2007 Schools Wikipedia Selection. Related subjects: Health and medicine

Classifications and external resources
ICD- 10 I 61.- I 64.
ICD- 9 435- 436
OMIM 601367
DiseasesDB 2247
MedlinePlus 000726
eMedicine neuro/9  emerg/558 emerg/557 pmr/187

A stroke, also known as cerebrovascular accident (CVA), is an acute neurologic injury in which the blood supply to a part of the brain is interrupted. That is, stroke involves sudden loss of neuronal function due to disturbance in cerebral perfusion. This disturbance in perfusion is commonly arterial, but can be venous.

The part of the brain with disturbed perfusion no longer receives adequate oxygen. This initiates the ischemic cascade which causes brain cells to die or be seriously damaged, impairing local brain function. Stroke is a medical emergency and can cause permanent neurologic damage or even death if not promptly diagnosed and treated. It is the third leading cause of death and adult disability in the United States and industrialized European nations. On average, a stroke occurs every 45 seconds and someone dies every 3 minutes. Of every 5 deaths from stroke, 2 occur in men and 3 in women.

Risk factors include advanced age, hypertension (high blood pressure), diabetes mellitus, high cholesterol, and cigarette smoking. Cigarette smoking is the most important modifiable risk factor of stroke.

The term "brain attack" is starting to come into use in the United States for stroke, just as the term "heart attack" is used for myocardial infarction, where a cutoff of blood causes necrosis to the tissue of the heart. Many hospitals have "brain attack" teams within their neurology departments specifically for swift treatment of stroke.

Types of stroke

Strokes can be classified into two major categories: ischemic and hemorrhagic. Ischemia can be due to thrombosis, embolism, or systemic hypoperfusion. Hemorrhage can be due to intracerebral hemorrhage or subarachnoid hemorrhage. ~80% of strokes are due to ischemia.

Ischemic stroke

In an ischemic stroke, which is the cause of approximately 85-90% of strokes, a blood vessel becomes occluded and the blood supply to part of the brain is totally or partially blocked. Ischemic stroke is commonly divided into thrombotic stroke, embolic stroke, systemic hypoperfusion (Watershed or Border Zone stroke), or venous thrombosis.

Thrombotic stroke

In thrombotic stroke, a thrombus-forming process develops in the affected artery. The thrombus — a built up clot — gradually narrows the lumen of the artery and impedes blood flow to distal tissue. These clots usually form 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 then called an "embolus." Thrombotic stroke can be divided into two types depending on the type of vessel the thrombus is formed on:

  • 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
    • Dissection
    • Takayasu arteritis
    • Giant cell arteritis
    • Arteritis/vasculitis
    • Noninflammatory vasculopathy
    • Moyamoya syndrome
    • Fibromuscular dysplasia
  • Small vessel disease involves the intracerebral arteries, 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 (lipid hyaline build-up secondary to hypertension and aging) and fibrinoid degeneration (stroke involving these vessels are known as lacunar infarcts)
    • Microatheromas from larger arteries that extend into the smaller arteries (atheromatous branch disease)

Embolic stroke

Embolic stroke refers to the blockage of arterial access to a part of the brain by an embolus -- a traveling particle or debris in the arterial bloodstream originating from elsewhere. An embolus is most frequently a blood clot, but it can also be a plaque broken off from an atherosclerotic blood vessel or a number of other substances including fat (e.g., from bone marrow in a broken bone), air, and even cancerous cells. Another cause is bacterial emboli released in infectious endocarditis.

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

  • those with known cardiac source
  • those with potential cardiac or aortic source (from transthoracic or transesophageal echocardiogram)
  • those with an arterial source
  • those with unknown source

High risk cardiac causes include:

  • Atrial fibrillation and paroxysmal atrial fibrillation
  • Rheumatic mitral or aortic valve disease
  • Bioprosthetic and mechanical heart valves
  • Atrial or ventricular thrombus
  • Sick sinus syndrome
  • Sustained atrial flutter
  • Recent myocardial infarction (within one month)
  • Chronic myocardial infarction together with ejection fraction <28 percent
  • Symptomatic congestive heart failure with ejection fraction <30 percent
  • Dilated cardiomyopathy
  • Libman-Sacks endocarditis
  • Antiphospholipid syndrome
  • Marantic endocarditis from cancer
  • Infective endocarditis
  • Papillary fibroelastoma
  • Left atrial myxoma
  • Coronary artery bypass graft ( CABG) surgery

Potential cardiac causes include:

  • Mitral annular calcification
  • Patent foramen ovale
  • Atrial septal aneurysm
  • Atrial septal aneurysm with patent foramen ovale
  • Left ventricular aneurysm without thrombus
  • Isolated left atrial smoke on echocardiography (no mitral stenosis or atrial fibrillation)
  • Complex atheroma in the ascending aorta or proximal arch

Systemic hypoperfusion ( Watershed stroke)

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. Blood flow to these areas does not necessarily stop, but instead it may lessen to the point where brain damage can occur.

Venous thrombosis

Veins in the brain function to drain the blood back to the body. When veins are blocked due to thrombosis, the draining of blood is prevented and the blood backs up, causing cerebral edema. This can result in both ischemic and hemorrhagic strokes. This commonly occurs in the rare disease sinus vein thrombosis>>

Background: Cerebral venous thrombosis is an elusive diagnosis because of its nonspecific presentation and its numerous predisposing causes. It is more common than previously thought. Imaging plays a key role in the diagnosis.

Cerebral venous thrombosis often presents with hemorrhagic infarction in areas atypical for arterial vascular distribution. Magnetic resonance venography (MRV) in conjunction with conventional MRI can accurately diagnose cerebral venous thrombosis. With careful interpretation and a high degree of clinical suspicion, CT also may lead to the diagnosis.

Pathophysiology: Cerebral venous thrombosis results from occlusion of a venous sinus and/or cortical vein and usually is caused by a partial thrombus or an extrinsic compression that subsequently progresses to complete occlusion. Once the vein is occluded, the thrombus may extend to veins draining into the sinus. This results in cortical venous infarction with petechial or overt hemorrhagic perivascular venous infarction.

Multiple pathophysiologic mechanisms and predisposing factors exist, including the following:

A hypercoagulable state

Extrinsic compression or local invasion of a venous by tumor or an adjacent infectious process (eg, mastoiditis)

A low-flow state within the venous sinus


Pregnancy and the postpartum state As many as 25% of patients present with no predisposing risk factor; however, in some patients, an etiologic factor is discovered subsequently.

When occlusion of a venous sinus occurs, the resulting venous congestion can lead to regional ischemia and infarction. Venous infarctions frequently are hemorrhagic and commonly occur within the white matter or at the gray-white matter junction. Involvement of the deep cerebral veins (eg, basal vein of Rosenthal) can progress to bilateral thrombosis of the internal cerebral veins with thalamic hemorrhagic infarction.


In the US: A range of occurrence in less than 1-9% of subjects has been suggested based on a limited autopsy series. The higher percentage may apply to older patients with concordant debilitating disease. Venous thrombosis is believed to be less common than arterial occlusive disease. Internationally: No current data are available. It is likely to be underdiagnosed since the availability of MR in developing countries is limited, and patients are not studied often by cerebral arteriography. Mortality/Morbidity:

A mortality range of 10-80% has been reported although the higher rate is based on older data. Recent studies estimate a morbidity range of 6-20%, including residual focal neurologic deficits and blindness secondary to optic nerve atrophy. The prognosis for return of function is believed to be somewhat better than for arterial stroke. Age:

Elderly or debilitated patients (eg, those with an underlying illness) are more likely to have spontaneous cerebral venous thrombosis. Neonates and infants suffering from dehydration may develop cerebral venous thrombosis. Clinical Details: The signs and symptoms of cerebral venous thrombosis occasionally are nonspecific and protean, making the clinical diagnosis difficult.

Patients may have generalized or focal neurologic symptoms and signs.




Possible seizures

Occasionally venous thrombosis may be mistaken for a psychiatric disorder (neurosis, hysteria, depression)

Physical examination findings may include the following:

Papilledema may be seen.

Forehead skin and eyelid edema, ocular chemosis, proptosis, and cranial nerve III, IV, and VI compromise can result from cavernous sinus thrombosis.

An isolated cortical venous thrombosis can result in focal neurologic symptoms and signs (related to the anatomic location of the thrombosis).

Predisposing factors include the following:

Hypercoagulable states including the use of oral contraceptives

Pregnancy and the postpartum period

Local or distant infection, including mastoiditis, otitis media, paranasal sinus infection, generalized sepsis, and facial or scalp cellulitis

Circulatory low-flow states resulting from blood volume depletion, dehydration, and/or cardiac disease

Behçet syndrome

Antiphospholipid antibody syndrome

Factor V Leiden genetic mutation and other hereditary thrombotic conditions

Arteriovenous malformations posttreatment

Direct trauma

Invasion of dural sinuses by adjacent tumor

Numerous chronic illnesses with sepsis, dehydration

In neonates and infants - Sepsis, dehydration, birth trauma, shock, and L-asparaginase therapy

Dural arteriovenous fistulas - May develop after dural sinus thrombosis

Intracranial hypotension - May occur in patients with extended thrombosis of the dural sinuses. Preferred Examination:

MRI with MRV is preferred for diagnosis. Clinical manifestations and physical findings may be nonspecific.

The diagnosis may be made or suggested by CT brain scan before and after intravenous contrast medium injection. Limitations of Techniques: Two-dimensional time-of-flight (2D TOF) MRV is performed in the coronal plane; however, in-plane signal loss that mimics thrombosis may occur with this technique. Thus, a review of source data and conventional MRI brain scan is necessary. Phase-contrast MRV techniques may help since small cortical venous infarcts may not be observed on 2D TOF MRV

Hemorrhagic stroke

A hemorrhagic stroke, or cerebral hemorrhage, is a form of stroke that occurs when a blood vessel in the brain ruptures or bleeds. Like ischemic strokes, hemorrhagic strokes interrupt the brain's blood supply because the bleeding vessel can no longer carry the blood to its target tissue. In addition, blood irritates brain tissue, disrupting the delicate chemical balance, and, if the bleeding continues, it can cause increased intracranial pressure which physically impinges on brain tissue and restricts blood flow into the brain. In this respect, hemorrhagic strokes are more dangerous than their more common counterpart, ischemic strokes. There are two types of hemorrhagic stroke: intracerebral hemorrhage, and subarachnoid hemorrhage.

Intracerebral hemorrhage

Intracerebral hemorrhage (ICH) is bleeding directly into the brain tissue, forming a gradually enlarging hematoma (pooling of blood). It generally occurs in small arteries or arterioles and is commonly due to hypertension, trauma, bleeding disorders, amyloid angiopathy, illicit drug use (e.g., amphetamines or cocaine), and vascular malformations. 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.

Subarachnoid hemorrhage

Subarachnoid hemorrhage (SAH) is bleeding into the cerebrospinal fluid (CSF) of the subarachnoid space surrounding the brain. The two most common causes of SAH are rupture of aneurysms from the base of the brain and bleeding from vascular malformations near the pial surface. Bleeding into the CSF from a ruptured aneurysm occurs very quickly, causing rapidly increased intracranial pressure. The bleeding usually only lasts a few seconds but rebleeding is common. Death or deep coma ensues if the bleeding continues. Hemorrhage from other sources is less abrupt and may continue for a longer period of time. SAH has a 40% mortality over 30 day period.

Signs and symptoms

The symptoms of stroke depend on the type of stroke and the area of the brain affected. Ischemic strokes usually only affect regional areas of the brain perfused by the blocked artery. Hemorrhagic strokes can affect local areas, but often can also cause more global symptoms due to bleeding and increased intracranial pressure.

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:

  • muscle weakness ( hemiplegia)
  • numbness
  • reduction in sensory or vibratory sensation

In most cases, the symptoms affect only one side of the body. The defect in the brain is usually on the opposite side of the body (depending on which part of the brain is affected). However, the presence of any one of these symptoms does not necessarily suggest a stroke, since these pathways also travel in the spinal cord and any lesion there can also produce these symptoms.

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

  • altered smell, taste, hearing, or vision (total or partial)
  • drooping of eyelid ( ptosis) and weakness of ocular muscles
  • decreased reflexes: gag, swallow, pupil reactivity to light
  • decreased sensation and muscle weakness of the face
  • balance problems and nystagmus
  • altered breathing and heart rate
  • weakness in sternocleidomastoid muscle (SCM) 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 (inability to speak or understand language from involvement of Broca's or Wernicke's area)
  • apraxia (altered voluntary movements)
  • visual field cut(involvement of occipital lobe)
  • memory deficits (involvement of temporal lobe)
  • hemineglect (involvement of parietal lobe)
  • disorganized thinking, confusion, hypersexual gestures (with involvement of frontal lobe)

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

  • trouble walking
  • altered movement coordination
  • vertigo and or disequilibrium

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

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

Subarachnoid hemorrhage

The symptoms of SAH occur abruptly due to the sudden onset of increased intracranial pressure. Often, patients complain of a sudden, extremely severe and widespread headache. The pain may or may not radiate down into neck and legs. Vomiting may occur soon after the onset of headache. Usually the neurologic exam is nonfocal -- meaning no deficits can be identified that attributes to certain areas of the brain -- unless the bleeding also occurs into the brain. The combination of headache and vomiting is uncommon in ischemic stroke.

Transient ischemic attack (TIA)

If the symptoms resolve within an hour, or maximum 24 hours, the diagnosis is transient ischemic attack (TIA), which is in essence a mini or brief stroke. This syndrome may be a warning sign, and a large proportion of patients develop strokes in the future. Recent data indicate that there is about a ten to fifteen percent chance of suffering a stroke in the year following a TIA, with half of that risk manifest in the first month, and, further, with much of that risk manifest in the first 48 hours. The chances of suffering an ischemic stroke can be reduced by using aspirin or related compounds such as clopidogrel, which inhibit platelets from aggregating and forming obstructive clots; but, for the same reason, such treatments (slightly) increase the likelihood and effects of hemorrhagic stroke since they impair clotting.


Stroke is diagnosed through several techniques: a neurological examination, blood tests, CT scans (without contrast enhancements) or MRI scans, Doppler ultrasound, and arteriography.

If a stroke is confirmed on imaging, various other studies may be performed to determine whether there is a peripheral source of emboli:

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


Early assessment

It is important to identify a stroke as early as possible because patients who are treated earlier are more likely to survive and have better recoveries. A simple set of tasks has been put forward by physicians to help those without medical training help to identify someone who is having a stroke. These are:

  • Ask the individual to smile.
  • Ask the individual to raise both arms and keep them raised.
  • Ask the individual to speak a simple sentence (coherently). For example, "It is sunny out today."

If the person has difficulty performing any of these tasks, emergency medical services should be contacted immediately, and the person's symptoms described.

The patient should be transported to the nearest hospital that can provide a rapid evaluation and treatment with the latest available therapies targeted to the type of stroke. The faster these therapies are started for hemorrhagic and ischemic stroke, the chances for recovery from each type improves greatly. Quick decisions about medication and the need for surgery have been shown to improve outcome.

Only detailed physical examination and medical imaging provide information on the presence, type, and extent of stroke.

Studies show that patients treated in hospitals with a dedicated Stroke Team or Stroke Unit and a specialized care program for stroke patients have improved odds of recovery.

Ischemic stroke

As ischemic stroke is due to a thrombus (blood clot) occluding a cerebral artery, a patient is given antiplatelet medication ( aspirin, clopidogrel, dipyridamole), or anticoagulant medication ( warfarin), dependent on the cause, when this type of stroke has been found. Hemorrhagic stroke must be ruled out with medical imaging, since this therapy would be harmful to patients with that type of stroke.

Whether thrombolysis is performed or not, the following investigations are required:

  • Stroke symptoms are documented, often using scoring systems such as the National Institutes of Health Stroke Scale, the Cincinnati Stroke Scale, and the Los Angeles Prehospital Stroke Screen. The latter is used by emergency medical technicians (EMTs) to determine whether a patient needs transport to a stroke centre.
  • A CT scan is performed to rule out hemorrhagic stroke
  • Blood tests, such as a full blood count, coagulation studies ( PT/INR and APTT), and tests of electrolytes, renal function, liver function tests and glucose levels are carried out.

Other immediate strategies to protect the brain during stroke include ensuring that blood sugar is as normal as possible (such as commencement of an insulin sliding scale in known diabetics), and that the stroke patient is receiving adequate oxygen and intravenous fluids. The patient may be positioned so that his or her head is flat on the stretcher, rather than sitting up, since studies have shown that this increases blood flow to the brain. Additional therapies for ischemic stroke include aspirin (50 to 325 mg daily), clopidogrel (75 mg daily), and combined aspirin and dipyridamole extended release (25/200 mg twice daily).

It is common for the blood pressure to be elevated immediately following a stroke. Studies indicated that while high blood pressure causes stroke, it is actually beneficial in the emergency period to allow better blood flow to the brain.

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 the stroke has been the result of cardiac arrhythmia (such as atrial fibrillation) with cardiogenic emboli, treatment of the arrhythmia and anticoagulation with warfarin or high-dose aspirin may decrease the risk of recurrence.


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 (eg, abnormal lab values, high blood pressure, recent surgery...). This position for tPA is based upon the findings of one study (NINDS; N Engl J Med 1995;333:1581-1587. ) which showed that tPA improves the chances for a good neurological outcome. When administered within the first 3 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. However, 55% of patients with large strokes developed substantial brain hemorrhage as a complication from being given tPA. tPA is often misconstrued in the news as a "magic bullet" and it is important for patients to be aware that despite the study that supports its use, some of the data were flawed and the safety and efficacy of tPA is controversial. A recent study (Neurology 2006:66, 1742-1744.) found the mortality to be higher among patients receiving tPA versus those who did not. 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. Until additional evidence clarifies such controversies, physicians are advised to use their discretion when considering its use. Given the cited absence of definitive evidence, AAEM believes it is inappropriate to claim that either use or non-use of intravenous thrombolytic therapy constitutes a standard of care issue in the treatment of stroke.

Mechanical Thrombectomy

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 up into the cerebral circulation, and deploying a corkscrew-like device to ensnare the clot, which is then withdrawn from the body. In August 2004, based on data from the MERCI (Mechanical Embolus Removal in Cerebral Ischemia) Trial, the FDA cleared one such device, called the Merci Retriever. Already newer generation devices are being tested in the Multi MERCI trial. Both the MERCI and Multi MERCI trials evaluated the use of mechanical thrombectomy up to 8 hours after onset of symptoms.

Hemorrhagic stroke

Patients with bleeding into ( intracerebral hemorrhage) or around the brain ( subarachnoid hemorrhage), require neurosurgical evaluation to detect and treat the cause of the bleeding. Anticoagulants and antithrombotics, key in treating ischemic stroke, can make bleeding worse and cannot be used in intracerebral hemorrhage. Patients are monitored and their blood pressure, blood sugar, and oxygenation are kept at optimum levels.

Care and rehabilitation

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

A rehabilitation team is usually multidisciplinary as it involves staff with different skills working together to help the patient. These include nursing staff, physiotherapy, occupational therapy, speech and language therapy, and usually a physician trained in rehabilitation medicine. Some teams may also include psychologists, social workers, and pharmacists since at least one third of the patients manifest post stroke depression.

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 is the cornerstone of the rehabilitation process. Often, assistive technology such as a wheelchair and standing frame may be beneficial. Another type of therapy involving relearning daily activities is occupational therapy (OT). OT involves exercise and training to help the stroke patient relearn everyday activities sometimes called the Activities of daily living (ADLs) such as eating, drinking and swallowing, dressing, bathing, cooking, reading and writing, and toileting. Speech and language therapy is appropriate for patients with problems understanding speech or written words, or problems forming speech.

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

Stroke rehabilitation can last anywhere from a few days to several months. Most return of function is seen in the first few days and weeks, and then improvement falls off. However, patients may continue to improve for years, regaining and strengthening abilities like writing, walking, running, and talking. Complete recovery is unusual but not impossible. Most patients will improve to some extent.


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

Some of the physical disabilities that can result from stroke include paralysis, numbness, pressure sores, pneumonia, incontinence, apraxia (inability to perform learned movements), difficulties carrying out daily activities, appetite loss, vision loss, and pain. If the stroke is severe enough, 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 ( Post stroke depression), which is characterized by lethargy, irritability, sleep disturbances, lowered self esteem, and withdrawal. 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. Some patients show the opposite of what they feel, for example crying when they are happy. 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.

Risk factors and prevention

The most important risk factors for stroke are hypertension, heart disease, diabetes, and cigarette smoking. Other risks include heavy alcohol consumption (see Alcohol consumption and health), high blood cholesterol levels, illicit drug use, and genetic or congenital conditions. 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. 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.

One of the most significant stroke risk factors is advanced age. 95% of strokes occur in people age 45 and older, and two-thirds of strokes occur in those over the age of 65. A person's risk of dying if he or she does have a stroke also increases with age. However, stroke can occur at any age, including in fetuses.

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

Men are 1.25 times more likely to suffer CVAs than women, yet 60% of deaths from stroke occur in women. Since women live longer, they are older on average when they have their strokes and thus more often killed (NIMH 2002). Some risk factors for stroke apply only to women. Primary among these are pregnancy, childbirth, menopause and the treatment thereof ( HRT). Stroke seems to run in some families.

Prevention is an important public health concern. Identification of patients with treatable risk factors for stroke is paramount. Treatment of risk factors in patients who have already had strokes (secondary prevention) is also very important as they are at high risk of subsequent events compared with those who have never had a stroke. Medication or drug therapy is the most common method of stroke prevention. Aspirin (usually at a low dose of 75 mg) is recommended for the primary and secondary prevention of stroke. Also see Antiplatelet drug treatment. Treating hypertension, diabetes mellitus, smoking cessation, control of hypercholesterolemia, physical exercise, and avoidance of illicit drugs and excessive alcohol consumption are all recommended ways of reducing the risk of stroke.

In patients who have strokes due to abnormalities of the heart, such as atrial fibrillation, anticoagulation with medications such as warfarin is often necessary for stroke prevention.

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. These procedures have been shown to prevent stroke in certain patients, especially where carotid stenosis leads to ischemic events such as transient ischemic attack.


Ischemic stroke occurs due to a loss of blood supply to part of the brain, initiating the Ischemic cascade. Brain tissue ceases to function if deprived of oxygen for more than 60 to 90 seconds and after a few hours will suffer irreversible injury possibly leading to death of the tissue, i.e., infarction. Atherosclerosis may disrupt the blood supply by narrowing the lumen of blood vessels leading to a reduction of blood flow, by causing the formation of blood clots within the vessel, or by releasing showers of small emboli through the disintegration of atherosclerotic plaques. Embolic infarction occurs when emboli formed elsewhere in the circulatory system, typically in the heart as a consequence of atria fibriliation, or in the carotid arteries. These break off, enter the cerebral circulation, then lodge in and occlude brain blood vessels.

Due to collateral circulation, within the region of brain tissue affected by ischemia there is a spectrum of severity. Thus, part of the tissue may immediately die while other parts may only be injured and could potentially recover. The ischemia area where tissue might recover is referred to as the ischemic penumbra.

As oxygen or glucose becomes depleted in ischemic brain tissue, the production of high energy phosphate compounds such as adenine triphosphate (ATP) fails leading to failure of energy dependent processes necessary for tissue cell survival. This sets off a series of interrelated events that result in cellular injury and death. These include the failure of mitochondria, which can lead further toward energy depletion and may trigger cell death due to apoptosis. Other processes include the loss of membrane ion pump function leading to electrolyte imbalances in brain cells. There is also the release of excitatory neurotransmitters, which have toxic effects in excessive concentrations.

Ischaemia 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 .

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 excitotoxic 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 be neuroprotective in stroke. 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 sofavorable results.

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 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.


Stroke will soon be the most common cause of death worldwide. Stroke is the third leading cause of death in the Western world, after heart disease and cancer, and causes 10% of world-wide deaths

The incidence of stroke increases exponentially from 30 years of age , and etiology varies by age .


Over 2,400 years ago, Hippocrates (460 to 370 BC) was first to describe the phenomenon of sudden paralysis, which we now know is caused by stroke. Apoplexy, from the Greek word meaning "struck down with violence,” first appeared in Hippocratic writings to describe stroke symptoms.

In 1658, in his Apoplexia, Johann Jacob Wepfer (1620-1695) identified the cause of hemorrhagic stroke when he suggested that people who had died of apoplexy had bleeding in their brains. Wepfer also identified the main arteries supplying the brain, the vertebral and carotid arteries, and identified the cause of ischemic stroke when he suggested that apoplexy might be caused by a blockage to those vessels.

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