Stroke

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Stroke
Classification and external resources

! scan slice of the brain sho"ing a right# hemispheric ischemic stroke (left side of image). ICD-10 $%&#$%'ner ICD-9 '('.)& OMIM %*&(%+ DiseasesDB ,,'+ MedlinePlus ***+,% neuro-) emerg-../ emerg-..+ eMedicine pmr-&/+ MeSH 0*,*.,& 1 stroke, or cerebrovascular accident (CVA), is the rapid loss of brain function(s) due to disturbance in the blood supply to the brain. !his can be due to ischemia (lack of blood flo") caused by blockage (thrombosis, arterial embolism), or a hemorrhage.2&3 1s a result, the affected area of the brain cannot function, "hich might result in an 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.2,3 1 stroke is a medical emergency and can cause permanent neurological damage, complications, and death. 4isk factors for stroke include old age, hypertension (high blood pressure), previous stroke or transient ischemic attack (!$1), diabetes, high cholesterol, cigarette smoking and atrial fibrillation.2,3 5igh blood pressure is the most important modifiable risk factor of stroke.2,3 $t is the second leading cause of death "orld"ide.2(3 1n ischemic stroke is occasionally treated in a hospital "ith thrombolysis (also kno"n as a 6clot buster6), and some hemorrhagic strokes benefit from neurosurgery. !reatment to recover any lost function is termed stroke rehabilitation, ideally in a stroke unit and involving health professions such as speech and language therapy, physical therapy and occupational therapy. 7revention of recurrence may involve the administration of antiplatelet drugs such as aspirin and dipyridamole, control and reduction of hypertension, and the use of statins. Selected patients may benefit from carotid endarterectomy and the use of anticoagulants.2,3

Contents

& lassification o &.& $schemic

o

&., 5emorrhagic

, Signs and symptoms

o o o

,.& 8arly recognition ,., Subtypes ,.( 1ssociated symptoms

( auses
o o o o o o

(.& !hrombotic stroke (., 8mbolic stroke (.( Systemic hypoperfusion (.' 9enous thrombosis (.. $ntracerebral hemorrhage (.% Silent stroke

' 7athophysiology
o o

'.& $schemic '., 5emorrhagic

. 0iagnosis
o o o o

..& 0efinition .., 7hysical e:amination ..( $maging ..' ;nderlying cause

% 7revention
o o

%.& 4isk factors %., Secondary prevention of ischemic stroke

+ <anagement
o o o o

+.& $schemic stroke +., 5emorrhagic stroke +.( Stroke unit +.' 4ehabilitation

/ 7rognosis ) 8pidemiology &* 5istory && 4esearch

o o

&&.& 1ngioplasty and stenting &&., =europrotection

&, 4eferences &( Further reading &' 8:ternal links

Classi ication
1 slice of brain from the autopsy of a person "ho suffered an acute middle cerebral artery (< 1) stroke Strokes can be classified into t"o ma>or categories: ischemic and hemorrhagic.2'3 $schemic strokes are those that are caused by interruption of the blood supply, "hile hemorrhagic strokes are the ones "hich result from rupture of a blood vessel or an abnormal vascular structure. 1bout /+? of strokes are caused by ischemia, and the remainder by hemorrhage. Some hemorrhages develop inside areas of ischemia (6hemorrhagic transformation6). $t is unkno"n ho" many hemorrhages actually start as ischemic stroke.2,3

Isc!e"ic
<ain articles: erebral infarction and @rain ischemia $n an ischemic stroke, blood supply to part of the brain is decreased, leading to dysfunction of the brain tissue in that area. !here are four reasons "hy this might happen: &. !hrombosis (obstruction of a blood vessel by a blood clot forming locally) 2. 8mbolism (obstruction due to an embolus from else"here in the body, see belo"),2,3 (. Systemic hypoperfusion (general decrease in blood supply, e.g., in shock)2.3

4. 9enous thrombosis.2%3

Stroke "ithout an obvious e:planation is termed 6cryptogenic6 (of unkno"n origin)A this constitutes (*#'*? of all ischemic strokes.2,32+3 !here are various classification systems for acute ischemic stroke. !he B:ford ommunity Stroke 7ro>ect classification (B S7, also kno"n as the @amford or B:ford classification) relies primarily on the initial symptomsA based on the e:tent of the symptoms, the stroke episode is classified as total anterior circulation infarct (!1 $), partial anterior circulation infarct (71 $), lacunar infarct (C1 $) or posterior circulation infarct (7B $). !hese four entities predict the e:tent of the stroke, the area of the brain affected, the underlying cause, and the prognosis. 2/32)3 !he !B1S! (!rial of Brg &*&+, in 1cute Stroke !reatment) classification is based on clinical symptoms as "ell as results of further investigationsA on this basis, a stroke is classified as being due to (&) thrombosis or embolism due to atherosclerosis of a large artery, (,) embolism of cardiac origin, (() occlusion of a small blood vessel, (') other determined cause, (.) undetermined cause (t"o possible causes, no cause identified, or incomplete investigation).2,32&*3

He"orr!a#ic
<ain articles: $ntracranial hemorrhage and intracerebral hemorrhage

1n intraparenchymal bleed (bottom arro") "ith surrounding edema (top arro") $ntracranial hemorrhage is the accumulation of blood any"here "ithin the skull vault. 1 distinction is made bet"een intra#a:ial hemorrhage (blood inside the brain) and e:tra#a:ial hemorrhage (blood inside the skull but outside the brain). $ntra#a:ial hemorrhage is due to intraparenchymal hemorrhage or intraventricular hemorrhage (blood in the ventricular system). !he main types of e:tra#a:ial hemorrhage are epidural hematoma (bleeding bet"een the dura mater and the skull), subdural hematoma (in the subdural space) and subarachnoid hemorrhage (bet"een the arachnoid mater and pia mater). <ost of the hemorrhagic stroke syndromes have specific symptoms (e.g., headache, previous head in>ury).

Si#ns and s$"%to"s

Stroke symptoms typically start suddenly, over seconds to minutes, and in most cases do not progress further. !he symptoms depend on the area of the brain affected. !he more e:tensive the area of brain affected, the more functions that are likely to be lost. Some forms of stroke can cause additional symptoms. For e:ample, in intracranial hemorrhage, the affected area may compress other structures. <ost forms of stroke are not associated "ith headache, apart from subarachnoid hemorrhage and cerebral venous thrombosis and occasionally intracerebral hemorrhage.

&arl$ reco#nition
9arious systems have been proposed to increase recognition of stroke. 0ifferent findings are able to predict the presence or absence of stroke to different degrees. Sudden#onset face "eakness, arm drift (i.e., if a person, "hen asked to raise both arms, involuntarily lets one arm drift do"n"ard) and abnormal speech are the findings most likely to lead to the correct identification of a case of stroke increasing the likelihood by ... "hen at least one of these is present). Similarly, "hen all three of these are absent, the likelihood of stroke is significantly decreased (D likelihood ratio of *.()).2&&3 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.

7roposed systems include F1S! (stroke) (face, arm, speech, and time),2&,3 as advocated by the 0epartment of 5ealth (;nited Eingdom) and !he Stroke 1ssociation, the 1merican Stroke 1ssociation (""".strokeassociation.org), =ational Stroke 1ssociation (;S """.stroke.org), the Cos 1ngeles 7rehospital Stroke Screen (C17SS)2&(3 and the incinnati 7rehospital Stroke Scale ( 7SS).2&'3 ;se of these scales is recommended by professional guidelines.2&.3 For people referred to the emergency room, early recognition of stroke is deemed important as this can e:pedite diagnostic tests and treatments. 1 scoring system called 4BS$84 (recognition of stroke in the emergency room) is recommended for this purposeA it is based on features from the medical history and physical e:amination.2&.32&%3

Subt$%es
$f the area of the brain affected contains one of the three prominent central nervous system path"aysFthe spinothalamic tract, corticospinal tract, and dorsal column (medial lemniscus), symptoms may include:

hemiplegia and muscle "eakness of the face numbness reduction in sensory or vibratory sensation initial flaccidity (hypotonicity), replaced by spasticity (hypertonicity), hyperrefle:ia, and obligatory synergies.2&+3

$n most cases, the symptoms affect only one side of the body (unilateral). 0epending on the part of the brain affected, the defect in the brain is usually on the opposite side of the body. 5o"ever, since these path"ays 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. $n addition to the above =S path"ays, the brainstem gives rise to most of the t"elve cranial nerves. 1 stroke affecting the brain stem and brain therefore can produce symptoms relating to deficits in these cranial nerves:

altered smell, taste, hearing, or vision (total or partial) drooping of eyelid (ptosis) and "eakness of ocular muscles decreased refle:es: gag, s"allo", pupil reactivity to light decreased sensation and muscle "eakness of the face balance problems and nystagmus altered breathing and heart rate "eakness in sternocleidomastoid muscle "ith inability to turn head to one side "eakness in tongue (inability to protrude and-or move from side to side)

$f the cerebral cortex is involved, the =S path"ays can again be affected, but also can produce the follo"ing symptoms:

aphasia (difficulty "ith verbal e:pression, auditory comprehension, reading and-or "riting @rocaGs or WernickeGs area typically involved) dysarthria (motor speech disorder resulting from neurological in>ury) apra:ia (altered voluntary movements) visual field defect memory deficits (involvement of temporal lobe) hemineglect (involvement of parietal lobe) disorganiHed thinking, confusion, hyperse:ual gestures ("ith involvement of frontal lobe) lack of insight of his or her, usually stroke#related, disability

$f the cerebellum is involved, the patient may have the follo"ing:

altered "alking gait altered movement coordination vertigo and or diseIuilibrium

Associated s$"%to"s
Coss 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. $f symptoms are ma:imal at onset, the cause is more likely to be a subarachnoid hemorrhage or an embolic stroke.

Causes
'!ro"botic stroke
$n thrombotic stroke a thrombus2&/3 (blood clot) usually forms around atherosclerotic plaIues. Since blockage of the artery is gradual, onset of symptomatic thrombotic strokes is slo"er. 1 thrombus itself (even if non#occluding) can lead to an embolic stroke (see belo") if the thrombus breaks off, at "hich point it is called an 6embolus.6 !"o types of thrombosis can cause stroke:

Large vessel disease involves the common and internal carotids, vertebral, and the ircle of Willis.2&)3 0iseases 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 "all (!akayasu arteritis, giant cell arteritis, vasculitis), noninflammatory vasculopathy, <oyamoya 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.2,*3 0iseases 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 degeneration2,&3 (stroke involving these vessels are kno"n as lacunar infarcts) and microatheroma (small atherosclerotic plaIues).2,,3

Sickle#cell anemia,2,(3 "hich can cause blood cells to clump up and block blood vessels, can also lead to stroke. 1 stroke is the second leading killer of people under ,* "ho suffer from sickle#cell anemia.2,'3

&"bolic stroke
1n embolic stroke refers to the blockage of an artery by an arterial embolus, a travelling particle or debris in the arterial bloodstream originating from else"here. 1n embolus is most freIuently a thrombus, but it can also be a number of other substances including fat (e.g., from bone marro" in a broken bone), air, cancer cells or clumps of bacteria (usually from infectious endocarditis). @ecause an embolus arises from else"here, local therapy solves the problem only temporarily. !hus, the source of the embolus must be identified. @ecause the embolic blockage is sudden in onset, symptoms usually are ma:imal at start. 1lso, symptoms may be transient as the embolus is partially resorbed and moves to a different location or dissipates altogether. 8mboli most commonly arise from the heart (especially in atrial fibrillation) but may originate from else"here in the arterial tree. $n parado:ical embolism, a deep vein thrombosis embolises through an atrial or ventricular septal defect in the heart into the brain. ardiac causes can be distinguished bet"een high and lo"#risk:2,.3

5igh risk: atrial fibrillation and paro:ysmal atrial fibrillation, rheumatic disease of the mitral or aortic valve disease, artificial heart valves, kno"n cardiac thrombus of the atrium or ventricle, sick sinus syndrome, sustained atrial flutter, recent myocardial infarction, chronic myocardial infarction together "ith e>ection fraction J,/ percent, symptomatic congestive heart failure "ith e>ection fraction J(* percent, dilated

cardiomyopathy, Cibman#Sacks endocarditis, <arantic endocarditis, infective endocarditis, papillary fibroelastoma, left atrial my:oma and coronary artery bypass graft ( 1@K) surgery. Co" risk-potential: calcification of the annulus (ring) of the mitral valve, patent foramen ovale (7FB), atrial septal aneurysm, atrial septal aneurysm with patent foramen ovale, left ventricular aneurysm "ithout thrombus, isolated left atrial 6smoke6 on echocardiography (no mitral stenosis or atrial fibrillation), comple: atheroma in the ascending aorta or pro:imal arch.

S$ste"ic !$%o%er usion

Systemic hypoperfusion is the reduction of blood flo" to all parts of the body. $t is most commonly due to heart failure from cardiac arrest or arrhythmias, or from reduced cardiac output as a result of myocardial infarction, pulmonary embolism, pericardial effusion, or bleeding. 5ypo:emia (lo" blood o:ygen content) may precipitate the hypoperfusion. @ecause the reduction in blood flo" is global, all parts of the brain may be affected, especially 6"atershed6 areas # border Hone regions supplied by the ma>or cerebral arteries. 1 "atershed stroke refers to the condition "hen blood supply to these areas is compromised. @lood flo" to these areas does not necessarily stop, but instead it may lessen to the point "here brain damage can occur. !his phenomenon is also referred to as 6last meado"6 to point to the fact that in irrigation the last meado" receives the least amount of "ater.

Venous t!ro"bosis
erebral venous sinus thrombosis leads to stroke due to locally increased venous pressure, "hich e:ceeds the pressure generated by the arteries. $nfarcts are more likely to undergo hemorrhagic transformation (leaking of blood into the damaged area) than other types of ischemic stroke.2%3

Intracerebral !e"orr!a#e
$t generally occurs in small arteries or arterioles and is commonly due to hypertension,2,%3 intracranial vascular malformations (including cavernous angiomas or arteriovenous malformations), cerebral amyloid angiopathy, or infarcts into "hich secondary haemorrhage has occurred.2,3 Bther potential causes are trauma, bleeding disorders, amyloid angiopathy, illicit drug use (e.g., amphetamines or cocaine). !he hematoma enlarges until pressure from surrounding tissue limits its gro"th, or until it decompresses by emptying into the ventricular system, SF or the pial surface. 1 third of intracerebral bleed is into the brainGs ventricles. $ 5 has a mortality rate of '' percent after (* days, higher than ischemic stroke or subarachnoid hemorrhage ("hich technically may also be classified as a type of stroke2,3).

Silent stroke
1 silent stroke is a stroke that does not have any out"ard symptoms, and the patients are typically una"are they have suffered a stroke. 0espite not causing identifiable symptoms, a silent stroke still causes damage to the brain, and places the patient at increased risk for both transient ischemic attack and ma>or stroke in the future. onversely, those "ho have suffered a ma>or stroke are at risk of having silent strokes.2,+3 $n a broad study in &))/, more than && million people "ere estimated to have e:perienced a stroke in the ;nited States. 1ppro:imately ++*,*** of these strokes "ere symptomatic and && million "ere first#ever silent <4$ infarcts or hemorrhages. Silent strokes typically cause lesions "hich are detected via the use of neuroimaging such as <4$. Silent strokes are estimated to occur at five times the rate of symptomatic strokes.2,/32,)3 !he risk of silent stroke increases "ith age, but may also affect younger adults and children, especially those "ith acute anemia.2,/32(*3

Pat!o%!$siolo#$
Isc!e"ic

<icrograph sho"ing cortical pseudolaminar necrosis, a finding seen in strokes on medical imaging and at autopsy. 5L8#CF@ stain.

<icrograph of the superficial cerebral corte: sho"ing neuron loss and reactive astrocytes in a person that suffered a stroke. 5L8#CF@ stain. $schemic stroke occurs because of a loss of blood supply to part of the brain, initiating the ischemic cascade.2(&3 @rain tissue ceases to function if deprived of o:ygen for more than %* to )* seconds and after appro:imately three hours, "ill suffer irreversible in>ury possibly leading to death of the tissue, i.e., infarction. (!his is "hy fibrinolytics such as alteplase are given only until three hours since the onset of the stroke.) 1therosclerosis may disrupt the blood supply by narro"ing the lumen of blood vessels leading to a reduction of blood flo", by causing the formation of blood clots "ithin the vessel, or by releasing sho"ers of small emboli through the disintegration of atherosclerotic plaIues.2(,3 8mbolic infarction occurs "hen emboli formed else"here in the circulatory system, typically in the heart as a conseIuence 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 no" occluded, the brain becomes lo" in energy, and thus it resorts into using anaerobic metabolism "ithin the region of brain tissue affected by ischemia. ;nfortunately, this kind of metabolism produces less adenosine triphosphate (1!7) but releases a by#product called lactic acid. Cactic acid is an irritant "hich could potentially destroy cells since it is an acid and disrupts the normal acid#base balance in the brain. !he ischemia area is referred to as the 6ischemic penumbra6.2((3 !hen, as o:ygen or glucose becomes depleted in ischemic brain tissue, the production of high energy phosphate compounds such as adenosine triphosphate (1!7) fails, leading to failure of energy#dependent processes (such as ion pumping) necessary for tissue cell survival. !his sets off a series of interrelated events that result in cellular in>ury and death. 1 ma>or cause of neuronal in>ury is release of the e:citatory neurotransmitter glutamate. !he concentration of glutamate outside the cells of the nervous system is normally kept lo" by so#called uptake carriers, "hich are po"ered by the concentration gradients of ions (mainly =aM) across the cell membrane. 5o"ever, stroke cuts off the supply of o:ygen and glucose "hich po"ers the ion pumps maintaining these gradients. 1s a result the transmembrane ion gradients run do"n, and glutamate transporters reverse their direction, releasing glutamate into the e:tracellular space. Klutamate acts on receptors in nerve cells (especially =<01 receptors), producing an influ: of calcium "hich activates enHymes that digest the cellsG proteins, lipids and nuclear material. alcium influ: can also lead to the failure of mitochondria, "hich can lead further to"ard energy depletion and may trigger cell death due to apoptosis. $schemia also induces production of o:ygen free radicals and other reactive o:ygen species. !hese react "ith and damage a number of cellular and e:tracellular elements. 0amage to the blood vessel lining or endothelium is particularly important. $n fact, many antio:idant neuroprotectants such as uric acid and =NO#*.) "ork 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 redo: signaling.2,'3 !hese processes are the same for any type of ischemic tissue and are referred to collectively as the ischemic cascade. 5o"ever, brain tissue is especially vulnerable to ischemia since it has little respiratory reserve and is completely dependent on aerobic metabolism, unlike most other organs. $n addition to in>urious 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 matri: metalloproteases, "hich are Hinc# and calcium# dependent enHymes that break do"n collagen, hyaluronic acid, and other elements of connective tissue. Bther

proteases also contribute to this process. !he loss of vascular structural integrity results in a breakdo"n of the protective blood brain barrier that contributes to cerebral edema, "hich can cause secondary progression of the brain in>ury. 1s is the case "ith any type of brain in>ury, the immune system is activated by cerebral infarction and may under some circumstances e:acerbate the in>ury caused by the infarction. $nhibition of the inflammatory response has been sho"n e:perimentally to reduce tissue in>ury due to cerebral infarction, but this has not proved out in clinical studies.

He"orr!a#ic
5emorrhagic strokes result in tissue in>ury by causing compression of tissue from an e:panding hematoma or hematomas. !his can distort and in>ure tissue. $n addition, the pressure may lead to a loss of blood supply to affected tissue "ith resulting infarction, and the blood released by brain hemorrhage appears to have direct to:ic effects on brain tissue and vasculature.2,'32('3 $nflammation contributes to the secondary brain in>ury after hemorrhage.2('3

Dia#nosis

1 ! sho"ing early signs of a middle cerebral artery stroke "ith loss of definition of the gyri and grey "hite boundary Stroke is diagnosed through several techniIues: a neurological e:amination (such as the =ihss), ! scans (most often "ithout contrast enhancements) or <4$ scans, 0oppler ultrasound, and arteriography. !he diagnosis of stroke itself is clinical, "ith assistance from the imaging techniIues. $maging techniIues also assist in determining the subtypes and cause of stroke. !here 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.2(.3

De inition
!he traditional definition of stroke, devised by the World 5ealth BrganiHation in the &)+*s,2(%3 is a 6neurological deficit of cerebrovascular cause that persists beyond ,' hours or is interrupted by death "ithin ,' hours6. !his definition "as supposed to reflect the reversibility of tissue damage and "as devised for the purpose, "ith the time frame of ,' hours being chosen arbitrarily. !he ,'#hour limit divides stroke from transient ischemic attack, "hich is a related syndrome of stroke symptoms that resolve completely "ithin ,' hours.2,3 With the availability of treatments that, "hen given early, can reduce stroke severity, many no" 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 s"iftly.2(+3

P!$sical e(a"ination
1 physical e:amination, including taking a medical history of the symptoms and a neurological status, helps giving an evaluation of the location and severity of a stroke. $t can give a standard score on e.g., the =$5 stroke scale.

I"a#in#

For diagnosing ischemic stroke in the emergency setting:2(/3

! scans (without contrast enhancements) sensitivityP &%? specificityP )%? <4$ scan sensitivityP /(? specificityP )/?

For diagnosing hemorrhagic stroke in the emergency setting:

! scans (without contrast enhancements) sensitivityP /)? specificityP &**? <4$ scan sensitivityP /&? specificityP &**?

For detecting chronic hemorrhages, <4$ scan is more sensitive.2()3 For the assessment of stable stroke, nuclear medicine scans S78 ! and 78!- ! may be helpful. S78 ! documents cerebral blood flo" and 78! "ith F0K isotope the metabolic activity of the neurons.

)nderl$in# cause

&,#lead 8 K of a patient "ith a stroke, sho"ing large deeply inverted !#"aves. 9arious 8 K changes may occur in people "ith strokes and other brain disorders. When a stroke has been diagnosed, various other studies may be performed to determine the underlying cause. With the current treatment and diagnosis options available, it is of particular importance to determine "hether there is a peripheral source of emboli. !est selection may vary, since the cause of stroke varies "ith age, comorbidity and the clinical presentation. ommonly used techniIues include:

an ultrasound-doppler study of the carotid arteries (to detect carotid stenosis) or dissection of the precerebral arteriesA an electrocardiogram (8 K) and echocardiogram (to identify arrhythmias and resultant clots in the heart "hich may spread to the brain vessels through the bloodstream)A a 5olter monitor study to identify intermittent arrhythmiasA an angiogram of the cerebral vasculature (if a bleed is thought to have originated from an aneurysm or arteriovenous malformation)A blood tests to determine hypercholesterolemia, bleeding diathesis and some rarer causes such as homocysteinuria.

Prevention
Kiven the disease burden of strokes, prevention is an important public health concern.2'*3 7rimary prevention is less effective than secondary prevention (as >udged by the number needed to treat to prevent one stroke per year).2'*3 4ecent guidelines detail the evidence for primary prevention in stroke.2'&3 @ecause stroke may indicate underlying atherosclerosis, it is important to determine the patientGs risk for other cardiovascular diseases such as coronary heart disease. onversely, aspirin confers some protection against first stroke in people "ho have had a myocardial infarction or those "ith a high cardiovascular risk.2',32'(3 $n those "ho have previously had a stroke treatment "ith medications such as aspirin, clopidogrel and dipyridamole may be given to prevent platelets from aggregating.2',3

*isk actors
!he 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 <edical 4esearch ouncil trials is that /(( patients have to be treated for & year to prevent one stroke2''32'.3). Bther modifiable risk factors include high blood cholesterol levels, diabetes, cigarette smoking2'%32'+3 (active and passive), heavy alcohol consumption2'/3 and drug use,2')3 lack of physical activity, obesity, processed red meat consumption2.*3 and unhealthy diet.2.&3 1lcohol use could predispose to ischemic stroke, and intracerebral and subarachnoid hemorrhage via multiple mechanisms (for e:ample via hypertension, atrial fibrillation, rebound thrombocytosis and platelet aggregation and clotting disturbances).2.,3 !he drugs most commonly associated "ith stroke are cocaine, amphetamines causing hemorrhagic stroke, but also over#the#counter cough and cold drugs containing sympathomimetics.2.(32.'3 =o high Iuality studies have sho"n the effectiveness of interventions aimed at "eight reduction, promotion of regular e:ercise, reducing alcohol consumption or smoking cessation.2..3 =onetheless, given the large body of circumstantial evidence, best medical management for stroke includes advice on diet, e:ercise, smoking and alcohol use.2.%3 <edication or drug therapy is the most common method of stroke preventionA carotid endarterectomy can be a useful surgical method of preventing stroke. Blood %ressure 5ypertension accounts for (.#.*? of stroke risk.2.+3 @lood pressure reduction of &* mm5g systolic or . mm5g diastolic reduces the risk of stroke by Q'*?.2./3 Co"ering blood pressure has been conclusively sho"n to prevent both ischemic and hemorrhagic strokes.2.)32%*3 $t is eIually important in secondary prevention.2%&3 8ven patients older than /* years and those "ith isolated systolic hypertension benefit from antihypertensive therapy.2%,32%(32%'3 !he available evidence does not sho" large differences in stroke prevention bet"een antihypertensive drugs F therefore, other factors such as protection against other forms of cardiovascular disease should be considered and cost.2%.32%%3 Atrial ibrillation !hose "ith atrial fibrillation have a .? a year risk of stroke, and this risk is higher in those "ith valvular atrial fibrillation.2%+3 0epending on the stroke risk, anticoagulation "ith medications such as "arfarin or aspirin is "arranted for stroke prevention.2%/3 Blood li%ids 5igh cholesterol levels have been inconsistently associated "ith (ischemic) stroke.2%*32%)3 Statins have been sho"n to reduce the risk of stroke by about &.?.2+*3 Since earlier meta#analyses of other lipid#lo"ering drugs did not sho" a decreased risk,2+&3 statins might e:ert their effect through mechanisms other than their lipid#lo"ering effects.2+*3 Diabetes "ellitus 0iabetes mellitus increases the risk of stroke by , to ( times. While intensive control of blood sugar has been sho"n to reduce microvascular complications such as nephropathy and retinopathy it has not been sho"n to reduce macrovascular complications such as stroke.2+,32+(3

Anticoa#ulation dru#s Bral anticoagulants such as "arfarin have been the mainstay of stroke prevention for over .* years. 5o"ever, several studies have sho"n that aspirin and antiplatelet drugs are highly effective in secondary prevention after a stroke or transient ischemic attack.2',3 Co" doses of aspirin (for e:ample +.D&.* mg) are as effective as high doses but have fe"er side effectsA the lo"est effective dose remains unkno"n.2+'3 !hienopyridines (clopidogrel, ticlopidine) 6might be slightly more effective6 than aspirin and have a decreased risk of gastrointestinal bleeding, but they are more e:pensive.2+.3 !heir e:act role remains controversial. !iclopidine has more skin rash, diarrhea, neutropenia and thrombotic thrombocytopenic purpura.2+.3 0ipyridamole can be added to aspirin therapy to provide a small additional benefit, even though headache is a common side effect.2+%3 Co"#dose aspirin is also effective for stroke prevention after sustaining a myocardial infarction.2'(3 8:cept for in atrial fibrillation, oral anticoagulants are not advised for stroke prevention Fany benefit is offset by bleeding risk.2++3 $n primary prevention ho"ever, antiplatelet drugs did not reduce the risk of ischemic stroke "hile increasing the risk of ma>or bleeding.2+/32+)3 Further studies are needed to investigate a possible protective effect of aspirin against ischemic stroke in "omen.2/*32/&3 Sur#er$ arotid endarterectomy or carotid angioplasty can be used to remove atherosclerotic narro"ing (stenosis) of the carotid artery. !here is evidence supporting this procedure in selected cases.2.%3 8ndarterectomy for a significant stenosis has been sho"n to be useful in the secondary prevention after a previous stroke.2/,3 arotid artery stenting has not been sho"n to be eIually useful.2/(32/'3 7atients are selected for surgery based on age, gender, degree of stenosis, time since symptoms and patientsG preferences.2.%3 Surgery is most efficient "hen not delayed too long F the risk of recurrent stroke in a patient "ho has a .*? or greater stenosis is up to ,*? after . years, but endarterectomy reduces this risk to around .?. !he number of procedures needed to cure one patient "as . for early surgery ("ithin t"o "eeks after the initial stroke), but &,. if delayed longer than &, "eeks.2/.32/%3 Screening for carotid artery narro"ing has not been sho"n to be a useful screening test in the general population.2/+3 Studies of surgical intervention for carotid artery stenosis "ithout symptoms have sho"n only a small decrease in the risk of stroke.2//32/)3 !o be beneficial, the complication rate of the surgery should be kept belo" '?. 8ven then, for &** surgeries, . patients "ill benefit by avoiding stroke, ( "ill develop stroke despite surgery, ( "ill develop stroke or die due to the surgery itself, and /) "ill remain stroke#free but "ould also have done so "ithout intervention.2.%3 Diet =utrition, specifically the <editerranean#style diet, has the potential for decreasing the risk of having a stroke by more than half.2)*3 $t does not appear that lo"ering levels of homocysteine "ith folic acid affects the risk of stroke.
2)&32),3

Secondar$ %revention o isc!e"ic stroke

1nticoagulation can prevent recurrent stroke. 1mong patients "ith nonvalvular atrial fibrillation, anticoagulation can reduce stroke by %*? "hile antiplatelet agents can reduce stroke by ,*?.2)(3 5o"ever, a recent meta#analysis suggests harm from anti#coagulation started early after an embolic stroke.2)'3 Stroke prevention treatment for atrial fibrillation is determined according to the 510S- 510S, system. !he most "idely used anticoagulant to prevent thromboembolic stroke in patients "ith nonvalvular atrial fibrillation is the oral agentWarfarin "hile dabigatran is a ne" alternative "hich does not reIuire prothrombin time monitoring. $f studies sho" 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.

Mana#e"ent
Isc!e"ic stroke
0efinitive therapy is aimed at removing the blockage by breaking the clot do"n (thrombolysis), or by removing it mechanically (thrombectomy). !he more rapidly blood flo" is restored to the brain, the fe"er brain cells die.2).3

!ight control of blood sugars in the first fe" hours does not improve outcomes and may cause harm.2)%3 5igh blood pressure is also not typically lo"ered as this has not been found to be helpful. '!ro"bol$sis !hrombolysis "ith recombinant tissue plasminogen activator (rt71) in acute ischemic stroke, "hen given before three hours of symptom onset increases the risk of death in the short term but in the long term improves the rate of independence and late mortalityA the increase in long term mortality is not significant.2)+3 When broken do"n by time to treatment it increases the chance of being alive and living independently by )? in those treated "ithin three hours, ho"ever the benefit for those treated bet"een three and si: hours is not significant.2)+3 !hese benefits or lack of benefits occurred regardless of the age of the person treated.2)+3 $t use is endorsed by the 1merican 5eart 1ssociation and the 1merican 1cademy of =eurology as the recommended treatment for acute stroke "ithin three hours of onset of symptoms as long as there are not other contraindications (such as abnormal lab values, high blood pressure, or recent surgery). !his position for t71 is based upon the findings of t"o studies by one group of investigators2)/3 "hich sho"ed that t71 improves the chances for a good neurological outcome. When administered "ithin the first three hours thrombolysis improves functional outcome "ithout affecting mortality.2))3 %.'? of people "ith large strokes developed substantial brain hemorrhage as a complication from being given t71 thus part of the reason for increased short term mortality. 2&**3 1dditionally, it is the position of the 1merican 1cademy of 8mergency <edicine that ob>ective evidence regarding the efficacy, safety, and applicability of t71 for acute ischemic stroke is insufficient to "arrant its classification as standard of care.2&*&3$ntra#arterial fibrinolysis, "here a catheter is passed up an artery into the brain and the medication is in>ected at the site of thrombosis, has been found to improve outcomes in people "ith acute ischemic stroke.2&*,3 Mec!anical t!ro"becto"$

4emoval of the clot may be attempted in those "here it occurs "ithin a large blood vessel and may be an option for those "ho either are not eligible for or do not improve "ith intravenous thrombolytics.2&*(3 Significant complications occur in about +?.2&*'3 1 randomiHed control trial of these procedures has not been done as of ,*&&.
2&*.3

He"icraniecto"$ Carge territory strokes can cause significant edema of the brain "ith secondary brain in>ury in surrounding tissue. !his phenomenon is mainly encountered in strokes of the middle cerebral artery territory, and is also called 6malignant cerebral infaction6 because it carries a dismal prognosis. 4elief of the pressure may be attempted "ith medication, but some reIuire hemicraniectomy, the temporary surgical removal of the skull on one side of the head. !his decreases the risk of death, although some more people survive "ith disability "ho "ould other"ise have died.2&*%3

He"orr!a#ic stroke
7eople "ith intracerebral hemorrhage reIuire neurosurgical evaluation to detect and treat the cause of the bleeding, although many may not need surgery. 1nticoagulants and antithrombotics, key in treating ischemic stroke, can make bleeding "orse. 7eople are monitored for changes in the level of consciousness, and their blood pressure, blood sugar, and o:ygenation are kept at optimum levels.2citation needed3

Stroke unit
$deally, people "ho have had a stroke are admitted to a 6stroke unit6, a "ard or dedicated area in hospital staffed by nurses and therapists "ith e:perience in stroke treatment. $t has been sho"n that people admitted to a stroke unit

have a higher chance of surviving than those admitted else"here in hospital, even if they are being cared for by doctors "ithout e:perience in stroke.2,3 When an acute stroke is suspected by history and physical e:amination, the goal of early assessment is to determine the cause. !reatment varies according to the underlying cause of the stroke, thromboembolic (ischemic) or hemorrhagic.

*e!abilitation
Stroke rehabilitation is the process by "hich patients "ith disabling strokes undergo treatment to help them return to normal life as much as possible by regaining and relearning the skills of everyday living. $t also aims to help the survivor understand and adapt to difficulties, prevent secondary complications and educate family members to play a supporting role. 1 rehabilitation team is usually multidisciplinary as it involves staff "ith different skills "orking together to help the patient. !hese 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 "orkers, and pharmacists since at least one third of the patients manifest post stroke depression. 9alidated instruments such as the @arthel scale may be used to assess the likelihood of a stroke patient being able to manage at home "ith or "ithout support subseIuent to discharge from hospital. Kood 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 (7!), occupational therapy (B!) and speech#language pathology (SC7) are the cornerstones of the rehabilitation process. Bften, assistive technology such as a "heelchair, "alkers, canes, and orthosis may be beneficial. 7! and B! have overlapping areas of e:pertise, ho"ever 7! focuses on >oint range of motion and strength by performing e:ercises and re#learning functional tasks such as bed mobility, transferring, "alking and other gross motor functions. 7hysiotherapists can also "ork "ith patients to improve a"areness and use of the hemiplegic side. 4ehabilitation involves "orking on the ability to produce strong movements or the ability to perform tasks using normal patterns. 8mphasis is often concentrated on functional tasks and patientRs goals. Bne e:ample physiotherapists employ to promote motor learning involves constraint#induced movement therapy. !hrough continuous practice the patient relearns to use and adapt the hemiplegic limb during functional activities to create lasting permanent changes.2&*+3 B! is involved in training to help relearn everyday activities kno"n as the 1ctivities of daily living (10Cs) such as eating, drinking, dressing, bathing, cooking, reading and "riting, and toileting. Speech and language therapy is appropriate for patients "ith the speech production disorders: dysarthria and apra:ia of speech, aphasia, cognitive#communication impairments and-or dysphagia (problems "ith s"allo"ing). 7atients may have particular problems, such as dysphagia, "hich can cause s"allo"ed material to pass into the lungs and cause aspiration pneumonia. !he condition may improve "ith time, but in the interim, a nasogastric tube may be inserted, enabling liIuid food to be given directly into the stomach. $f s"allo"ing is still deemed unsafe, then a percutaneous endoscopic gastrostomy (78K) tube is passed and this can remain indefinitely. !reatment of spasticity related to stroke often involves early mobilisations, commonly performed by a physiotherapist, combined "ith elongation of spastic muscles and sustained stretching through various positioning. 2&+3 Kaining initial improvements in range of motion is often achieved through rhythmic rotational patterns associated "ith the affected limb.2&+3 1fter full range has been achieved by the therapist, the limb should be positioned in the lengthened positions to prevent against further contractures, skin breakdo"n, and disuse of the limb "ith the use of splints or other tools to stabiliHe the >oint.2&+3 old in the form of ice "raps or ice packs have been proven to briefly reduce spasticity by temporarily dampening neural firing rates.2&+3 8lectrical stimulation to the antagonist muscles or vibrations has also been used "ith some success.2&+3 Stroke rehabilitation should be started as Iuickly as possible and can last any"here from a fe" days to over a year. <ost return of function is seen in the first fe" months, and then improvement falls off "ith the 6"indo"6 considered officially by ;.S. state rehabilitation units and others to be closed after si: months, "ith little chance of further improvement. 5o"ever, patients have been kno"n to continue to improve for years, regaining and strengthening abilities like "riting, "alking, running, and talking. 0aily rehabilitation e:ercises should continue to be part of the stroke patientGs routine. omplete recovery is unusual but not impossible and most patients "ill improve to some e:tent: proper diet and e:ercise are kno"n to help the brain to recover.

Some current and future therapy methods include the use of virtual reality and video games for rehabilitation. !hese forms of rehabilitation offer potential for motivating patients to perform specific therapy tasks that many other forms do not.2&*/3 <any clinics and hospitals are adopting the use of these off#the#shelf devices for e:ercise, social interaction and rehabilitation because they are affordable, accessible and can be used "ithin the clinic and home.2&*/3. Bther novel non#invasive rehabilitation methods are currently being developed to augment physical therapy to improve motor function of stroke patients, such as transcranial magnetic stimulation (!<S) and transcranial direct# current stimulation (t0 S)2&*)3 and robotic therapies.2&&*3

Pro#nosis
0isability affects +.? of stroke survivors enough to decrease their employability.2&&&3 Stroke can affect peoples physically, mentally, emotionally, or a combination of the three. !he results of stroke vary "idely depending on siHe and location of the lesion.2&&,3 0ysfunctions correspond to areas in the brain that have been damaged. Some of the physical disabilities that can result from stroke include muscle "eakness, numbness, pressure sores, pneumonia, incontinence, apra:ia (inability to perform learned movements), difficulties carrying out daily activities, appetite loss, speech loss, vision loss, and pain. $f the stroke is severe enough, or in a certain location such as parts of the brainstem, coma or death can result. 8motional problems resulting from stroke can result from direct damage to emotional centers in the brain or from frustration and difficulty adapting to ne" limitations. 7ost#stroke emotional difficulties include an:iety, panic attacks, flat affect (failure to e:press emotions), mania, apathy, and psychosis. (* to .*? of stroke survivors suffer post stroke depression, "hich is characteriHed by lethargy, irritability, sleep disturbances, lo"ered self esteem, and "ithdra"al.2&&(3 0epression can reduce motivation and "orsen outcome, but can be treated "ith antidepressants. 8motional lability, another conseIuence of stroke, causes the patient to s"itch Iuickly bet"een emotional highs and lo"s and to e:press emotions inappropriately, for instance "ith an e:cess of laughing or crying "ith little or no provocation. While these e:pressions of emotion usually correspond to the patientGs actual emotions, a more severe form of emotional lability causes patients to laugh and cry pathologically, "ithout regard to conte:t or emotion.2&&&3 Some patients sho" the opposite of "hat they feel, for e:ample crying "hen they are happy.2&&'3 8motional lability occurs in about ,*? of stroke patients. ognitive deficits resulting from stroke include perceptual disorders, 1phasia, dementia, and problems "ith attention and memory. 1 stroke sufferer may be una"are of his or her o"n disabilities, a condition called anosognosia. $n a condition called hemispatial neglect, a patient is unable to attend to anything on the side of space opposite to the damaged hemisphere. ;p to &*? of people follo"ing a stroke develop seiHures, most commonly in the "eek subseIuent to the eventA the severity of the stroke increases the likelihood of a seiHure.2&&.32&&%3

&%ide"iolo#$
0isability#ad>usted life year for cerebral vascular disease per &**,*** inhabitants in ,**'.2&&+3 no data &&,.#&(** J,.* &(**#&'+. ,.*#',. &'+.#&%.* ',.#%** &%.*#&/,. %**#++. &/,.#,*** ++.#).* S,*** ).*#&&,. Stroke "as the second most common cause of death "orld"ide in ,**', resulting in ..+ million deaths (Q&*? of the total).2(3 1ppro:imately ) million people had a stroke in ,**/ and (* million people have previously had a stroke and are still alive.2&&/3 $t is ranked after heart disease and before cancer.2,3 Keographic disparities in stroke incidence have been observed, including the e:istence of a 6stroke belt6 in the southeastern ;nited States, but causes of these disparities have not been e:plained.

!he incidence of stroke increases e:ponentially from (* years of age, and etiology varies by age.2&&)3 1dvanced age is one of the most significant stroke risk factors. ).? of strokes occur in people age '. and older, and t"o#thirds of strokes occur in those over the age of %..2&&(32,'3 1 personGs risk of dying if he or she does have a stroke also increases "ith age. 5o"ever, 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. 5igher levels of 9on Willebrand factor are more common amongst people "ho have had ischemic stroke for the first time. 2&,*3 !he results of this study found that the only significant genetic factor "as the personGs blood type. 5aving had a stroke in the past greatly increases oneGs risk of future strokes. <en are ,.? more likely to suffer strokes than "omen,2,'3 yet %*? of deaths from stroke occur in "omen.2&&'3 Since "omen live longer, they are older on average "hen they have their strokes and thus more often killed (=$<5 ,**,).2,'3 Some risk factors for stroke apply only to "omen. 7rimary among these are pregnancy, childbirth, menopause and the treatment thereof (54!).

Histor$
5ippocrates first described the sudden paralysis that is often associated "ith stroke. 8pisodes of stroke and familial stroke have been reported from the ,nd millennium @ on"ard in ancient <esopotamia and 7ersia.2&,&3 5ippocrates ('%* to (+* @ ) "as first to describe the phenomenon of sudden paralysis that is often associated "ith ischemia. 1pople:y, from the Kreek "ord meaning 6struck do"n "ith violence,6 first appeared in 5ippocratic "ritings to describe this phenomenon.2&,,32&,(3 !he "ord stroke "as used as a synonym for apoplectic seiHure as early as &.)),2&,'3 and is a fairly literal translation of the Kreek term. $n &%./, in his Apoplexia, Johann Jacob Wepfer (&%,*D&%).) identified the cause of hemorrhagic stroke "hen he suggested that people "ho had died of apople:y had bleeding in their brains.2&,,32,'3 Wepfer also identified the main arteries supplying the brain, the vertebral and carotid arteries, and identified the cause of ischemic stroke 2also kno"n as cerebral infarction3 "hen he suggested that apople:y might be caused by a blockage to those vessels.2,'3 4udolf 9ircho" first described the mechanism of thromboembolism as a ma>or factor.2&,.3

*esearc!
An#io%last$ and stentin#
1ngioplasty and stenting have begun to be looked at as possible viable options in treatment of acute ischemic stroke. $ntra#cranial stenting in symptomatic intracranial arterial stenosis, the rate of technical success (reduction to stenosis of J.*?) ranged from )*#)/?, and the rate of ma>or peri#procedural complications ranged from '#&*?. !he rates of restenosis and-or stroke follo"ing the treatment "ere also favorable.2&,%3 !his data suggests that a randomiHed controlled trial is needed to more completely evaluate the possible therapeutic advantage of this preventative measure.

+euro%rotection
@rain tissue survival can be improved to some e:tent if one or more of these processes is inhibited. 0rugs that scavengereactive o:ygen species, inhibit apoptosis, or inhibit e:citatory neurotransmitters, for e:ample, have been sho"n e:perimentally to reduce tissue in>ury caused by ischemia. 1gents that "ork in this "ay are referred to as beingneuroprotective. ;ntil recently, human clinical trials "ith neuroprotective agents have failed, "ith the probable e:ception of deep barbiturate coma. 5o"ever, more recently =NO#*.), the disulfonyl derivative of the radical#scavengin phenylbutylnitrone, is reported to be neuroprotective in stroke.2&,+3 !his agent appears to "ork at the level of the blood vessel lining or endothelium. ;nfortunately, after producing favorable results in one large# scale clinical trial, a second trial failed to sho" favorable results.2,'3 @enefit of =NO#*.) is Iuestionable.2&,/3