1. Any acute clinical event, related to impairment of cerebral circulation, that lasts more than 24 hours. SYN: apoplexy, brain attack. 2. A harmful discharge of lightning, particularly one that affects a human being. 3. A pulsation. 4. To pass the hand or any instrument gently over a surface. SEE ALSO: stroking. 5. A gliding movement over a surface. [A.S. strac] Acute neurologic deficits resulting from circulatory impairment that resolve within 24 hours are called transient ischemic attacks (TIAs); most TIAs last only 15–20 minutes. In contrast, a s. 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 s. varies from minimal impairment to rapid onset of coma followed quickly by death. S. ranks third as a cause of death in adults in the U.S., after ischemic heart disease and cancer. About 700,000 people a year experience strokes in this country, and at any given time the population includes about 3 million s. survivors. The incidence of s. has gradually declined during the past generation. Risk factors for s. include hypertension, valvular heart disease, atrial fibrillation, hyperlipidemia, diabetes mellitus, cigarette smoking, and a family history of s.. In addition, recent studies have shown that 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 s., 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 s. 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 s. is 15–30% within the first 30 days. Hemorrhagic s., which makes up the other 15%, has a graver prognosis, with a 30-day mortality rate of 40–80%. The diagnostic evaluation of the patient with s. includes history, physical examination, blood count, blood chemistries, coagulation profile, electrocardiogram, and imaging studies. While cranial CT is the procedure of choice to identify subarachnoid hemorrhage, MRI is a more sensitive indicator of parenchyal hemorrhage as well as of ischemia and infarction. About 20% of persons initially thought to have had a s. 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 s., 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 s. (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. In limited studies, intraarterial injection of prourokinase up to 6 hours after stoke onset has favorably influenced outcome. During the acute phase of a s., 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. Effective measures for the prevention of s. include aggressive management of hypertension, hyperlipidemia, and diabetes mellitus, cessation of smoking, and chemoprophylaxis in persons at high risk. Administration of aspirin (acetylsalicylic acid) prophylactically inhibits platelet aggregation by suppressing thromboxane A2. A meta-analysis of randomized controlled trials involving a total of more than 50,000 people indicated that low-dosage aspirin (80–325 mg/day) reduces the risk of ischemic s. by 39 events per 10,000 persons but increases the risk of hemorrhagic s. by 12 events per 10,000 persons. Other studies suggest that aspirin at higher dosage (1.3 g/day in divided doses) protects men but not women from ischemic s. 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 s. risk by two-thirds. Most studies show that, in persons with carotid artery stenosis of at least 60%, carotid endarterectomy reduces the risk of s.. The National S. Association has recommended adoption of the term brain attack for s., 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.
- effective s. the rapid forward movement of cilia.
- heart s. impact of the apex of the heart against the wall of the chest.
- recovery s. the slow return movement of cilia.
- spinal s. abrupt onset of focal spinal cord dysfunction caused by a disturbance in its blood supply.
- sun s. sunstroke.

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stroke 'strōk n sudden diminution or loss of consciousness, sensation, and voluntary motion caused by rupture or obstruction (as by a clot) of a blood vessel of the brain called also apoplexy, brain attack, cerebral accident, cerebrovascular accident see hemorrhagic stroke, ischemic stroke, LITTLE STROKE

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a sudden attack of weakness affecting one side of the body. It is the consequence of an interruption to the flow of blood to the brain. An ischaemic stroke occurs when the flow of blood is prevented by clotting (see thrombosis) or by a detached clot, either from the heart or a large vessel (such as the carotid artery), that lodges in an artery (see embolism). A haemorrhagic stroke results from rupture of an artery wall (see cerebral haemorrhage). Prolonged reduction of blood pressure may result in more diffuse brain damage, as after a cardiorespiratory arrest. A stroke can vary in severity from a passing weakness or tingling in a limb (see transient ischaemic attack) to a profound paralysis, coma, and death.

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(strōk) 1. a sudden and severe attack; called also ictus. 2. stroke syndrome. 3. a pulsation.

Medical dictionary. 2011.

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