stroke(redirected from Cerebrovascular accidents)
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- more than one-half million people in the United States experience a new or recurrent stroke each year
- stroke is the third leading cause of death in the United States and the leading cause of disability
- stroke kills about 160,000 Americans each year, or almost one out of three stroke victims
- three million Americans are currently permanently disabled from stroke
- in the United States, stroke costs about $30 billion per year in direct costs and loss of productivity
- two-thirds of strokes occur in people over age 65 but they can occur at any age
- strokes affect men more often than women, although women are more likely to die from a stroke
- strokes affect blacks more often than whites, and are more likely to be fatal among blacks
Causes and symptoms
- Age and sex. The risk of stroke increases with age, doubling for each decade after age 55. Men are more likely to have a stroke than women.
- Heredity. Blacks, Asians, and Hispanics have higher rates of stroke than do whites, related partly to higher blood pressure. People with a family history of stroke are at greater risk.
- Diseases. Stroke risk is increased for people with diabetes, heart disease (especially atrial fibrillation), high blood pressure, prior stroke, or TIA. Risk of stroke increases tenfold for someone with one or more TIAs.
- Other medical conditions. Stroke risk increases with obesity, high blood cholesterol level, or high red blood cell count.
- Hormone replacement therapy. In mid-2003, a large clinical trial called the Women's Health Initiative was halted when researchers discovered several potentially dangerous effects of combined hormone replacement therapy on postmenopausal women. In addition to increasing the risk of some cancers and dementia, combined estrogen and progesterone therapy increased risk of ischemic stroke by 31% among study participants.
- Lifestyle choices. Stroke risk increases with cigarette smoking (especially if combined with the use of oral contraceptives), low level of physical activity, alcohol consumption above two drinks per day, or use of cocaine or intravenous drugs.
- blurring or decreased vision in one or both eyes
- severe headache, often described as "the worst headache of my life"
- weakness, numbness, or paralysis of the face, arm, or leg, usually confined to one side of the body
- dizziness, loss of balance or coordination, especially when combined with other symptoms
- quitting smoking
- controlling blood pressure
- getting regular exercise
- keeping body weight down
- avoiding excessive alcohol consumption
- getting regular checkups and following the doctor's advice regarding diet and medicines, particularly hormone replacement therapy.
See also: stroking. Synonym(s): apoplexy, brain attack
See also: stroking.
See also: stroking.
See also: stroking.
An acute neurologic deficit resulting from circulatory impairment that resolves within 24 hours is called a transient ischemic attack (TIA); most TIAs last only 15-20 minutes. In contrast, a stroke involves irreversible brain damage, the type and severity of symptoms depending on the location and extent of brain tissue whose circulation has been compromised. The outcome of a stroke varies from minimal impairment to rapid onset of coma followed quickly by death. Stroke ranks third as a cause of death in adults in the U.S., after ischemic heart disease and cancer. About 600,000 people a year experience strokes in this country, of which about one fourth are fatal. At any given time the population includes about 3 million stroke survivors. Stroke costs the U.S. national economy more than $40 billion a year. The incidence of stroke has gradually declined during the past generation. Risk factors for stroke include hypertension, valvular heart disease or the presence of a prosthetic valve, atrial fibrillation, left ventricular dysfunction, hyperlipidemia, diabetes mellitus, cigarette smoking, obstructive sleep apnea, a history of previous stroke or TIA, and a family history of stroke. In addition, prolonged estrogen replacement therapy, elevation of plasma homocysteine, low circulating levels of folic acid and pyridoxine (vitamin B6), periodontal disease, and chronic bronchitis are all independent risk factors. Ischemic stroke, which accounts for about 85% of all strokes, is generally caused by atherothrombosis or embolism of a major cerebral artery. Less common causes of ischemic stroke include nonatheromatous vascular disease and coagulation disorders. Severe, acute ischemia in nerve tissue triggers cellular changes (calcium influx, protease activation) that can swiftly cause irreversible damage (infarction). Around the infarct zone lies a so-called penumbra of ischemic, electrically silent tissue that may be salvageable by prompt reperfusion. The mortality of ischemic stroke is 15-30% within the first 30 days. Hemorrhagic stroke, which makes up the other 15%, has a graver prognosis, with a 30-day mortality rate of 40-80%. Carriers of either the e2 or e4 allele of the apolipoprotein E (APOE) gene have an elevated risk of intracerebral hemorrhage. About 30% of ischemic infarcts, including most of those with severe impairment of cerebral blood flow and extensive tissue death, eventually develop a hemorrhagic component. The diagnostic evaluation of the patient with stroke includes history, physical examination, hematologic studies with coagulation profile, blood chemistries, electrocardiogram, and imaging studies. Although cranial CT without contrast enhancement is the procedure of choice to distinguish ischemic from hemorrhagic stroke and to identify subarachnoid hemorrhage, MRI is a more sensitive indicator of parenchymal hemorrhage as well as of early ischemia and infarction, and is more useful in assessing the brainstem and cerebellum and in identifying underlying nonvascular lesions. About 20% of people initially thought to have had a stroke prove to have some other disorder, and as many as 20% of strokes are missed on initial evaluation by emergency department physicians. Early and aggressive treatment is crucial in limiting damage to brain tissue and achieving an optimal outcome. In ischemic stroke, intravenous administration of tissue plasminogen activator (TPA) within the first 3 hours, with the purpose of dissolving an obstructing thrombus, has been shown to improve overall outcome at 90 days. Limiting factors in the use of thrombolytic therapy are the need to rule out hemorrhagic stroke (sometimes difficult with available imaging methods) and the fact that the therapy itself may induce hemorrhage. Intravenous thrombolytic agents other than TPA are not only less effective but also more likely to cause hemorrhage. During the acute phase of a stroke, respiratory and circulatory support and attention to fluid and electrolyte balance and nutrition are vitally important. Hypothermia and intravenous administration of heparin and magnesium also improve outcome in selected cases. Long-term consequences may depend on the aggressiveness and persistence of physical therapy and rehabilitation. About 40% of stroke victims develop depression, a complication that aggravates cognitive impairment and delays recovery. Effective measures for the prevention of stroke include aggressive management of hypertension (relative risk reduction, 30-50%), hyperlipidemia (30-40%), and diabetes mellitus; cessation of smoking; and chemoprophylaxis in patients at high risk. Administration of aspirin (acetylsalicylic acid) prophylactically inhibits platelet aggregation by suppressing thromboxane A2. Metaanalysis of randomized controlled trials involving a total of more than 50,000 people indicated that low-dose aspirin (81-325 mg/day) reduces the risk of ischemic stroke by 39 events per 10,000 people but increases the risk of hemorrhagic stroke by 12 events per 10,000 people. Other studies suggest that aspirin at higher dosage (1.3 g/day in divided doses) protects men but not women from ischemic stroke because in women aspirin also suppresses prostacyclin, a natural inhibitor of platelet aggregation. Prophylaxis with other antiplatelet agents (clopidogrel, ticlopidine) is equally effective in men and women and at least as protective as aspirin. In nonvalvular atrial fibrillation, warfarin prophylaxis reduces stroke risk by two thirds. In people with carotid artery stenosis of more than 70%, carotid endarterectomy clearly reduces the risk of stroke. The National Stroke Association has recommended adoption of the term brain attack for stroke, by analogy with the familiar heart attack, to emphasize to the public both the location of the lesion and the urgency of the need for assessment and treatment. see also tissue plasminogen activator.
strokeA clinical syndrome consisting of rapidly developing clinical signs of focal (at times global) disturbance of cerebral function, lasting more than 24 hours or leading to death, with no apparent cause other than that of vascular origin.
strokeCerebrovascular accident Neurology A sudden focal neurologic defect lasting > 24 hrs, which is characterized by abrupt loss of consciousness due to either hemorrhage or vascular occlusion of cerebral blood vessels, leading to immediate paralysis, weakness, speech defects; a sudden onset of neurologic deficit of vascular origin; strokes are a leading cause of disability in developed countries–500,000 new victims/yr, US, 20-30% of whom are left with severe residua; strokes are the 3rd leading cause of death–20-30% early mortality; the incidence of stroke rises dramatically with age; the risk doubles every decade after age 35 Statistics, mortality < 80 deaths/105: Whites in US–especially in the midwest, Australia, New Zealand, northern Europe, Egypt; >130 deaths/105: Black US–especially in south, Russia, mainland China, former Eastern Blocks, Argentina Clinical Paralysis, weakness, sensory loss, speech defects Etiology ASHD, dissection or stenosis of carotid artery, cocaine, embolism, HTN, fibromuscular dysplasia, syphilis Treatment Warfarin ↓ risk of stroke in Pts with A Fib or previous MI; in poor candidates for warfarin therapy, aspirin–which is less protective ± ticlopidine; carotid endarterectomy–useful if 70+% stenosis; CE's role in asymptomatic Pts is uncertain; dipyridamole and sulfinpyrazone are useless. See Completed stroke, Delayed stroke, Embolic stroke, Hemorrhagic stroke, Recent completed small stroke, Sunstroke, Working stroke.
See also: cerebrovascular accident
See also: stroking
Risk factors for stroke include advanced age (esp. older than 65 years), atherosclerosis of the aortic arch, atrial fibrillation, carotid artery disease, cigarette use, excessive alcohol use (more than 5 drinks daily), heart failure, hyperlipidemia, hypertension, a history of myocardial infarction, diabetes mellitus, male gender, close relation of someone who has had a stroke, nonwhite race, peripheral vascular disease, physical inactivity, obesity, using combination hormonal contraception (the pill, ring, patch), being pregnant or immediately postpartum, or a recent transient ischemic attack.
The National Institute of Neurological Disorders and Stroke lists the following symptoms as warning signs of stroke: sudden weakness or numbness of the face, arm, or leg; sudden loss of vision, double vision, dimming of vision in one or both eyes; sudden difficulty speaking or understanding speech; sudden severe headache; and sudden falling, gait disturbance, or dizziness. The patient who experiences these problems should call 911 immediately. If symptoms disappear in a few minutes, the individual may have experienced a transient ischemic attack (TIA [informally known as a “ministroke” or a “warning stroke”]) and should notify his/her primary care provider immediately for preventive care. In clinical practice, stroke patients often present with more than one stroke symptom (e.g., limb paralysis and aphasia; severe headache and hemibody deficits). It is also important to note that these symptoms are not specific for stroke: sudden dizziness or gait disturbance can occur as a result of intoxication with drugs or alcohol, for example, and sudden severe head pain can result from cluster headache, migraine, and many other disorders.
Acute ischemic stroke can be treated with recombinant tissue plasminogen activator (rt-PA) if the disease is recognized in the first 90 to 180 min and intracerebral hemorrhage has been excluded with urgent computed tomography (CT) or magnetic resonance imaging (MRI) scanning of the brain. This form of therapy is not without risk; thrombolytic drugs can reduce the potential for long-term disability and death by 20%, but increase the risk of hemorrhage. Hemorrhagic strokes, which have about a 50% mortality, can sometimes be treated by evacuating blood clots from the brain or by repairing intracerebral aneurysms.
CAUTION!Patients with hemorrhagic stroke should never receive fibrinolytic drugs. Other contraindications to fibrinolysis in stroke include recent or active bleeding or a known propensity for abnormal bleeding; recent lumbar puncture; recent arterial puncture; recent myocardial infarction; recent surgery or major trauma; seizure at the onset of the stroke; or blood pressure over 185/110 that does not improve with simple therapies.
Acute phase: The health care team performs a history and physical assessment, including a careful examination of airway, breathing, circulation, and neurological functions. The Glasgow Coma Scale should be used to assess level of consciousness. The severity of a stroke should be assessed with a valid scale, such as the National Institute’s of Health Stroke Scale (NIHSS) or other well-publicized assessment tools. Staff provides oxygen by nasal cannula, establishes venous access via two large-bore catheters, and infuses saline intravenously; obtains blood samples for complete blood count, blood glucose, electrolytes, and coagulation studies; and obtains a 12-lead ECG and initiates cardiac monitoring. The stroke team, neurologist, radiologist, and MRI and/or CT technician are alerted. Fever and hyperglycemia are treated aggressively because elevated body temperatures and elevated blood glucose levels have been linked to poorer outcomes. Blood pressure is gently controlled to a level less than 180/110: more aggressive pressure control may be hazardous. The patient is positioned in the lateral or semiprone position with the head elevated 15 to 30 degrees to decrease cerebral venous pressure. Neurological status is monitored for signs of deterioration or improvement, and findings are documented on a flow sheet. The National Institute of Neurological Disorders and Stroke (NINDS) suggests the following order of assessment in patients with suspected stroke: level of consciousness, eye movements, visual fields, facial movements, motor function of arms and legs, limb coordination, sensory responses, and language use including clarity of speech. A history of the incident is obtained, including how and when symptoms started. Past medical history should be reviewed (hypertension, use of anticoagulant drugs, cardiac dysrhythmias). The patient is prepared for prescribed diagnostic studies, including MRI and/or CT, and possibly arteriography.
The patient is oriented frequently and reassured with verbal and tactile contacts. Attention is focused on determining the patient’s candidacy for emergent use of thrombolytic therapy. If potential benefits are established, recombinant tissue plasminogen activator (rt-PA) is administered intravenously over 60 min, with 10% of the determined dosage as a bolus in the first 60 sec. Blood pressure is monitored closely once the infusion is started, and any elevation treated aggressively. The patient also is monitored for indications of systemic bleeding (tachycardia, tachypnea, hypotension or acute hypertension, rapid mental status deterioration, severe headache, and nausea and vomiting). When rt-PA administration is complete, the patient is transferred to the neurologic ICU or neurology unit. If clot-busting drugs cannot or should not be administered, monitoring and supportive care is provided. The ability to speak is assessed, and if aphasia is present, a consultation by a speech therapist is obtained. Bladder function is assessed; noninvasive measures are used to encourage voiding in the presence of urinary retention, voiding pattern is determined, and the incontinent patient is kept clean and dry. Use of indwelling catheters is limited because these promote urinary tract infection. Bowel function is assessed, and dietary intervention and stool softeners or laxatives as necessary are used to prevent constipation. Straining at stool or use of enemas is avoided. Fluid and electrolyte balance (intake, output, daily weight, laboratory values) is monitored and maintained. Adequate enteral or parenteral nutrition is provided as appropriate. Nursing measures are instituted to prevent complications of immobility. In consultation with occupational therapists and physical therapists, a program of positioning and mobility is initiated, as appropriate. Examples of activities include repositioning at least every 2 hr, maintaining correct body alignment, supporting joints to prevent flexion and rotation contractures, and providing range-of-motion exercises (passive to involved joints, active-assisted or active to uninvolved joints). Irrigation and lubrication prevent oral mucous membranes and eyes (cornea) from drying. Prescribed medical therapy is administered to decrease cerebral edema, and antihypertensives or anticoagulants are given as appropriate for etiology. The patient is observed for seizure activity, and drug therapy and safety precautions are initiated. Most stroke patients are hospitalized for a few days. Patient education about risk modification begins prior to discharge.
Rehabilitative phase: After the acute phase of stroke, rehabilitation goals depend on the severity of the patient's deficit, the age of the patient, the presence of comorbidities and prior functional status, his or her ability to perform activities of daily living independently, and the family and social support systems available. The rehabilitation program will consist of various types of exercises, including neuromuscular retraining, motor learning and motor control, and functional activities that emphasize relearning or retraining in basic skills required for self-care. This may include instruction in the use of adaptive and supportive devices to facilitate independence in daily tasks. The goal of rehabilitation is to achieve an optimal functional outcome that will allow the patient to be discharged to the least restrictive environment. Ideally, the patient will achieve sufficient independence to return to community living, either independently or with family and community support.
All patient efforts should receive positive reinforcement. Patient communication is a priority. Exercises, proper positioning, and supportive devices help to prevent deformities. Quiet rest periods are provided based on the patient's response to activity. The patient should either assist with or perform own personal hygiene and establish independence in other activities of daily living. The rehabilitation team evaluates the patient's ability to feed self and continues to provide enteral feeding as necessary. A bowel and bladder retraining program is initiated, and both patient and family receive instruction in its management. Both patient and family are taught about the therapeutic regimen (activity and rest, diet, and medications), including desired effects and adverse reactions to report. Emotional lability, a consequence of some strokes, is recognized and explained, and assistance is provided to help the patient deal with changes in affect.
The best results are achieved by patients treated in specialized treatment centers with demonstrably low complication rates. All stroke patients are advised to reduce their risk for future stroke by taking prescribed antihypertensive drugs as directed; losing excess weight; exercising regularly; eating a well-balanced diet low in fat, cholesterol, sugar, and salt; stopping smoking; limiting alcohol intake; and maintaining glycemic control. Patient and family are referred to the American Stroke Association or local stroke groups for information and support (http://www.strokeassociation.org).
|Cause of Stroke||Frequency of Occurrence|
|Emboli from other organs, e.g., heart||about 15%|
|Cerebrovascular disease||greater than 50%|
|Trauma||less than 5%|
|Hypercoagulable states||less than 5%|
strokeThe effect of acute deprivation of blood to a part of the brain by narrowing or obstruction of an artery, usually by thrombosis (80 %), or of damage to the brain substance from bleeding into it (CEREBRAL HAEMORRHAGE) (15%). Subarachnoid haemorrhage is the cause in 5%. The results of such damage are most obvious if they involve the nerve tracts concerned with movement, sensation, speech and vision. These are situated close together, in the internal capsule of the brain, and are often involved together. There may be paralysis and loss of sensation down one side of the body or of one side of the face, loss of corresponding halves of the fields of vision, a range of speech disturbances or various disorders of comprehension or expression. In most cases a degree of recovery, sometimes considerable, may be expected. Haemorrhage into the brainstem, where the centres for the control of the vital functions of breathing and heart-beat are situated, is the most immediately dangerous to life. Diagnosis of the type of stroke is important and this requires neuroimaging of the brain.
Patient discussion about stroke
Q. Stroke My granny got stroke. Now she is in the hospital, but she doesn't identify me or my mother. When I asked her what are the season now - she answers that it's winter now. I don't know how to help her. What I have to prepare for?
Q. Migraine stroke Hi, I'm 58 years-old male and I have migraines with aura since age 14. Two weeks ago, I felt weakness in the left side of my body, and at the hospital the doctors told me I had a stroke. I underwent several tests, but they still don't know the cause for the stroke (my lab tests are normal; I don't have diabetes or hypertension). My neurologist said that although it's very rare, he thinks that my stroke was caused by my migraine. I tried to find information about it, but couldn't find much – do you know where I can get some more info? Thanks!
Q. What Are the Risk Factors for Developing Stroke? My father had a stroke recently, at the age of 73. What are the risk factors for developing this?
2) excessive alcohol intake
3) uncontrolled high blood pressure
4) high cholesterol
5) overweight/unhealthy diet
6) illegal drugs/abuse of Rx drugs
7) known or unknown heart problems
9) known or unknown vascular brain defects - aneurysm, etc.
10)family history of stroke