Stroke Clasificacion

8/17/2019 Stroke Clasificacion

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INTRODUCTION — The two broad categories of stroke, hemorrhage and ischemia,

are diametrically opposite conditions: hemorrhage is characterized by too much blood

within the closed cranial cavity, while ischemia is characterized by too little blood to

supply an adequate amount of oxygen and nutrients to a part of the brain [ !"

#ach of these categories can be divided into subtypes that have somewhat differentcauses, clinical pictures, clinical courses, outcomes, and treatment strategies" $s an

example, intracranial hemorrhage can be caused by intracerebral hemorrhage %&'(,

also called parenchymal hemorrhage), which involves bleeding directly into brain

tissue, and subarachnoid hemorrhage %*$(), which involves bleeding into the

cerebrospinal fluid that surrounds the brain and spinal cord [ !"

This topic will review the classification of stroke" The clinical diagnosis of stroke

subtypes and an overview of stroke evaluation are discussed separately" %*ee +'linical

diagnosis of stroke subtypes+ and +verview of the evaluation of stroke+ ")

DEFINITIONS — *troke is classified into two ma-or types:

• .rain ischemia due to thrombosis, embolism, or systemic hypoperfusion

• .rain hemorrhage due to intracerebral hemorrhage or subarachnoid

hemorrhage

$ stroke is the acute neurologic in-ury that occurs as a result of one of these pathologic

processes" $pproximately /0 percent of strokes are due to ischemic cerebral infarction

and 10 percent to brain hemorrhage"

$n infarcted brain is pale initially" 2ithin hours to days, the gray matter becomes

congested with engorged, dilated blood vessels and minute petechial hemorrhages"

2hen an embolus blocking a ma-or vessel migrates, lyses, or disperses within minutes

to days, recirculation into the infarcted area can cause a hemorrhagic infarction and

may aggravate edema formation due to disruption of the blood3brain barrier"

$ primary intracerebral hemorrhage damages the brain directly at the site of the

hemorrhage by compressing the surrounding tissue" 4hysicians must initially consider

whether the patient with suspected cerebrovascular disease is experiencing symptoms

and signs suggestive of ischemia or hemorrhage"

The great ma-ority of ischemic strokes are caused by a diminished supply of arterial

blood, which carries sugar and oxygen to brain tissue" $nother cause of stroke that is

difficult to classify is stroke due to occlusion of veins that drain the brain of blood"5enous occlusion causes a back3up of fluid resulting in brain edema, and in addition it

may cause both brain ischemia and hemorrhage into the brain"

BRAIN ISCHEMIA — There are three main subtypes of brain ischemia [ 1 !:

• Thrombosis %see 6Thrombosis6 below) generally refers to local in situ obstruction

of an artery" The obstruction may be due to disease of the arterial wall, such as


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arteriosclerosis, dissection, or fibromuscular dysplasia7 there may or may not

be superimposed thrombosis"

• #mbolism %see 6#mbolism6 below) refers to particles of debris originating

elsewhere that block arterial access to a particular brain region [ 8 !" *ince theprocess is not local %as with thrombosis), local therapy only temporarily solves

the problem7 further events may occur if the source of embolism is notidentified and treated"

• *ystemic hypoperfusion %see 6*ystemic hypoperfusion6 below) is a more general

circulatory problem, manifesting itself in the brain and perhaps other organs"

.lood disorders %see 6.lood disorders6 below) are an uncommon primary cause of

stroke" (owever, increased blood coagulability can result in thrombus formation and

subsequent cerebral embolism in the presence of an endothelial lesion located in the

heart, aorta, or large arteries that supply the brain"

Transient ischemic attack %T&$) is defined clinically by the temporary nature of the

associated neurologic symptoms, which last less than 19 hours by the classic

definition" The definition is changing with recognition that transient neurologic

symptoms are frequently associated with permanent brain tissue in-ury" The definition

of T&$ is discussed in more detail separately" %*ee +efinition of transient ischemic

attack+ ")

Thrombosis — Thrombotic strokes are those in which the pathologic process giving

rise to thrombus formation in an artery produces a stroke either by reduced blood flow

distally %low flow) or by an embolic fragment that breaks off and travels to a more

distant vessel %artery3to3artery embolism)" Thrombotic strokes can be divided into

either large or small vessel disease % table )" These two subtypes of thrombosis are

worth distinguishing since the causes, outcomes, and treatments are different"

Large vessel disease — ;arge vessels include both the extracranial %common and

internal carotids, vertebral) and intracranial arterial system %'ircle of 2illis and

proximal branches) % figure and figure 1 )"

&ntrinsic lesions in large extracranial and intracranial arteries cause symptoms by

reducing blood flow beyond obstructive lesions, and by serving as the source of

intraarterial emboli" $t times a combination of mechanisms is operant" *evere stenosis

promotes the formation of thrombi which can break off and embolize, and the reduced

blood flow caused by the vascular obstruction makes the circulation less competent at

washing out and clearing these emboli"

4athologies affecting large extracranial vessels include:

• $therosclerosis

• issection

• Takayasu arteritis


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• vasculitis

• ?oninflammatory vasculopathy

• @oyamoya syndrome

• 5asoconstriction

$therosclerosis is by far the most common cause of in situ local disease within the

large extracranial and intracranial arteries that supply the brain" 2hite platelet3fibrin

and red erythrocyte3fibrin thrombi are often superimposed upon the atherosclerotic

lesions, or they may develop without severe vascular disease in patients with

hypercoagulable states" 5asoconstriction %eg, with migraine) is probably the next most

common, followed in frequency by arterial dissection %a disorder much more common

than previously recognized) and traumatic occlusion" =ibromuscular dysplasia is an

uncommon arteriopathy, while arteritis is frequently mentioned in the differential

diagnosis, but it is an extremely rare cause of thrombotic stroke"

$ortic disease is really a form of proximal extracranial large vessel disease, but it isoften considered together with cardioembolic sources because of anatomic proximity"

%*ee 6$ortic atherosclerosis6 below")

&dentification of the specific focal vascular lesion, including its nature, severity, and

localization, is important for treatment since local therapy may be effective %eg,

surgery, angioplasty, intraarterial thrombolysis)" &t should be possible clinically in most

patients to determine whether the local vascular disease is within the anterior %carotid)

or posterior %vertebrobasilar) circulation and whether the disorder affects large or

penetrating arteries" %*ee+'linical diagnosis of stroke subtypes+, section on 6?eurologic

examination6 ")

elivery of adequate blood through a blocked or partially blocked artery depends upon

many factors, including blood pressure, blood viscosity, and collateral flow" ;ocal

vascular lesions also may throw off emboli, which can cause transient symptoms" &n

patients with thrombosis, the neurologic symptoms often fluctuate, remit, or progress

in a sputtering fashion % figure 8 )" %*ee +'linical diagnosis of stroke subtypes+, section

on 6'linical course6and +#tiology and clinical manifestations of transient ischemic

attack+, section on 6'linical manifestations6 ")


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Small vessel disease — *mall vessel disease affects the intracerebral arterial

system, specifically penetrating arteries that arise from the distal vertebral artery, the

basilar artery, the middle cerebral artery stem, and the arteries of the circle of 2illis"

These arteries thrombose due to:

•

;ipohyalinosis %a lipid hyaline build3up distally secondary to hypertension) andfibrinoid degeneration

• $theroma formation at their origin or in the parent large artery

The most common cause of obstruction of the smaller arteries and arterioles that

penetrate at right angles to supply the deeper structures within the brain %eg, basal

ganglia, internal capsule, thalamus, pons) is lipohyalinosis, blockage of an artery by

medial hypertrophy, and lipid admixed with fibrinoid material in the hypertrophied

arterial wall" $ stroke due to obstruction of these vessels is referred to as a lacunar

stroke" %*ee +;acunar infarcts+ ") ;ipohyalinosis is most often related to hypertension,

but aging may play a role"

@icroatheromas can also block these small penetrating arteries, as can plaques within

the larger arteries that block or extend into the orifices of the branches %called

atheromatous branch disease) [ !"

4enetrating artery occlusions usually cause symptoms that develop during a short

period of time, hours or at most a few days % figure 9 ), compared with large artery3

related brain ischemia, which can evolve over a longer period"

Embolism — #mbolic strokes are divided into four categories % table )"

• Those with a known source that is cardiac

• Those with a possible cardiac or aortic source based upon

transthoracic and>or transesophageal echocardiographic findings

• Those with an arterial source %artery to artery embolism)

• Those with a truly unknown source in which tests for embolic sources are

negative

The symptoms depend upon the region of brain rendered ischemic [ 9,A !" The

embolus suddenly blocks the recipient site so that the onset of symptoms is abrupt and

usually maximal at the start % figure A )" Bnlike thrombosis, multiple sites withindifferent vascular territories may be affected when the source is the heart %eg, left

atrial appendage or left ventricular thrombus) or aorta" Treatment will depend upon the

source and composition of the embolus" %*ee +*econdary prevention for specific causes

of ischemic stroke and transient ischemic attack+ ")

'ardioembolic strokes usually occur abruptly, although they occasionally present with

stuttering, fluctuating symptoms" The symptoms may clear entirely since emboli can


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migrate and lyse, particularly those composed of thrombus" 2hen this occurs,

infarction generally also occurs but is silent7 the area of infarction is smaller than the

area of ischemia that gave rise to the symptoms" This process is often referred to as a

T&$ due to embolism, although it is more correctly termed an embolic infarction or

stroke in which the symptoms clear within 19 hours"

'ardioembolic strokes can be divided into those with a known source and those with a

possible cardiac or ascending aortic source based upon

transthoracic and>or transesophageal echocardiographic findings [ 8 !"

High-ris !ardia! so"r!e — The diagnosis of embolic strokes with a known cardiac

source is generally agreed upon by physicians % table 1 ) [ C,D !7 included in this

category are those due to:

• $trial fibrillation and paroxysmal atrial fibrillation

• Eheumatic mitral or aortic valve disease

• .ioprosthetic and mechanical heart valves

• $trial or ventricular thrombus

• *ick sinus syndrome

• *ustained atrial flutter

• Eecent myocardial infarction %within one month)

• 'hronic myocardial infarction together with e-ection fraction F1/ percent

• *ymptomatic congestive heart failure with e-ection fraction F80 percent

• ilated cardiomyopathy

• =ibrous nonbacterial endocarditis as found in patients with systemic lupus %ie,

;ibman3*acks endocarditis), antiphospholipid syndrome, and cancer %maranticendocarditis)

• &nfective endocarditis

• 4apillary fibroelastoma

• ;eft atrial myxoma

• 'oronary artery bypass graft %'$.


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associated with ascending aortic atherosclerosis is probably the most common cause"

%*ee +?eurologic complications of cardiac surgery+ ")

#o$e%$ial !ardia! so"r!e — #mbolic strokes considered to have a potential cardiac

source % table 1 ) are ones in which a possible source is detected %usually) by

echocardiographic methods [ C,D !, including:

• @itral annular calcification

• 4atent foramen ovale

• $trial septal aneurysm

• $trial septal aneurysm with patent foramen ovale

• ;eft ventricular aneurysm without thrombus

• &solated left atrial smoke on echocardiography %no mitral stenosis or atrialfibrillation)

• 'omplex atheroma in the ascending aorta or proximal arch %see 6$ortic

atherosclerosis6 below)

&n this group, the association of the cardiac or aortic lesion and the rate of embolism is

often uncertain, since some of these lesions do not have a high frequency of embolism

and are often incidental findings unrelated to the stroke event [ G !" Thus, they are

considered potential sources of embolism" $ truly unknown source represents embolic

strokes in which no clinical evidence of heart disease is present % table )"

Aor$i! a$heros!lerosis — &n longitudinal population studies with nonselected

patients, complex aortic atherosclerosis does not appear to be associated with any

increased primary ischemic stroke risk [ 031 !" (owever, most studies evaluating

secondary stroke risk have found that complex aortic atherosclerosis is a risk factor for

recurrent stroke [ 83C !"

The range of findings is illustrated by the following studies:

• $ prospective case3control study examined the frequency and thickness of

atherosclerotic plaques in the ascending aorta and proximal arch in 1A0 patients

admitted to the hospital with ischemic stroke and 1A0 consecutive controls, allover the age of C0 years [ 9 !" $therosclerotic plaques H9 mm in thickness

were found in 9 percent of patients compared with 1 percent of controls, andthe odds ratio for ischemic stroke among patients with such plaques was G"

after ad-ustment for atherosclerotic risk factors" &n addition, aorticatherosclerotic plaques H9 mm were much more common in patients with brain

infarcts of unknown cause %relative risk 9"D)"

• &n contrast, a population3based study of 8A sub-ects who had

transesophageal echocardiography %T##) found that complex atherosclerotic


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plaque %I9 mm with or without mobile debris) in the ascending and transverse

aortic arch was not a significant risk factor for cryptogenic ischemic stroke orT&$ after ad-usting for age, gender, and other clinical risk factors [ !"

(owever, there was an association between complex aortic plaque andnoncryptogenic stroke" The investigators concluded that complex aortic arch

debris is a marker for the presence of generalized atherosclerosis"

@ethodologic differences are a potential explanation for the discrepant results of these

reports assessing the risk of ischemic stroke related to aortic atherosclerosis, as the

earlier case3control studies may have been skewed by selection and referral bias"

(owever, many patients with aortic atherosclerosis also have cardiac or large artery

lesions, a problem that may confound purely epidemiologic studies"

&n the author6s opinion, there is no question that large protruding plaques in the

ascending aorta and arch, particularly mobile plaques, are an important cause of

stroke [ D !"

S&s$emi! h&'o'er("sio% — Eeduced blood flow is more global in patients with

systemic hypoperfusion and does not affect isolated regions" The reduced perfusion

can be due to cardiac pump failure caused by cardiac arrest or arrhythmia, or to

reduced cardiac output related to acute myocardial ischemia, pulmonary embolism,

pericardial effusion, or bleeding" (ypoxemia may further reduce the amount of oxygen

carried to the brain"

*ymptoms of brain dysfunction typically are diffuse and nonfocal in contrast to the

other two categories of ischemia" @ost affected patients have other evidence of

circulatory compromise and hypotension such as pallor, sweating, tachycardia or

severe bradycardia, and low blood pressure" The neurologic signs are typically bilateral,

although they may be asymmetric when there is preexisting asymmetrical

craniocerebral vascular occlusive disease"

The most severe ischemia may occur in border zone %watershed) regions between the

ma-or cerebral supply arteries since these areas are most vulnerable to systemic

hypoperfusion" The signs that may occur with borderzone infarction include cortical

blindness, or at least bilateral visual loss7 stupor7 and weakness of the shoulders and

thighs with sparing of the face, hands, and feet %a pattern likened to a +man3in3a3

barrel+)"

Blood disorders — .lood and coagulation disorders are an uncommon primary cause

of stroke and T&$, but they should be considered in patients younger than age 9A,

patients with a history of clotting dysfunction, and in patients with a history of

cryptogenic stroke [ G !" The blood disorders associated with arterial cerebral infarctioninclude:

• *ickle cell anemia

• 4olycythemia vera

• #ssential thrombocytosis


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• (eparin induced thrombocytopenia

• 4rotein ' or * deficiency, acquired or congenital

• 4rothrombin gene mutation

• =actor 5 ;eiden %resistance to activated protein ')

• $ntithrombin &&& deficiency

• $ntiphospholipid syndrome

• (yperhomocysteinemia

=actor 5 ;eiden mutation and prothrombin 1010 mutations are associated mostly with

venous rather than arterial thrombosis" They can result in cerebral venous thrombosis

or deep venous thrombosis with paradoxical emboli" %*ee +#tiology, clinical features,

and diagnosis of cerebral venous thrombosis+ ")

&nfectious and inflammatory disease such as pneumonia, urinary tract infections,

'rohn6s disease, ulcerative colitis, (&5>$&*, and cancers result in a rise in acute

phase reactants such as fibrinogen, '3reactive protein, and coagulation factors 5&& and

5&&&" &n the presence of an endothelial cardiac or vascular lesion, this increase can

promote active thrombosis and embolism"

TOAST !lassi(i!a$io% — The T$*T classification scheme for ischemic stroke is

widely used and has good interobserver agreement [ / !" The T$*T system % table

8 ) attempts to classify ischemic strokes according to the ma-or pathophysiologic

mechanisms that are recognized as the cause of most ischemic strokes % table )" &t

assigns ischemic strokes to five subtypes based upon clinical features and the results

of ancillary studies including brain imaging, neurovascular evaluations, cardiac tests,

and laboratory evaluations for a prothrombotic state"

The five T$*T subtypes of ischemic stroke are:

• ;arge artery atherosclerosis

• 'ardioembolism

• *mall vessel occlusion

• *troke of other determined etiology

• *troke of undetermined etiology

The last subtype 3 stroke of undetermined etiology 3 involves cases where the cause of

a stroke cannot be determined with any degree of confidence, and by definition


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includes those with two or more potential causes identified, those with a negative

evaluation, and those with an incomplete evaluation" %*ee+'ryptogenic stroke+ ")

SSS-TOAST a%d CCS !lassi(i!a$io% — *ince the original T$*T classification

scheme was developed in the early GG0s, advances in stroke evaluation and

diagnostic imaging have allowed more frequent identification of potential vascular and

cardiac causes of stroke [ C !" These advances could cause an increasing proportion of

ischemic strokes to be classified as +undetermined+ if the strict definition of this

category %cases with two or more potential causes) is applied"

$s a result, an evidenced3based modification of the T$*T criteria called ***3T$*T

has been developed [ C !" The ***3T$*T system divides each of the original T$*T

subtypes into three subcategories as +evident,+ +probable,+ or +possible+ based upon

the weight of diagnostic evidence as determined by predefined clinical and imaging

criteria % table 9 )"

&n a study that compared the original T$*T and the ***3T$*T criteria applied to a

series of A0 patients with acute ischemic stroke, patients classified as +undetermined3

unclassified+ decreased for T$*T and ***3T$*T were 8/ to 90 versus 9 percent,

respectively, and inter3examiner reliability for ***3T$*T was higher than for T$*T,

although the difference was not statistically significant [ C !"

&n a further refinement, an automated version of the ***3T$*T called the 'ausative

'lassification *ystem %''*) was devised to improve its usefulness and accuracy for

stroke subtyping [ G !" The ''* is a computerized algorithm that consists of

questionnaire3style classification scheme" The ''* appears to have good inter3rater

reliability among multiple centers [ 10 !" &t is available online

at https:>>ccs"mgh"harvard"edu "

BRAIN HEMORRHA)E — There are two main subtypes of brain hemorrhage [ 1 !:

• &ntracerebral hemorrhage refers to bleeding directly into the brain parenchyma

• *ubarachnoid hemorrhage refers to bleeding into the cerebrospinal fluid within

the subarachnoid space that surrounds the brain

I%$ra!erebral hemorrhage — .leeding in intracerebral hemorrhage %&'() is usually

derived from arterioles or small arteries" The bleeding is directly into the brain, forming

a localized hematoma that spreads along white matter pathways" $ccumulation of

blood occurs over minutes or hours7 the hematoma gradually enlarges by adding blood

at its periphery like a snowball rolling downhill" The hematoma continues to grow untilthe pressure surrounding it increases enough to limit its spread or until the

hemorrhage decompresses itself by emptying into the ventricular system or into the

cerebrospinal fluid %'*=) on the pial surface of the brain [ 1,11 !"

The most common causes of &'( are hypertension, trauma, bleeding diatheses,

amyloid angiopathy, illicit drug use %mostly amphetamines and cocaine), and vascular

malformations [ 1,11 !" %*ee +*pontaneous intracerebral hemorrhage: 4athogenesis,

https://ccs.mgh.harvard.edu/https://ccs.mgh.harvard.edu/


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clinical features, and diagnosis+ ") ;ess frequent causes include bleeding into tumors,

aneurysmal rupture, and vasculitis"

The earliest symptoms of &'( relate to dysfunction of the portion of the brain that

contains the hemorrhage [ 1,11 !" $s examples:

• .leeding into the right putamen and internal capsule region causes left limbmotor and>or sensory signs

• .leeding into the cerebellum causes difficulty walking

• .leeding into the left temporal lobe presents as aphasia

The neurologic symptoms usually increase gradually over minutes or a few hours" &n

contrast to brain embolism and *$(, the neurologic symptoms related to &'( may not

begin abruptly and are not maximal at onset % figure C ) %and see below)"

(eadache, vomiting, and a decreased level of consciousness develop if the hematomabecomes large enough to increase intracranial pressure or cause shifts in intracranial

contents % figure D ) [ 1,11 !" These symptoms are absent with small hemorrhages7

the clinical presentation in this setting is that of a gradually progressing stroke"

&'( destroys brain tissue as it enlarges" The pressure created by blood and

surrounding brain edema is life3threatening7 large hematomas have a high mortality

and morbidity" The goal of treatment is to contain and limit the bleeding" Eecurrences

are unusual if the causative disorder is controlled %eg, hypertension or bleeding

diathesis)"

S"bara!h%oid hemorrhage — The two ma-or causes of *$( are rupture of arterial

aneurysms that lie at the base of the brain and bleeding from vascular malformationsthat lie near the pial surface" .leeding diatheses, trauma, amyloid angiopathy, and

illicit drug use are less common" %*ee+#tiology, clinical manifestations, and diagnosis of

aneurysmal subarachnoid hemorrhage+ ")

Eupture of an aneurysm releases blood directly into the cerebrospinal fluid %'*=) under

arterial pressure" The blood spreads quickly within the '*=, rapidly increasing

intracranial pressure" eath or deep coma ensues if the bleeding continues" The

bleeding usually lasts only a few seconds but rebleeding is very common" 2ith causes

of *$( other than aneurysm rupture, the bleeding is less abrupt and may continue

over a longer period of time"

*ymptoms of *$( begin abruptly in contrast to the more gradual onset of &'(" Thesudden increase in pressure causes a cessation of activity %eg, loss of memory or focus

or knees buckling)" (eadache is an invariable symptom and is typically instantly severe

and widespread7 the pain may radiate into the neck or even down the back into the

legs" 5omiting occurs soon after onset" There are usually no important focal neurologic

signs unless bleeding occurs into the brain and '*= at the same time %meningocerebral

hemorrhage)" nset headache is more common than in &'(, and the combination of

onset headache and vomiting is infrequent in ischemic stroke % figure D ) [ 18 !"


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%*ee +#tiology, clinical manifestations, and diagnosis of aneurysmal subarachnoid

hemorrhage+ ")

$pproximately 80 percent of patients have a minor hemorrhage manifested only by

sudden and severe headache %the so3called sentinel headache) that precedes a ma-or

*$( % figure D ) [ 18 !" The complaint of the sudden onset of severe headache is

sufficiently characteristic that a minor *$( should always be considered" &n a

prospective study of 9/ patients presenting with sudden and severe headache, for

example, subarachnoid hemorrhage was present in 1A percent overall and 1 percent

in patients in whom headache was the only symptom [ 19 !"

The goal of treatment of *$( is to identify the cause and quickly treat it to prevent

rebleeding" The other goal of treatment is to prevent brain damage due to delayed

ischemia related to vasoconstriction of intracranial arteries7 blood within the '*=

induces vasoconstriction, which can be intense and severe" The treatment of *$( is

discussed separately" %*ee +Treatment of aneurysmal subarachnoid hemorrhage+ ")

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Stroke Clasificacion