User:CFCF/sandbox/Stroke

A stroke, sometimes referred to as a cerebrovascular accident (CVA), cerebrovascular insult (CVI), or colloquially brain attack is the loss of

Strokes can be classified into two major categories: ischemic and hemorrhagic.^[7] Ischemic strokes are caused by interruption of the blood supply, while hemorrhagic strokes result from the rupture of a blood vessel or an abnormal vascular structure. About 87% of strokes are ischemic, the rest are hemorrhagic. Some hemorrhages develop inside areas of ischemia ("hemorrhagic transformation"). It is unknown how many hemorrhagic strokes actually start as ischemic stroke.^[5]

In the 1970s the World Health Organization defined stroke as a "neurological deficit of cerebrovascular cause that persists beyond 24 hours or is interrupted by death within 24 hours",^[8] although the word "stroke" is centuries old. This definition was supposed to reflect the reversibility of tissue damage and was devised for the purpose, with the time frame of 24 hours being chosen arbitrarily. The 24-hour limit divides stroke from transient ischemic attack, which is a related syndrome of stroke symptoms that resolve completely within 24 hours.^[5] With the availability of treatments which can reduce stroke severity when given early, many now prefer alternative terminology, such as brain attack and acute ischemic cerebrovascular syndrome (modeled after heart attack and acute coronary syndrome, respectively), to reflect the urgency of stroke symptoms and the need to act swiftly.^[9]

In an ischemic stroke, blood supply to part of the brain is decreased, leading to dysfunction of the brain tissue in that area. There are four reasons why this might happen:

1. Thrombosis (obstruction of a blood vessel by a blood clot forming locally)
2. Embolism (obstruction due to an embolus from elsewhere in the body, see below),^[5]
3. Systemic hypoperfusion (general decrease in blood supply, e.g., in shock)^[10]
4. Venous thrombosis.^[11]

Stroke without an obvious explanation is termed "cryptogenic" (of unknown origin); this constitutes 30-40% of all ischemic strokes.^[5][12]

There are various classification systems for acute ischemic stroke. The Oxford Community Stroke Project classification (OCSP, also known as the Bamford or Oxford classification) relies primarily on the initial symptoms; based on the extent of the symptoms, the stroke episode is classified as

Intracranial hemorrhage is the accumulation of blood anywhere within the skull vault. A distinction is made between

Stroke symptoms typically start suddenly, over seconds to minutes, and in most cases do not progress further. The symptoms depend on the area of the brain affected. The more extensive the area of brain affected, the more functions that are likely to be lost. Some forms of stroke can cause additional symptoms. For example, in intracranial hemorrhage, the affected area may compress other structures. Most forms of stroke are not associated with headache, apart from subarachnoid hemorrhage and cerebral venous thrombosis and occasionally intracerebral hemorrhage.

Various systems have been proposed to increase recognition of stroke. Different findings are able to predict the presence or absence of stroke to different degrees. Sudden-onset face weakness, arm drift (i.e., if a person, when asked to raise both arms, involuntarily lets one arm drift downward) and abnormal speech are the findings most likely to lead to the correct identification of a case of stroke increasing the likelihood by 5.5 when at least one of these is present). Similarly, when all three of these are absent, the likelihood of stroke is significantly decreased (– likelihood ratio of 0.39).^[17] While these findings are not perfect for diagnosing stroke, the fact that they can be evaluated relatively rapidly and easily make them very valuable in the acute setting.

Proposed systems include

• hemiplegia and muscle weakness of the face
• numbness
• reduction in sensory or vibratory sensation
• initial
  flaccidity (hypotonicity), replaced by spasticity (hypertonicity), hyperreflexia, and obligatory synergies.^[23]

In addition to the above CNS pathways, the brainstem gives rise to most of the twelve cranial nerves. A stroke affecting the brain stem and brain therefore can produce symptoms relating to deficits in these cranial nerves:

• altered smell, taste, hearing, or vision (total or partial)
• drooping of eyelid (ptosis) and weakness of ocular muscles
• decreased reflexes: gag, swallow, pupil reactivity to light
• decreased sensation and muscle weakness of the face
• balance problems and nystagmus
• altered breathing and heart rate
• weakness in sternocleidomastoid muscle with inability to turn head to one side
• weakness in tongue (inability to protrude and/or move from side to side)

If the cerebral cortex is involved, the CNS pathways can again be affected, but also can produce the following symptoms:

• reading and/or writing Broca's or Wernicke's area
  typically involved)
• dysarthria (motor speech disorder resulting from neurological injury)
• apraxia (altered voluntary movements)
• visual field defect
• memory deficits (involvement of temporal lobe)
• hemineglect (involvement of parietal lobe
  )
• disorganized thinking, confusion,
  hypersexual
  gestures (with involvement of frontal lobe)
• lack of insight of his or her, usually stroke-related, disability

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

• altered walking gait
• 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 the brain.

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

In thrombotic stroke a thrombus^[24] (blood clot) usually forms around atherosclerotic plaques. Since blockage of the artery is gradual, onset of symptomatic thrombotic strokes is slower. A thrombus itself (even if non-occluding) can lead to an embolic stroke (see below) if the thrombus breaks off, at which point it is called an "embolus." Two types of thrombosis can cause stroke:

• Large vessel disease involves the common and
  Takayasu arteritis, giant cell arteritis, vasculitis), noninflammatory vasculopathy, Moyamoya disease and fibromuscular dysplasia
  .
• Small vessel disease involves the smaller arteries inside the brain: branches of the
  lacunar infarcts) and microatheroma (small atherosclerotic plaques).^[27]

An embolic stroke refers to the blockage of an artery by an arterial embolus, a traveling particle or debris in the arterial bloodstream originating from elsewhere. An embolus is most frequently a thrombus, but it can also be a number of other substances including fat (e.g., from bone marrow in a broken bone), air, cancer cells or clumps of bacteria (usually from infectious endocarditis).^[3]

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

Emboli most commonly arise from the heart (especially in atrial fibrillation) but may originate from elsewhere in the arterial tree. In paradoxical embolism, a deep vein thrombosis embolizes through an atrial or ventricular septal defect in the heart into the brain.^[3]

Cardiac causes can be distinguished between high and low-risk:^[29]

• High risk: atrial fibrillation and
  coronary artery bypass graft
  (CABG) surgery.
• Low risk/potential: calcification of the annulus (ring) of the mitral valve, patent foramen ovale (PFO), atrial septal aneurysm, atrial septal aneurysm with patent foramen ovale, left ventricular aneurysm without thrombus, isolated left atrial "smoke" on echocardiography (no mitral stenosis or atrial fibrillation), complex atheroma in the ascending aorta or proximal arch.

Cerebral hypoperfusion is the reduction of blood flow to all parts of the body. It is most commonly due to

Cerebral venous sinus thrombosis leads to stroke due to locally increased venous pressure, which exceeds the pressure generated by the arteries. Infarcts are more likely to undergo hemorrhagic transformation (leaking of blood into the damaged area) than other types of ischemic stroke.^[11]

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

Stroke is diagnosed through several techniques: a neurological examination (such as the

For diagnosing ischemic stroke in the emergency setting:[42]

• CT scans (without contrast enhancements)

sensitivity

= 16%

specificity

= 96%

• MRI scan

sensitivity= 83%

specificity= 98%

For diagnosing hemorrhagic stroke in the emergency setting:

• CT scans (without contrast enhancements)

sensitivity= 89%

specificity= 100%

• MRI scan

sensitivity= 81%

specificity= 100%

For detecting chronic hemorrhages, MRI scan is more sensitive.^[43]

For the assessment of stable stroke, nuclear medicine scans SPECT and PET/CT may be helpful. SPECT documents cerebral blood flow and PET with FDG isotope the metabolic activity of the neurons.

When a stroke has been diagnosed, various other studies may be performed to determine the underlying cause. With the current treatment and diagnosis options available, it is of particular importance to determine whether there is a peripheral source of emboli. Test selection may vary, since the cause of stroke varies with age, comorbidity and the clinical presentation. Commonly used techniques include:

• an
  carotid stenosis
  ) or dissection of the precerebral arteries;
• an
  arrhythmias
  and resultant clots in the heart which may spread to the brain vessels through the bloodstream);
• a Holter monitor study to identify intermittent arrhythmias;
• an
  angiogram of the cerebral vasculature (if a bleed is thought to have originated from an aneurysm or arteriovenous malformation
  );
• blood tests to determine hypercholesterolemia,
  homocysteinuria
  .

No high-quality studies have shown the effectiveness of interventions aimed at weight reduction, promotion of regular exercise, reducing alcohol consumption or smoking cessation.^[59] Nonetheless, given the large body of circumstantial evidence, best medical management for stroke includes advice on diet, exercise, smoking and alcohol use.^[60] Medication or drug therapy is the most common method of stroke prevention; carotid endarterectomy can be a useful surgical method of preventing stroke.

Those with atrial fibrillation have a 5% a year risk of stroke, and this risk is higher in those with valvular atrial fibrillation.^[71] Depending on the stroke risk, anticoagulation with medications such as warfarin or aspirin is useful for prevention.^[72]

High cholesterol levels have been inconsistently associated with (ischemic) stroke.

In primary prevention however, antiplatelet drugs did not reduce the risk of ischemic stroke while increasing the risk of major bleeding.[82]^[83] Further studies are needed to investigate a possible protective effect of aspirin against ischemic stroke in women.^[84][85]

Carotid endarterectomy or carotid angioplasty can be used to remove atherosclerotic narrowing (stenosis) of the carotid artery. There is evidence supporting this procedure in selected cases.^[60] Endarterectomy for a significant stenosis has been shown to be useful in the prevention of further strokes in those who have already had one.^[86] Carotid artery stenting has not been shown to be equally useful.^[87][88] Patients are selected for surgery based on age, gender, degree of stenosis, time since symptoms and patients' preferences.^[60] Surgery is most efficient when not delayed too long —the risk of recurrent stroke in a patient who has a 50% or greater stenosis is up to 20% after 5 years, but endarterectomy reduces this risk to around 5%. The number of procedures needed to cure one patient was 5 for early surgery (within two weeks after the initial stroke), but 125 if delayed longer than 12 weeks.^[89][90]

Screening for carotid artery narrowing has not been shown to be a useful screening test in the general population.^[91] Studies of surgical intervention for carotid artery stenosis without symptoms have shown only a small decrease in the risk of stroke.^[92][93] To be beneficial, the complication rate of the surgery should be kept below 4%. Even then, for 100 surgeries, 5 patients will benefit by avoiding stroke, 3 will develop stroke despite surgery, 3 will develop stroke or die due to the surgery itself, and 89 will remain stroke-free but would also have done so without intervention.^[60]

Nutrition, specifically the

Anticoagulants, when used following stroke, should not be stopped for dental procedures.[101]

If studies show carotid stenosis, and the person has residual function in the affected side, carotid endarterectomy (surgical removal of the stenosis) may decrease the risk of recurrence if performed rapidly after stroke.

Definitive therapy is aimed at removing the blockage by breaking the clot down (thrombolysis), or by removing it mechanically (thrombectomy). The philosophical premise underlying the importance of rapid stroke intervention was crystallized as Time is Brain! in the early 1990s.^[102] Years later, that same idea, that rapid cerebral blood flow restoration results in fewer brain cells dying, has been proved and quantified.^[103]

Tight control of blood sugars in the first few hours does not improve outcomes and may cause harm.^[104] High blood pressure is also not typically lowered as this has not been found to be helpful.

Thrombolysis with

People with intracerebral hemorrhage require neurosurgical evaluation to detect and treat the cause of the bleeding, although many may not need surgery. Anticoagulants and antithrombotics, key in treating ischemic stroke, can make bleeding worse. People are monitored for changes in the level of consciousness, and their blood pressure, blood sugar, and oxygenation are kept at optimum levels.^{[citation needed]}

Ideally, people who have had a stroke are admitted to a "stroke unit", a ward or dedicated area in hospital staffed by nurses and therapists with experience in stroke treatment. It has been shown that people admitted to a stroke unit have a higher chance of surviving than those admitted elsewhere in hospital, even if they are being cared for by doctors without experience in stroke.^[5][113]

When an acute stroke is suspected by history and physical examination, the goal of early assessment is to determine the cause. Treatment varies according to the underlying cause of the stroke, thromboembolic (ischemic) or hemorrhagic.

A rehabilitation team is usually multidisciplinary as it involves staff with different skills working together to help the patient. These include physicians trained in rehabilitation medicine,

Treatment of spasticity related to stroke often involves early mobilizations, commonly performed by a physiotherapist, combined with elongation of spastic muscles and sustained stretching through various positionings.[23] Gaining initial improvement in range of motion is often achieved through rhythmic rotational patterns associated with the affected limb.^[23] After full range has been achieved by the therapist, the limb should be positioned in the lengthened positions to prevent against further contractures, skin breakdown, and disuse of the limb with the use of splints or other tools to stabilize the joint.^[23] Cold in the form of ice wraps or ice packs have been proven to briefly reduce spasticity by temporarily dampening neural firing rates.^[23] Electrical stimulation to the antagonist muscles or vibrations has also been used with some success.^[23]

Some current and future therapy methods include the use of virtual reality and video games for rehabilitation. These forms of rehabilitation offer potential for motivating patients to perform specific therapy tasks that many other forms do not.^[119] Many clinics and hospitals are adopting the use of these off-the-shelf devices for exercise, social interaction and rehabilitation because they are affordable, accessible and can be used within the clinic and home.^[119]

Other novel non-invasive rehabilitation methods are currently being developed to augment physical therapy to improve motor function of stroke patients, such as transcranial magnetic stimulation (TMS) and transcranial direct-current stimulation (tDCS)^[120] and robotic therapies.^[121]

A stroke can also reduce people's general fitness.^[122] Reduced fitness can reduce capacity for rehabilitation as well as general health.^[123] A systematic review found that there are inadequate long-term data about the effects of exercise and training on death, dependence and disability after a stroke.^[122] However, cardiorespiratory training added to walking programs in rehabilitation can improve speed, tolerance and independence during walking.^[122]

Disability affects 75% of stroke survivors enough to decrease their employability.^[124] Stroke can affect peoples physically, mentally, emotionally, or a combination of the three. The results of stroke vary widely depending on size and location of the lesion.^[125] Dysfunctions correspond to areas in the brain that have been damaged.

Some of the physical disabilities that can result from stroke include muscle weakness, numbness,

30 to 50% of stroke survivors suffer post stroke depression, which is characterized by lethargy, irritability, sleep disturbances, lowered self esteem, and withdrawal.^[126]

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.^[124] Some patients show the opposite of what they feel, for example crying when they are happy.^[127] Emotional lability occurs in about 20% of stroke patients.

Cognitive deficits resulting from stroke include perceptual disorders, Aphasia,^[128] dementia,^[129] and problems with attention^[130] and memory.^[131] 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.

Cognitive and psychological outcome after a stroke can be affected by the age at which the stroke happened, pre-stroke baseline intellectual functioning, psychiatric history and whether there is pre-existing brain pathology.^[132]

Up to 10% of people following a stroke develop seizures, most commonly in the week subsequent to the event; the severity of the stroke increases the likelihood of a seizure.^[133][134]

Stroke was the second most frequent cause of death worldwide in 2011, accounting for 6.2 million deaths (~11% of the total). ^[136] Approximately 17 million people had a stroke in 2010 and 33 million people have previously had a stroke and were still alive.^[137] Between 1990 and 2010 the number of strokes decrease by approximately 10% in the developed world and increased by 10% in the developing world.^[137] Overall two thirds of strokes occurred in those over 65 years old.^[137]

It is ranked after heart disease and before cancer.

The incidence of stroke increases exponentially from 30 years of age, and etiology varies by age.^[139] Advanced age is one of the most significant stroke risk factors. 95% of strokes occur in people age 45 and older, and two-thirds of strokes occur in those over the age of 65.^[126][28] A person's risk of dying if he or she does have a stroke also increases with age. However, stroke can occur at any age, including in childhood.

Family members may have a genetic tendency for stroke or share a lifestyle that contributes to stroke. Higher levels of Von Willebrand factor are more common amongst people who have had ischemic stroke for the first time.^[140] The results of this study found that the only significant genetic factor was the person's blood type. Having had a stroke in the past greatly increases one's risk of future strokes.

Men are 25% more likely to suffer strokes than women,

Episodes of stroke and familial stroke have been reported from the 2nd millennium BC onward in ancient Mesopotamia and Persia.^[141] Hippocrates (460 to 370 BC) was first to describe the phenomenon of sudden paralysis that is often associated with ischemia. Apoplexy, from the Greek word meaning "struck down with violence," first appeared in Hippocratic writings to describe this phenomenon.^[142][143] The word stroke was used as a synonym for apoplectic seizure as early as 1599,^[144] and is a fairly literal translation of the Greek term.

In 1658, in his Apoplexia,

The term cerebrovascular accident was introduced in 1927, reflecting a "growing awareness and acceptance of vascular theories and (...) recognition of the consequences of a sudden disruption in the vascular supply of the brain".[146] Its use is now discouraged by a number of neurology textbooks, reasoning that the connotation of fortuitousness carried by the word accident insufficiently highlights the modifiability of the underlying risk factors.^{[147][148][149]} Cerebrovascular insult may be used interchangeably.^[150]

The term brain attack was introduced for use to underline the acute nature of stroke according to the

Angioplasty and stenting have begun to be looked at as possible viable options in treatment of acute ischemic stroke. Intra-cranial stenting in symptomatic intracranial arterial stenosis, the rate of technical success (reduction to stenosis of <50%) ranged from 90-98%, and the rate of major peri-procedural complications ranged from 4-10%. The rates of restenosis and/or stroke following the treatment were also favorable. This data suggests that a randomized controlled trial is needed to more completely evaluate the possible therapeutic advantage of this preventative measure.^[153]

Removal of the clot may be attempted in those where it occurs within a large blood vessel and may be an option for those who either are not eligible for or do not improve with intravenous thrombolytics.^[154] Significant complications occur in about 7%.^[155] As of October 2013^[update], trials have not shown positive results.^[156]

Drugs that scavenge

Further reading

• J. P. Mohr, Dennis Choi, James Grotta, Philip Wolf (2004). Stroke: Pathophysiology, Diagnosis, and Management. New York: Churchill Livingstone.
  OCLC 50477349 52990861. {{cite book}}: Check |oclc= value (help)CS1 maint: multiple names: authors list (link
  )
• Charles P. Warlow, Jan van Gijn, Martin S. Dennis, Joanna M. Wardlaw, John M. Bamford, Graeme J. Hankey, Peter A. G. Sandercock, Gabriel Rinkel, Peter Langhorne, Cathie Sudlow, Peter Rothwell (2008). Stroke: Practical Management (3rd ed.). Wiley-Blackwell.
  ISBN 978-1-4051-2766-0.{{cite book}}: CS1 maint: multiple names: authors list (link
  )

External links

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