Stroke - Wikipedia, The Free Encyclopedia

Stroke - Wikipedia, the free encyclopedia http://en.wikipedia.org/w/index.php?
title=Stroke&printable=yes
Stroke
From Wikipedia, the free encyclopedia
A stroke, previously known medically as a Stroke

cerebrovascular accident (CVA), is the
Classification and external resources
rapidly developing loss of brain function(s)
due 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 an inability to see one side of the
visual field.[2]
CT scan slice of the brain showing a right-
A stroke is a medical emergency and can hemispheric ischemic stroke (left side of image).
cause permanent neurological damage,
ICD-10 I61. (http://apps.who.int
complications, and lead to death. It is the
/classifications/apps/icd/icd10online
leading cause of adult disability in the
United States and Europe and it is the /?gi60.htm+i61) -I64.
(http://apps.who.int/classifications
second leading cause of death worldwide.[3]
/apps/icd/icd10online
Risk factors for stroke include advanced
age, hypertension (high blood pressure), /?gi60.htm+i64)
previous stroke or transient ischemic attack ICD-9 434.91 (http://www.icd9data.com
(TIA), diabetes, high cholesterol, cigarette /getICD9Code.ashx?icd9=434.91)
smoking and atrial fibrillation.[2] High
OMIM 601367
blood pressure is the most important
(http://www.ncbi.nlm.nih.gov
modifiable risk factor of stroke.[2] /omim/601367)
An ischemic stroke is occasionally treated in DiseasesDB 2247
a hospital with thrombolysis (also known as (http://www.diseasesdatabase.com
a "clot buster"), and some hemorrhagic /ddb2247.htm)
strokes benefit from neurosurgery.
Treatment to recover any lost function is MedlinePlus 000726 (http://www.nlm.nih.gov
termed stroke rehabilitation, ideally in a /medlineplus/ency/article
stroke unit and involving health professions /000726.htm)
such as speech and language therapy, eMedicine neuro/9 (http://www.emedicine.com
physical therapy and occupational therapy. /neuro/topic9.htm) emerg/558
Prevention of recurrence may involve the
(http://www.emedicine.com/emerg
administration of antiplatelet drugs such as
/topic558.htm#) emerg/557
aspirin and dipyridamole, control and
reduction of hypertension, and the use of
1 of 31 13/03/11 10:42 PM
Stroke - Wikipedia, the free encyclopedia http://en.wikipedia.org/w/index.php?title=Stroke&printable=yes
statins. Selected patients may benefit from

carotid endarterectomy and the use of (http://www.emedicine.com/emerg
anticoagulants.[2] /topic557.htm#) pmr/187
(http://www.emedicine.com
/pmr/topic187.htm#)
Contents MeSH D020521 (http://www.nlm.nih.gov

/cgi/mesh/2010/MB_cgi?field=uid&
1 Definition term=D020521)
2 Classification
2.1 Ischemic
2.2 Hemorrhagic
3 Signs and symptoms
3.1 Early recognition
3.2 Subtypes
3.3 Associated symptoms
4 Causes
5 Pathophysiology
5.1 Ischemic
5.2 Hemorrhagic
6 Diagnosis
6.1 Physical examination
6.2 Imaging
6.3 Underlying etiology
7 Prevention
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 interventions
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
8.3 Secondary prevention of
ischemic stroke
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8.4 Treatment of hemorrhagic

stroke
9 Care and rehabilitation
10 Prognosis
11 Epidemiology
12 History
13 External Links
14 References
15 Further reading
Definition
The traditional definition of stroke , devised by the World Health Organization in the 1970s,[4]
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.[5]
Classification
Strokes can be classified into two major categories: ischemic
and hemorrhagic.[6] 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. About 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 A slice of brain from the
actually start as ischemic stroke.[2] autopsy of a person who
suffered an acute middle
Ischemic cerebral artery (MCA) stroke
Main articles: Cerebral infarction and Brain ischemia
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)
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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)[7]
4. Venous thrombosis.[8]
Stroke without an obvious explanation is termed "cryptogenic" (of unknown origin); this
constitutes 30-40% of all ischemic strokes.[2][9]
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.
[10][11]
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][12]
Hemorrhagic
Main articles: Intracranial hemorrhage and intracerebral hemorrhage
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
with associated
Signs and symptoms intraventricular
hemorrhage.
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 brain
affected, the more functions that are likely to be lost. Some forms of stroke can cause
additional symptoms. For example, in intracranial hemorrhage, the affected area may compress
other structures. Most forms of stroke are not associated with headache, apart from
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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).[13] 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 (stroke) (face, arm, speech, and time),[14] 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)[15] and the Cincinnati Prehospital Stroke
Scale (CPSS).[16] Use of these scales is recommended by professional guidelines.[17]
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.[17][18]
Subtypes
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:
hemiplegia and muscle weakness of the face

numbness
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
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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 symptoms:
aphasia (difficulty with verbal expression, auditory comprehension, reading and/or

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)
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 the brain.
If symptoms are maximal at onset, the cause is more likely to be a subarachnoid hemorrhage or
an embolic stroke.
Causes
Thrombotic stroke
In thrombotic stroke a thrombus (blood clot) usually forms around atherosclerotic plaques.
Since blockage of the artery is gradual, onset of symptomatic thrombotic strokes is slower. A
thrombus itself (even if non-occluding) can lead to an embolic stroke (see below) if the
thrombus breaks off, at which point it is called an "embolus." Two types of thrombosis can
cause stroke:
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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
plaques).
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.[19]
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 solves the problem only 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:[20]
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), complex atheroma in the
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ascending aorta or proximal arch
Systemic hypoperfusion
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.[8]
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]).
Pathophysiology
Ischemic
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Ischemic stroke occurs due to a loss of blood supply to part

of the brain, initiating the ischemic cascade.[21] 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 Micrograph showing cortical
narrowing the lumen of blood vessels leading to a reduction pseudolaminar necrosis, a
of blood flow, by causing the formation of blood clots within finding seen in strokes on
the vessel, or by releasing showers of small emboli through medical imaging and at autopsy.
the disintegration of atherosclerotic plaques. Embolic H&E-LFB stain.
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 adenosine triphosphate (ATP) but
releases a by-product called lactic acid. Lactic acid is an
irritant which could potentially destroy cells since it is an
acid and disrupts the normal acid-base balance in the brain.
The ischemia area is referred to as the "ischemic
penumbra".[22]
Then, as oxygen or glucose becomes depleted in ischemic

brain tissue, the production of high energy phosphate
compounds such as adenosine triphosphate (ATP) fails, Micrograph of the superficial
leading to failure of energy-dependent processes (such as ion cerebral cortex showing neuron
pumping) necessary for tissue cell survival. This sets off a loss and reactive astrocytes in a
series of interrelated events that result in cellular injury and person that suffered a stroke.
death. A major cause of neuronal injury is release of the H&E-LFB stain.
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.
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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.[19]
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.[23]
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.[19]
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.
Hemorrhagic
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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 vasculature.[19]
Diagnosis
Stroke is diagnosed through several techniques: a
neurological examination (such as the Nihss), CT scans Head CT showing deep
(most often without contrast enhancements) or MRI intracerebral hemorrhage due to
scans, Doppler ultrasound, and arteriography. The bleeding within the cerebellum,
diagnosis of stroke itself is clinical, with assistance from approximately 30 hours old.
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.[24]
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 scale.
Imaging
For diagnosing ischemic stroke in the emergency setting:[25]
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%
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MRI scan
sensitivity= 81%
specificity= 100%
For detecting chronic hemorrhages, MRI scan is more sensitive.[26]
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 homocysteinuria
Prevention
Given the disease burden of strokes, prevention is an important public health concern.[27]
Primary prevention is less effective than secondary prevention (as judged by the number
needed to treat to prevent one stroke per year).[27] Recent guidelines detail the evidence for
primary prevention in stroke.[28] 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.[29][30]
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[31][32]).
Other modifiable risk factors include high blood cholesterol levels, diabetes, cigarette
smoking[33][34] (active and passive), heavy alcohol consumption[35] and drug use,[36] lack of
12 of 31 13/03/11 10:42 PM
physical activity, obesity and unhealthy diet.[37] 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).[38] The drugs most commonly associated with stroke are cocaine,
amphetamines causing hemorrhagic stroke, but also over-the-counter cough and cold drugs
containing sympathomimetics.[39][40]
No high quality studies have shown the effectiveness of interventions aimed at weight
reduction, promotion of regular exercise, reducing alcohol consumption or smoking
cessation.[41] Nonetheless, given the large body of circumstantial evidence, best medical
management for stroke includes advice on diet, exercise, smoking and alcohol use.[42]
Medication or drug therapy is the most common method of stroke prevention; carotid
endarterectomy can be a useful surgical method of preventing stroke.
Blood pressure
Hypertension accounts for 35-50% of stroke risk.[43] 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.[44] Lowering blood pressure has been conclusively shown to
prevent both ischemic and hemorrhagic strokes.[45][46] It is equally important in secondary
prevention.[47] Even patients older than 80 years and those with isolated systolic hypertension
benefit from antihypertensive therapy.[48][49][50] Studies show that intensive antihypertensive
therapy results in a greater risk reduction.[51] 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.[51][52]
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.[53] Depending on the stroke risk,
anticoagulation with medications such as coumarins or aspirin is warranted for stroke
prevention.[54]
Blood lipids
High cholesterol levels have been inconsistently associated with (ischemic) stroke.[46][55]
Statins have been shown to reduce the risk of stroke by about 15%.[56] Since earlier
meta-analyses of other lipid-lowering drugs did not show a decreased risk,[57] statins might
exert their effect through mechanisms other than their lipid-lowering effects.[56]
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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.[58][59]
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.[29] 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.[60] Thienopyridines (clopidogrel, ticlopidine) "might
be slightly more effective" than aspirin and have a decreased risk of gastrointestinal bleeding,
but they are more expensive.[61] Their exact role remains controversial. Ticlopidine has more
skin rash, diarrhea, neutropenia and thrombotic thrombocytopenic purpura.[61] Dipyridamole
can be added to aspirin therapy to provide a small additional benefit, even though headache is a
common side effect.[62] Low-dose aspirin is also effective for stroke prevention after
sustaining a myocardial infarction.[30] Except for in atrial fibrillation, oral anticoagulants are
not advised for stroke prevention —any benefit is offset by bleeding risk.[63]
In primary prevention however, antiplatelet drugs did not reduce the risk of ischemic stroke
while increasing the risk of major bleeding.[64][65] Further studies are needed to investigate a
possible protective effect of aspirin against ischemic stroke in women.[66][67]
Surgery
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.[42] Endarterectomy for a significant stenosis has been shown to be useful in the
secondary prevention after a previous symptomatic stroke.[68] Carotid artery stenting has not
been shown to be equally useful.[69][70] Patients are selected for surgery based on age, gender,
degree of stenosis, time since symptoms and patients' preferences.[42] Surgery is most efficient
when not delayed too long —the risk of recurrent stroke in a patient who has a 50% or greater
stenosis is up to 20% after 5 years, but endarterectomy reduces this risk to around 5%. The
number of procedures needed to cure one patient was 5 for early surgery (within two weeks
after the initial stroke), but 125 if delayed longer than 12 weeks.[71][72]
Screening for carotid artery narrowing has not been shown to be a useful screening test in the
general population.[73] Studies of surgical intervention for carotid artery stenosis without
14 of 31 13/03/11 10:42 PM
symptoms have shown only a small decrease in the risk of stroke.[74][75] 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.[42]
Nutritional and metabolic interventions
Nutrition, specifically the Mediterranean-style diet, has the potential of more than halving
stroke risk.[76]
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.[77]
However, the two largest randomized controlled trials included in the meta-analysis had
conflicting results. One reported positive results;[78] whereas the other was negative.[79]
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.[80]
Treatment
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 (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 die.[81]
15 of 31 13/03/11 10:42 PM
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.[29]
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.
Thrombolysis
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[82] 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.[83] 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.[84] 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.[85]
Intra-arterial 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.[86]
Mechanical thrombectomy
16 of 31 13/03/11 10:42 PM
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,[87][88][89][90] though
no differences have been found between newer and older versions
of the devices.[91] The devices have only been tested on patients
treated with mechanical clot embolectomy within eight hours of the
Merci Retriever L5.
onset of symptoms.
Angioplasty and stenting
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.[92] This data suggests that a large, randomized
controlled trial is needed to more completely evaluate the possible therapeutic advantage of
this treatment.
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%.[93] However, a recent meta-analysis suggests harm from anti-coagulation
started early after an embolic stroke.[94] Stroke prevention treatment for atrial fibrillation is
determined according to the CHADS/CHADS2 system. The most widely used anticoagulant to
prevent thromboembolic stroke in patients with nonvalvular atrial fibrillation is the oral agent
Warfarin while dabigatran is a new alternative which does not require prothrombin time
monitoring.
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 stroke.
Treatment of hemorrhagic stroke

Patients with intracerebral hemorrhage require neurosurgical evaluation to detect and treat the
cause of the bleeding, although many may not need surgery. Anticoagulants and
antithrombotics, key in treating ischemic stroke, can make bleeding worse and cannot be used
in intracerebral hemorrhage. Patients are monitored for changes in the level of consciousness,
17 of 31 13/03/11 10:42 PM
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), speech-
language pathology (SLP) are the cornerstones of the rehabilitation process. 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 the speech production disorders:
dysarthria and apraxia of speech, aphasia, cognitive-communication impairments and/or
dysphagia (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 deemed unsafe,
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
18 of 31 13/03/11 10:42 PM
impossible and most patients will improve to some extent : proper diet and exercise are known
to help the brain to recover.
Prognosis
Disability affects 75% of stroke survivors enough to decrease their employability.[95] 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.[96] Dysfunctions
correspond to areas in the brain that have been damaged.
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.[97] 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.[95] Some
patients show the opposite of what they feel, for example crying when they are happy.[98]
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.[99][100]
Epidemiology
19 of 31 13/03/11 10:42 PM
Stroke could soon be the most common cause of death worldwide.[101] 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.[102] 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.[103] 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.[97][19]
A person's risk of dying if he or she does have a stroke also increases with age. However,
stroke can occur at any age, including in childhood.
Family members may have a genetic tendency for stroke or share a lifestyle that contributes to
stroke. Higher levels of Von Willebrand factor are more common amongst people who have
had ischemic stroke for the first time.[104] 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,[19] yet 60% of deaths from stroke
occur in women.[98] Since women live longer, they are older on average when they have their
strokes and thus more often killed (NIMH 2002).[19] 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.[105] 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.[106][107]
The word stroke was used as a synonym for apoplectic seizure as

early as 1599,[108] and is a fairly literal translation of the Greek Hippocrates first described
term. the sudden paralysis that is
often associated with
In 1658, in his Apoplexia, Johann Jacob Wepfer (1620–1695) stroke.
identified the cause of hemorrhagic stroke when he suggested
that people who had died of apoplexy had bleeding in their
brains.[106][19] Wepfer also identified the main arteries supplying the brain, the vertebral and
carotid arteries, and identified the cause of ischemic stroke [also known as cerebral infarction]
20 of 31 13/03/11 10:42 PM
when he suggested that apoplexy might be caused by a blockage to those vessels.[19]
Rudolf Virchow first described the mechanism of thromboembolism as a major factor.[109]
External Links
Imaging CVA (http://rad.usuhs.edu/medpix/master.php3?mode=image_finder&
action=search&srchstr=stroke#top) CT, MR, Angiography of Stroke
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Further reading
J. P. Mohr, Dennis Choi, James Grotta, Philip Wolf (2004). Stroke: Pathophysiology,
Diagnosis, and Management. New York: Churchill Livingstone. ISBN 0-443-06600-0.
OCLC 52990861 50477349 52990861 (http://www.worldcat.org/oclc/50477349) .
Charles P. Warlow, Jan van Gijn, Martin S. Dennis, Joanna M. Wardlaw, John M.
Bamford, Graeme J. Hankey, Peter A. G. Sandercock, Gabriel Rinkel, Peter Langhorne,
Cathie Sudlow, Peter Rothwell (2008). Stroke: Practical Management (3rd ed.). Wiley-
Blackwell. ISBN 1-4051-2766-X.
Retrieved from "http://en.wikipedia.org/wiki/Stroke"
Categories: Stroke | Aging-associated diseases | Cerebrovascular diseases
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A stroke, previously known medically as a Stroke

statins. Selected patients may benefit from

Contents MeSH D020521 (http://www.nlm.nih.gov

8.4 Treatment of hemorrhagic

Main articles: Cerebral infarction and Brain ischemia

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

Intracranial hemorrhage is the accumulation of blood anywhere

subarachnoid hemorrhage and cerebral venous thrombosis and occasionally intracerebral

hemiplegia and muscle weakness of the face

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

aphasia (difficulty with verbal expression, auditory comprehension, reading and/or

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

An embolic stroke refers to the blockage of an artery by an arterial embolus, a travelling

Cardiac causes can be distinguished between high and low-risk:[20]

ascending aorta or proximal arch

It generally occurs in small arteries or arterioles and is commonly due to hypertension,

Ischemic stroke occurs due to a loss of blood supply to part

Then, as oxygen or glucose becomes depleted in ischemic

Hemorrhagic strokes result in tissue injury by causing

For diagnosing ischemic stroke in the emergency setting:[25]

CT scans (without contrast enhancements)

For diagnosing hemorrhagic stroke in the emergency setting:

CT scans (without contrast enhancements)

For detecting chronic hemorrhages, MRI scan is more sensitive.[26]

an ultrasound/doppler study of the carotid arteries (to detect carotid stenosis) or

Surgical procedures such as carotid endarterectomy or carotid angioplasty can be used to

Nutritional and metabolic interventions

Treatment of ischemic stroke

In addition to definitive therapies, management of acute stroke includes control of blood

In increasing numbers of primary stroke centers, pharmacologic thrombolysis ("clot busting")

Another intervention for acute ischemic stroke is removal of the

Angioplasty and stenting

Secondary prevention of ischemic stroke

Treatment of hemorrhagic stroke

Care and rehabilitation

A rehabilitation team is usually multidisciplinary as it involves staff with different skills

The word stroke was used as a synonym for apoplectic seizure as

when he suggested that apoplexy might be caused by a blockage to those vessels.[19]

Rudolf Virchow first described the mechanism of thromboembolism as a major factor.[109]

thrombolysis.". Pathophysiology : the (http://www.ncbi.nlm.nih.gov/pubmed

artid=64503. /presenter.jhtml?identifier=4716) . American

(http://www.ncbi.nlm.nih.gov/pubmed 49. ^ Staessen JA, Gasowski J, Wang JG, et al.

(http://www.ncbi.nlm.nih.gov/pubmed diabetes (UKPDS 33). UK Prospective

. PMID 16087900 doi:10.1056/NEJMoa060900

(http://www.ncbi.nlm.nih.gov/pubmed (2008). "Vertebrobasilar revascularization

(http://dx.doi.org Global Burden of Disease Study". Lancet

/strokeintime.html) . MERGINET.com 6 (9). PMC 1034034

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