depolarization in the brain
Cerebrovascular disease
Cerebral palsy
Dejerine–Roussy syndrome
Functional Independence Measure
Lipoprotein(a)
Mobile Stroke Unit
Ultrasound-enhanced systemic thrombolysis
Weber's syndrome
World Stroke Day

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Further reading
Gijn, Jan van (2023). Stroke: A History of Ideas. Cambridge University Press. ISBN 978-1-108-
83254-0.
Mohr JP, Choi D, Grotta J, Wolf P (2004). Stroke: Pathophysiology, Diagnosis, and Management.
New York: Churchill Livingstone. ISBN 978-0-443-06600-9. OCLC 50477349 ([Link]
[Link]/oclc/50477349).
Warlow CP, van Gijn J, Dennis MS, Wardlaw JM, Bamford JM, Hankey GJ, et al. (2008). Stroke:
Practical Management (3rd ed.). Wiley-Blackwell. ISBN 978-1-4051-2766-0.

External links
DRAGON Score for Post-Thrombolysis ([Link]
come/) Archived ([Link]
core-post-tpa-stroke-outcome) 2020-10-27 at the Wayback Machine
THRIVE score for stroke outcome ([Link]
Archived ([Link]
roke-outcome/) 2016-09-13 at the Wayback Machine

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National Institute of Neurological Disorders and Stroke ([Link]

orders)

Retrieved from "[Link]

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