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Stroke

2007 Schools Wikipedia Selection. Related subjects: Health and medicine

   CAPTION: Stroke
   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

   Dehydration

   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.

   Frequency:

   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.

   Headaches

   Nausea

   Vomiting

   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.

Diagnosis

   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)

Treatment

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.

Thrombolysis

   In increasing numbers of primary stroke centers, pharmacologic
   thrombolysis ("clot busting") with the drug Tissue plasminogen
   activator, tPA, is used to dissolve the clot and unblock the artery.
   However, the use of tPA in acute stroke is controversial. On one hand,
   it is endorsed by the American Heart Association and the American
   Academy of Neurology as the recommended treatment for acute stroke
   within three hours of onset of symptoms as long as there are not other
   contraindications (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.

Prognosis

   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.

Pathophysiology

   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.

Epidemiology

   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 .

History

   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.

   Retrieved from " http://en.wikipedia.org/wiki/Stroke"
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