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Related to brain attack: heart attack, stroke
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.
brain attackA lay term for an abrupt, nonpsychogenic change in mental status, unrelated to infection or trauma; BAs correspond to either a transient ischaemic attack or cerebrovascular accident.
brain attackNeurology A lay term for an abrupt, nonpsychogenic change in mental status, unrelated to infection or trauma; BAs correspond to either a TIA or CVA. See Cerebrovascular accident, Stroke, Transient ischemic attack.
a·cute is·che·mic stroke(AIS) (ă-kyūt' is-kē'mik strōk)
Synonym(s): brain attack, cerebral vascular attack.
Patient discussion about brain attack
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