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Stroke - Wikipedia, the free encyclopedia http://en.wikipedia.


From Wikipedia, the free encyclopedia

A stroke (sometimes called a cerebrovascular accident Stroke

(CVA)) is the rapidly developing loss of brain function(s) due
Classification and external resources
to disturbance in the blood supply to the brain. This can be
due to ischemia (lack of blood flow) caused by blockage
(thrombosis, arterial embolism), or a hemorrhage (leakage of
blood).[1] As a result, the affected area of the brain is unable
to function, leading to inability to move one or more limbs on
one side of the body, inability to understand or formulate
speech, or inability to see one side of the visual field.[2]

A stroke is a medical emergency and can cause permanent

neurological damage, complications, and even death. It is the
leading cause of adult disability in the United States and
Europe and it is the number two cause of death worldwide.[3]
Risk factors for stroke include advanced age, hypertension
CT scan slice of the brain showing a right-
(high blood pressure), previous stroke or transient ischemic
attack (TIA), diabetes, high cholesterol, cigarette smoking hemispheric ischemic stroke (left side of image).

and atrial fibrillation.[4] High blood pressure is the most ICD-10 I61. (http://apps.who.int
important modifiable risk factor of stroke.[2] /classifications/apps/icd/icd10online
/?gi60.htm+i61) -I64.
A stroke is occasionally treated with thrombolysis ("clot (http://apps.who.int/classifications
buster"), in the "stroke unit" of a hospital. Secondary /apps/icd/icd10online
prevention may involve antiplatelet drugs (aspirin and often
dipyridamole), blood pressure control, statins, and in selected
patients with carotid endarterectomy and anticoagulation.[2] ICD-9 434.91 (http://www.icd9data.com
Treatment to recover lost function is stroke rehabilitation, /getICD9Code.ashx?icd9=434.91)
involving health professions such as speech and language OMIM 601367
therapy, physical therapy and occupational therapy.

DiseasesDB 2247
1 Definition
2 Classification MedlinePlus 000726 (http://www.nlm.nih.gov
2.1 Ischemic stroke /medlineplus/ency/article
2.2 Hemorrhagic stroke /000726.htm)
3 Signs and symptoms eMedicine neuro/9 (http://www.emedicine.com
3.1 Early recognition /neuro/topic9.htm) emerg/558
3.2 Subtypes
3.3 Associated symptoms
/topic558.htm#) emerg/557
4 Causes

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5 Pathophysiology
5.1 Ischemic
/topic557.htm#) pmr/187
5.2 Hemorrhagic
6 Diagnosis /pmr/topic187.htm#)
6.1 Physical examination
6.2 Imaging MeSH D020521 (http://www.nlm.nih.gov
6.3 Underlying etiology /cgi/mesh/2010/MB_cgi?field=uid&
7 Prevention term=D020521)
7.1 Risk factors
7.1.1 Blood pressure
7.1.2 Atrial fibrillation
7.1.3 Blood lipids
7.1.4 Diabetes mellitus
7.1.5 Anticoagulation drugs
7.1.6 Surgery
7.1.7 Nutritional and metabolic
8 Treatment
8.1 Stroke unit
8.2 Treatment of ischemic stroke
8.2.1 Thrombolysis
8.2.2 Mechanical thrombectomy
8.2.3 Angioplasty and stenting
8.2.4 Therapeutic hypothermia
8.3 Secondary prevention of ischemic stroke
8.4 Treatment of hemorrhagic stroke
8.5 Care and rehabilitation
9 Prognosis
10 Epidemiology
11 History
12 References
13 Further reading

The traditional definition of stroke, devised by the World Health Organization in the 1970s,[5] is a "neurological
deficit of cerebrovascular cause that persists beyond 24 hours or is interrupted by death within 24 hours". This
definition was supposed to reflect the reversibility of tissue damage and was devised for the purpose, with the
time frame of 24 hours being chosen arbitrarily. The 24-hour limit divides stroke from transient ischemic attack,
which is a related syndrome of stroke symptoms that resolve completely within 24 hours.[2] With the availability
of treatments that, when given early, can reduce stroke severity, many now prefer alternative concepts, such as
brain attack and acute ischemic cerebrovascular syndrome (modeled after heart attack and acute coronary
syndrome respectively), that reflect the urgency of stroke symptoms and the need to act swiftly.[6]

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Strokes can be classified into two major categories: ischemic and

hemorrhagic.[7] Ischemic strokes are those that are caused by interruption of
the blood supply, while hemorrhagic strokes are the ones which result from
rupture of a blood vessel or an abnormal vascular structure. 87% of strokes are
caused by ischemia, and the remainder by hemorrhage. Some hemorrhages
develop inside areas of ischemia ("hemorrhagic transformation"). It is unknown
how many hemorrhages actually start off as ischemic stroke.[2]
A slice of brain from the
Ischemic stroke autopsy of a person who
suffered an acute middle
Main articles: Cerebral infarction and Brain ischemia cerebral artery (MCA) stroke
In an ischemic stroke, blood supply to part of the brain is decreased, leading to
dysfunction of the brain tissue in that area. There are four reasons why this might happen:

1. Thrombosis (obstruction of a blood vessel by a blood clot forming locally)

2. Embolism (obstruction due to an embolus from elsewhere in the body, see below),[2]
3. Systemic hypoperfusion (general decrease in blood supply, e.g. in shock)[8]
4. Venous thrombosis.[9]

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

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

Hemorrhagic stroke

Main articles: Intracranial hemorrhage and intracerebral hemorrhage

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Intracranial hemorrhage is the accumulation of blood anywhere within the skull

vault. A distinction is made between intra-axial hemorrhage (blood inside the
brain) and extra-axial hemorrhage (blood inside the skull but outside the brain).
Intra-axial hemorrhage is due to intraparenchymal hemorrhage or
intraventricular hemorrhage (blood in the ventricular system). The main types of
extra-axial hemorrhage are epidural hematoma (bleeding between the dura mater
and the skull), subdural hematoma (in the subdural space) and subarachnoid
hemorrhage (between the arachnoid mater and pia mater). Most of the
hemorrhagic stroke syndromes have specific symptoms (e.g. headache, previous
head injury).

CT scan showing an
intracerebral hemorrhage
Stroke symptoms typically start suddenly, over seconds to minutes, and in most with associated
cases do not progress further. The symptoms depend on the area of the brain intraventricular
affected. The more extensive the area of brain affected, the more functions that hemorrhage.
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 headache, apart from subarachnoid hemorrhage and cerebral venous thrombosis and
occasionally intracerebral hemorrhage.

Early recognition

Various systems have been proposed to increase recognition of stroke by patients, relatives and emergency first
responders. A systematic review, updating a previous systematic review from 1994, looked at a number of trials
to evaluate how well different physical examination findings are able to predict the presence or absence of
stroke. It was found that sudden-onset face weakness, arm drift (e.g. if a person, when asked to raise both arms,
involuntarily lets one arm drift downward) and abnormal speech are the findings most likely to lead to the
correct identification of a case of stroke (+ likelihood ratio of 5.5 when at least one of these is present).
Similarly, when all three of these are absent, the likelihood of stroke is significantly decreased (– likelihood ratio
of 0.39).[14] While these findings are not perfect for diagnosing stroke, the fact that they can be evaluated
relatively rapidly and easily make them very valuable in the acute setting.

Proposed systems include FAST (face, arm, speech, and time),[15] as advocated by the Department of Health
(United Kingdom) and The Stroke Association, the American Stroke Association (www.strokeassociation.org) ,
National Stroke Association (US www.stroke.org), the Los Angeles Prehospital Stroke Screen (LAPSS)[16] and
the Cincinnati Prehospital Stroke Scale (CPSS).[17] Use of these scales is recommended by professional

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.


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

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hemiplegia and muscle weakness of the face

reduction in sensory or vibratory sensation

In most cases, the symptoms affect only one side of the body (unilateral). Depending on the part of the brain
affected, 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 a stroke.

In addition to the above CNS pathways, the brainstem also consists of the 12 cranial nerves. A stroke affecting
the brain stem therefore can produce symptoms relating to deficits in these cranial nerves:

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

drooping of eyelid (ptosis) and weakness of ocular muscles
decreased reflexes: gag, swallow, pupil reactivity to light
decreased sensation and muscle weakness of the face
balance problems and nystagmus
altered breathing and heart rate
weakness in sternocleidomastoid muscle with inability to turn head to one side
weakness in tongue (inability to protrude and/or move from side to side)

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

aphasia (inability to speak or understand language from involvement of Broca's or Wernicke's area)
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)
anosognosia (persistent denial of the existence of a, usually stroke-related, deficit)

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

trouble walking
altered movement coordination
vertigo and or disequilibrium

Associated symptoms

Loss of consciousness, headache, and vomiting usually occurs more often in hemorrhagic stroke than in
thrombosis because of the increased intracranial pressure from the leaking blood compressing on the brain.

If symptoms are maximal at onset, the cause is more likely to be a subarachnoid hemorrhage or an embolic

Thrombotic stroke

In thrombotic stroke a thrombus (blood clot) usually forms around atherosclerotic plaques. Since blockage of the

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artery is gradual, onset of symptomatic thrombotic strokes is slower. A thrombus itself (even if non-occluding)
can lead to an embolic stroke (see below) if the thrombus breaks off, at which point it is called an "embolus."
Two types of thrombosis can cause stroke:

Large vessel disease involves the common and internal carotids, vertebral, and the Circle of Willis.
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, various
inflammatory diseases of the blood vessel wall (Takayasu arteritis, giant cell arteritis, vasculitis),
noninflammatory vasculopathy, Moyamoya disease and fibromuscular dysplasia.
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. 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 are known as lacunar infarcts) and microatheroma (small atherosclerotic

Sickle cell anemia, which can cause blood cells to clump up and block blood vessels, can also lead to stroke. A
stroke is the second leading killer of people under 20 who suffer from sickle-cell anemia.[20]

Embolic stroke

An embolic stroke refers to the blockage of an artery by an arterial embolus, a travelling particle or debris in the
arterial bloodstream originating from elsewhere. An embolus is most frequently a thrombus, but it can also be a
number of other substances including fat (e.g. from bone marrow in a broken bone), air, cancer cells or clumps
of bacteria (usually from infectious endocarditis).

Because an embolus arises from elsewhere, local therapy only solves the problem temporarily. Thus, the source
of the embolus must be identified. Because the embolic blockage is sudden in onset, symptoms usually are
maximal at start. Also, symptoms may be transient as the embolus is partially resorbed and moves to a different
location or dissipates altogether.

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

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

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 vertricle, 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)
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), complex atheroma in the ascending aorta or proximal arch

Systemic hypoperfusion

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Systemic hypoperfusion is the reduction of blood flow to all parts of the body. It is most commonly due to
cardiac pump failure from cardiac arrest or arrhythmias, or from reduced cardiac output as a result of
myocardial infarction, pulmonary embolism, pericardial effusion, or bleeding. Hypoxemia (low blood oxygen
content) may precipitate the hypoperfusion. Because the reduction in blood flow is global, all parts of the brain
may be affected, especially "watershed" areas - border zone regions supplied by the major cerebral arteries. A
watershed stroke refers to the condition when blood supply to these areas is compromised. Blood flow to these
areas does not necessarily stop, but instead it may lessen to the point where brain damage can occur. This
phenomenon is also referred to as "last meadow" to point to the fact that in irrigation the last meadow receives
the least amount of water.

Venous thrombosis

Cerebral venous sinus thrombosis leads to stroke due to locally increased venous pressure, which exceeds the
pressure generated by the arteries. Infarcts are more likely to undergo hemorrhagic transformation (leaking of
blood into the damaged area) than other types of ischemic stroke.[9]

Intracerebral hemorrhage

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


Ischemic stroke occurs due to a loss of blood supply to part of the brain, initiating the ischemic cascade.[22]
Brain tissue ceases to function if deprived of oxygen for more than 60 to 90 seconds and after approximately
three hours, will suffer irreversible injury possibly leading to death of the tissue, i.e., infarction. (This is why
TPA's (e.g. Streptokinase, Altapase) are given only until three hours since the onset of the stroke.)
Atherosclerosis may disrupt the blood supply by narrowing the lumen of blood vessels leading to a reduction of
blood flow, by causing the formation of blood clots within the vessel, or by releasing showers of small emboli
through the disintegration of atherosclerotic plaques. Embolic infarction occurs when emboli formed elsewhere
in the circulatory system, typically in the heart as a consequence of atrial fibrillation, or in the carotid arteries,
break off, enter the cerebral circulation, then lodge in and occlude brain blood vessels. Since blood vessels in the
brain are now occluded, the brain becomes low in energy, and thus it resorts into using anaerobic respiration
within the region of brain tissue affected by ischemia. Unfortunately, this kind of respiration produces less ATP
but releases a by-product called lactic acid. Lactic acid is an irritant which could potentially destroy cells since it
is an acid and disrupts the normal acid-bace balance in the brain. The ischemia area is referred to as the
"ischemic penumbra".[23]

Then, as oxygen or glucose becomes depleted in ischemic brain tissue, the production of high energy phosphate
compounds such as adenosine triphosphate (ATP) fails, leading to failure of energy-dependent processes (such
as ion pumping) necessary for tissue cell survival. This sets off a series of interrelated events that result in

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cellular injury and death. A major cause of neuronal injury is release of the excitatory neurotransmitter
glutamate. The concentration of glutamate outside the cells of the nervous system is normally kept low by
so-called uptake carriers, which are powered by the concentration gradients of ions (mainly Na+) across the cell
membrane. However, stroke cuts off the supply of oxygen and glucose which powers the ion pumps maintaining
these gradients. As a result the transmembrane ion gradients run down, and glutamate transporters reverse their
direction, releasing glutamate into the extracellular space. Glutamate acts on receptors in nerve cells (especially
NMDA receptors), producing an influx of calcium which activates enzymes that digest the cells' proteins, lipids
and nuclear material. Calcium influx can also lead to the failure of mitochondria, which can lead further toward
energy depletion and may trigger cell death due to apoptosis.

Ischemia also induces production of oxygen free radicals and other reactive oxygen species. These react with
and damage a number of cellular and extracellular elements. Damage to the blood vessel lining or endothelium is
particularly important. In fact, many antioxidant neuroprotectants such as uric acid and NXY-059 work at the
level of the endothelium and not in the brain per se. Free radicals also directly initiate elements of the apoptosis
cascade by means of redox signaling.[20]

These processes are the same for any type of ischemic tissue and are referred to collectively as the ischemic
cascade. However, brain tissue is especially vulnerable to ischemia since it has little respiratory reserve and is
completely dependent on aerobic metabolism, unlike most other organs.

Brain tissue survival can be improved to some extent if one or more of these processes is inhibited. Drugs that
scavenge reactive oxygen species, inhibit apoptosis, or inhibit excitatory neurotransmitters, for example, have
been shown experimentally to reduce tissue injury due to ischemia. Agents that work in this way are referred to
as being neuroprotective. Until recently, human clinical trials with neuroprotective agents have failed, with the
probable exception of deep barbiturate coma. However, more recently NXY-059, the disulfonyl derivative of
the radical-scavenging spintrap phenylbutylnitrone, is reported to be neuroprotective in stroke.[24] This agent
appears to work at the level of the blood vessel lining or endothelium. Unfortunately, after producing favorable
results in one large-scale clinical trial, a second trial failed to show favorable results.[20]

In addition to injurious effects on brain cells, ischemia and infarction can result in loss of structural integrity of
brain tissue and blood vessels, partly through the release of matrix metalloproteases, which are zinc- and
calcium-dependent enzymes that break down collagen, hyaluronic acid, and other elements of connective tissue.
Other proteases also contribute to this process. The loss of vascular structural integrity results in a breakdown of
the protective blood brain barrier that contributes to cerebral edema, which can cause secondary progression of
the brain injury.

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


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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

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 Head CT showing deep
techniques. Imaging techniques also assist in determining the subtypes intracerebral hemorrhage due to
and cause of stroke. There is yet no commonly used blood test for the bleeding within the cerebellum,
stroke diagnosis itself, though blood tests may be of help in finding out approximately 30 hours old.
the likely cause of stroke.[25]

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 a stroke. It can give a standard score on e.g. the NIH stroke


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

CT scans (without contrast enhancements)

sensitivity= 16%
specificity= 96%

MRI scan

sensitivity= 83%
specificity= 98%

For diagnosing hemorrhagic stroke in the emergency setting:

CT scans (without contrast enhancements)

sensitivity= 89%
specificity= 100%

MRI scan

sensitivity= 81%
specificity= 100%

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

For the assessment of stable stroke, nuclear medicine scans SPECT and PET/CT may be helpful. SPECT
documents cerebral blood flow and PET with FDG isotope the metabolic activity of the neurons.

Underlying etiology

When a stroke has been diagnosed, various other studies may be performed to determine the underlying
etiology. With the current treatment and diagnosis options available, it is of particular importance to determine
whether there is a peripheral source of emboli. Test selection may vary, since the cause of stroke varies with
age, comorbidity and the clinical presentation. Commonly used techniques include:

an ultrasound/doppler study of the carotid arteries (to detect carotid stenosis) or dissection of the
precerebral arteries
an electrocardiogram (ECG) and echocardiogram (to identify 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)
blood tests to determine hypercholesterolemia, bleeding diathesis and some rarer causes such as

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

Risk factors

The most important modifiable risk factors for stroke are high blood pressure and atrial fibrillation (although
magnitude of this effect is small: the evidence from the Medical Research Council trials is that 833 patients have
to be treated for 1 year to prevent one stroke[32][33]). Other modifiable risk factors include high blood
cholesterol levels, diabetes, cigarette smoking[34][35] (active and passive), heavy alcohol consumption[36] and
drug use,[37] lack of physical activity, obesity and unhealthy diet.[38] Alcohol use could predispose to ischemic
stroke, and intracerebral and subarachnoid hemorrhage via multiple mechanisms (for example via hypertension,
atrial fibrillation, rebound thrombocytosis and platelet aggregation and clotting disturbances).[39] The drugs most
commonly associated with stroke are cocaine, amphetamines causing hemorrhagic stroke, but also over-the-
counter cough and cold drugs containing sympathomimetics.[40][41]

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

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Blood pressure

Hypertension accounts for 35-50% of stroke risk.[44] Epidemiological studies suggest that even a small blood
pressure reduction (5 to 6 mmHg systolic, 2 to 3 mmHg diastolic) would result in 40% fewer strokes.[45]
Lowering blood pressure has been conclusively shown to prevent both ischemic and hemorrhagic strokes.[46][47]
It is equally important in secondary prevention.[48] Even patients older than 80 years and those with isolated
systolic hypertension benefit from antihypertensive therapy.[49][50][51] Studies show that intensive
antihypertensive therapy results in a greater risk reduction.[52] The available evidence does not show large
differences in stroke prevention between antihypertensive drugs —therefore, other factors such as protection
against other forms of cardiovascular disease should be considered and cost.[52][53]

Atrial fibrillation

Patients with atrial fibrillation have a risk of 5% each year to develop stroke, and this risk is even higher in those
with valvular atrial fibrillation.[54] Depending on the stroke risk, anticoagulation with medications such as
coumarins or aspirin is warranted for stroke prevention.[55]

Blood lipids

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

Diabetes mellitus

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

Anticoagulation drugs

Oral anticoagulants such as warfarin have been the mainstay of stroke prevention for over 50 years. However,
several studies have shown that aspirin and antiplatelet drugs are highly effective in secondary prevention after
a stroke or transient ischemic attack[30]. Low doses of aspirin (for example 75–150 mg) are as effective as high
doses but have fewer side effects; the lowest effective dose remains unknown.[61] Thienopyridines (clopidogrel,
ticlopidine) "might be slightly more effective" than aspirin and have a decreased risk of gastrointestinal bleeding,
but they are more expensive.[62] Their exact role remains controversial. Ticlopidine has more skin rash,
diarrhea, neutropenia and thrombotic thrombocytopenic purpura.[62] Dipyridamole can be added to aspirin
therapy to provide a small additional benefit, even though headache is a common side effect.[63] Low-dose
aspirin is also effective for stroke prevention after sustaining a myocardial infarction.[31] Oral anticoagulants are
not advised for stroke prevention —any benefit is offset by bleeding risk.[64]

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

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against ischemic stroke in women.[67][68]


Surgical procedures such as carotid endarterectomy or carotid angioplasty can be used to remove significant
atherosclerotic narrowing (stenosis) of the carotid artery, which supplies blood to the brain. There is a large
body of evidence supporting this procedure in selected cases.[43] Endarterectomy for a significant stenosis has
been shown to be useful in the secondary prevention after a previous symptomatic stroke.[69] Carotid artery
stenting has not been shown to be equally useful.[70][71] Patients are selected for surgery based on age, gender,
degree of stenosis, time since symptoms and patients' preferences.[43] Surgery is most efficient when not
delayed too long —the risk of recurrent stroke in a patient who has a 50% or greater stenosis is up to 20% after
5 years, but endarterectomy reduces this risk to around 5%. The number of procedures needed to cure one
patient was 5 for early surgery (within two weeks after the initial stroke), but 125 if delayed longer than 12

Screening for carotid artery narrowing has not been shown to be a useful screening test in the general
population.[74] Studies of surgical intervention for carotid artery stenosis without symptoms have shown only a
small decrease in the risk of stroke.[75][76] To be beneficial, the complication rate of the surgery should be kept
below 4%. Even then, for 100 surgeries, 5 patients will benefit by avoiding stroke, 3 will develop stroke despite
surgery, 3 will develop stroke or die due to the surgery itself, and 89 will remain stroke-free but would also have
done so without intervention.[43]

Nutritional and metabolic interventions

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

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

The European Society of Cardiology and the European Association for Cardiovascular Prevention and
Rehabilitation have developed an interactive tool for prediction and managing the risk of heart attack and stroke
in Europe. HeartScore is aimed at supporting clinicians in optimising individual cardiovascular risk reduction.
The Heartscore Programme is available in 12 languages and offers web based or PC version [81].

Stroke unit

Ideally, people who have had a stroke are admitted to a "stroke unit", a ward or dedicated area in hospital
staffed by nurses and therapists with experience in stroke treatment. It has been shown that people admitted to a
stroke unit have a higher chance of surviving than those admitted elsewhere in hospital, even if they are being
cared for by doctors without experience in stroke.[2]

When an acute stroke is suspected by history and physical examination, the goal of early assessment is to
determine the cause. Treatment varies according to the underlying cause of the stroke, thromboembolic

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(ischemic) or hemorrhagic. A non-contrast head CT scan can rapidly identify a hemorrhagic stroke by imaging
bleeding in or around the brain. If no bleeding is seen, a presumptive diagnosis of ischemic stroke is made.

Treatment of ischemic stroke

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

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

In addition to definitive therapies, management of acute stroke includes control of blood sugars, ensuring the
patient has adequate oxygenation and adequate intravenous fluids. Patients may be positioned with their heads
flat on the stretcher, rather than sitting up, to increase blood flow to the brain. It is common for the blood
pressure to be elevated immediately following a stroke. Although high blood pressure may cause some strokes,
hypertension during acute stroke is desirable to allow adequate blood flow to the brain.


In increasing numbers of primary stroke centers, pharmacologic thrombolysis ("clot busting") with the drug
tissue plasminogen activator (tPA), is used to dissolve the clot and unblock the artery. However, the use of tPA
in acute stroke is controversial. On one hand, it is endorsed by the American Heart Association and the
American Academy of Neurology as the recommended treatment for acute stroke within three hours of onset of
symptoms as long as there are not other contraindications (such as abnormal lab values, high blood pressure, or
recent surgery). This position for tPA is based upon the findings of two studies by one group of investigators[83]
which showed that tPA improves the chances for a good neurological outcome. When administered within the
first three hours, 39% of all patients who were treated with tPA had a good outcome at three months, only 26%
of placebo controlled patients had a good functional outcome. A recent study using alteplase for thrombolysis in
ischemic stroke suggests clinical benefit with administration 3 to 4.5 hours after stroke onset.[84] However, in
the NINDS trial 6.4% of patients with large strokes developed substantial brain hemorrhage as a complication
from being given tPA. A recent study found the mortality to be higher among patients receiving tPA versus those
who did not.[85] 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.[86].

Intra-artial fibrinolysis, where a catherter 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.[87]

Mechanical thrombectomy

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Another intervention for acute ischemic stroke is removal of the offending

thrombus directly. This is accomplished by inserting a catheter into the femoral
artery, directing it into the cerebral circulation, and deploying a corkscrew-like
device to ensnare the clot, which is then withdrawn from the body. Mechanical
embolectomy devices have been demonstrated effective at restoring blood flow in
patients who were unable to receive thrombolytic drugs or for whom the drugs were
ineffective,[88][89][90][91] though no differences have been found between newer
and older versions of the devices.[92] The devices have only been tested on patients
treated with mechanical clot embolectomy within eight hours of the onset of

Angioplasty and stenting Merci Retriever L5.

Angioplasty and stenting have begun to be looked at as possible viable options in

treatment of acute ischemic stroke. In a systematic review of six uncontrolled, single-center trials, involving a
total of 300 patients, of intra-cranial stenting in symptomatic intracranial arterial stenosis, the rate of technical
success (reduction to stenosis of <50%) ranged from 90-98%, and the rate of major peri-procedural
complications ranged from 4-10%. The rates of restenosis and/or stroke following the treatment were also
favorable.[93] This data suggests that a large, randomized controlled trial is needed to more completely evaluate
the possible therapeutic advantage of this treatment.

Therapeutic hypothermia

Main article: therapeutic hypothermia

Most of the data concerning therapeutic hypothermia’s effectiveness in treating ischemic stroke is limited to
animal studies. These studies have focused primarily on ischemic as opposed to hemorrhagic stroke, as
hypothermia has been associated with a lower clotting threshold. In these animal studies investigating the effect
of temperature decline following ischemic stroke, hypothermia has been shown to be an effective all-purpose
neuroprotectant.[94] This promising data has led to the initiation of a variety of human studies. At the time of
this article’s publishing, this research has yet to return results. However, in terms of feasibility, the use of
hypothermia to control intracranial pressure (ICP) after an ischemic stroke was found to be both safe and
practical. The device used in this study was called the Arctic Sun.[95]

Secondary prevention of ischemic stroke

Anticoagulation can prevent recurrent stroke. Among patients with nonvalvular atrial fibrillation,
anticoagulation can reduce stroke by 60% while antiplatelet agents can reduce stroke by 20%.[96]. However, a
recent meta-analysis suggests harm from anti-coagulation started early after an embolic stroke.[97] Stroke
prevention treatment for atrial fibrillation is determined according to the CHADS/CHADS2 system.

If studies show carotid stenosis, and the patient has residual function in the affected side, carotid
endarterectomy (surgical removal of the stenosis) may decrease the risk of recurrence if performed rapidly after

Treatment of hemorrhagic stroke

Patients with intracerebral hemorrhage require neurosurgical evaluation to detect and treat the cause of the

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bleeding, although many may not need surgery. Anticoagulants and antithrombotics, key in treating ischemic
stroke, can make bleeding worse and cannot be used in intracerebral hemorrhage. Patients are monitored and
their blood pressure, blood sugar, and oxygenation are kept at optimum levels.

Care and rehabilitation

Stroke rehabilitation is the process by which patients with disabling strokes undergo treatment to help them
return to normal life as much as possible by regaining and relearning the skills of everyday living. It also aims to
help the survivor understand and adapt to difficulties, prevent secondary complications and educate family
members to play a supporting role.

A rehabilitation team is usually multidisciplinary as it involves staff with different skills working together to help
the patient. These include nursing staff, physiotherapy, occupational therapy, speech and language therapy, and
usually a physician trained in rehabilitation medicine. Some teams may also include psychologists, social
workers, and pharmacists since at least one third of the patients manifest post stroke depression. Validated
instruments such as the Barthel scale may be used to assess the likelihood of a stroke patient being able to
manage at home with or without support subsequent to discharge from hospital.

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

For most stroke patients, physical therapy (PT) and occupational therapy (OT) are the cornerstones of the
rehabilitation process, but in many countries Neurocognitive Rehabilitation is used, too. Often, assistive
technology such as a wheelchair, walkers, canes, and orthosis may be beneficial. PT and OT have overlapping
areas of working but their main attention fields are; PT involves re-learning functions as transferring, walking
and other gross motor functions. OT focusses on exercises and training to help relearn everyday activities
known as the Activities of daily living (ADLs) such as eating, drinking, dressing, bathing, cooking, reading and
writing, and toileting. Speech and language therapy is appropriate for patients with problems understanding
speech or written words, problems forming speech and problems with swallowing.

Patients may have particular problems, such as complete or partial inability to swallow, which can cause
swallowed material to pass into the lungs and cause aspiration pneumonia. The condition may improve with
time, but in the interim, a nasogastric tube may be inserted, enabling liquid food to be given directly into the
stomach. If swallowing is still unsafe after a week, then a percutaneous endoscopic gastrostomy (PEG) tube is
passed and this can remain indefinitely.

Stroke rehabilitation should be started as 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, 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 : proper diet and exercise are known to help the brain to recover.

Disability affects 75% of stroke survivors enough to decrease their employability.[98] 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.[99] Dysfunctions correspond to areas in the brain that have been damaged.

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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.

Emotional problems resulting from stroke can result from direct damage to emotional centers in the brain or
from frustration and difficulty adapting to new limitations. Post-stroke emotional difficulties include anxiety,
panic attacks, flat affect (failure to express emotions), mania, apathy, and psychosis.

30 to 50% of stroke survivors suffer post stroke depression, which is characterized by lethargy, irritability, sleep
disturbances, lowered self esteem, and withdrawal.[100] Depression can reduce motivation and worsen outcome,
but can be treated with antidepressants.

Emotional lability, another consequence of stroke, causes the patient to switch quickly between emotional highs
and lows and to express emotions inappropriately, for instance with an excess of laughing or crying with little or
no provocation. While these expressions of emotion usually correspond to the patient's actual emotions, a more
severe form of emotional lability causes patients to laugh and cry pathologically, without regard to context or
emotion.[98] Some patients show the opposite of what they feel, for example crying when they are happy.[101]
Emotional lability occurs in about 20% of stroke patients.

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

Up to 10% of all stroke patients develop seizures, most commonly in the week subsequent to the event; the
severity of the stroke increases the likelihood of a seizure.[102][103]

Stroke could soon be the most common cause of death worldwide.[104] Stroke is currently the second leading
cause of death in the Western world, ranking after heart disease and before cancer,[2] and causes 10% of deaths
worldwide.[105] 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.[106] Advanced
age is one of the most significant stroke risk factors. 95% of strokes occur in people age 45 and older, and
two-thirds of strokes occur in those over the age of 65.[100][20] A person's risk of dying if he or she does have a
stroke also increases with age. However, stroke can occur at any age, including in fetuses.

Family members may have a genetic tendency for stroke or share a lifestyle that contributes to stroke. Higher
levels of Von Willebrand factor are more common amongst people who have had ischemic stroke for the first
time.[107] The results of this study found that the only significant genetic factor was the person's blood type.
Having had a stroke in the past greatly increases one's risk of future strokes.

Men are 25% more likely to suffer strokes than women,[20] yet 60% of deaths from stroke occur in women.[101]
Since women live longer, they are older on average when they have their strokes and thus more often killed
(NIMH 2002).[20] Some risk factors for stroke apply only to women. Primary among these are pregnancy,

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childbirth, menopause and the treatment thereof (HRT).

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.[108][109]

The word stroke was used as a synonym for apoplectic seizure as early as
1599,[110] and is a fairly literal translation of the Greek term.

In 1658, in his Apoplexia, Johann Jacob Wepfer (1620–1695) identified the

cause of hemorrhagic stroke when he suggested that people who had died of
apoplexy had bleeding in their brains.[108][20] Wepfer also identified the main Hippocrates first described
arteries supplying the brain, the vertebral and carotid arteries, and identified the the sudden paralysis that is
cause of ischemic stroke [also known as cerebral infarction] when he suggested often associated with
that apoplexy might be caused by a blockage to those vessels.[20] stroke.

Rudolf Virchow first described the mechanism of thromboembolism as a major factor.[111]

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