The most important risk factors for stroke are hypertension, heart disease, diabetes, and cigarette smoking. Other risks include heavy alcohol consumption, 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. 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 anemia.
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. 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.
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 apoptotis 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.
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.
Taking fish oil supplements (eg. Maxepa) may prevent stroke to some extent.
2006-09-27 22:14:19
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answer #1
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answered by Ajeesh Kumar 4
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Causes of ischemic stroke
An ischemic stroke is caused by a blood clot that blocks blood flow to the brain. A blood clot can develop in a narrowed artery that supplies the brain or can travel from the heart (or elsewhere in the body) to an artery that supplies the brain.
Blood clots are usually the result of other problems in the body that affect the normal flow of blood, such as:
Hardening of the arteries (atherosclerosis). This is caused by high blood pressure, diabetes, and high cholesterol.
Atrial fibrillation or other irregular heart rhythms.
Certain heart valve problems, including having an artificial heart valve, a repaired heart valve, heart valve disease such as mitral valve prolapse, or narrowing (stenosis) of a heart valve.
Infection of the heart valves (endocarditis).
A patent foramen ovale, which is a congenital heart defect.
Blood-clotting disorders.
Inflammation of blood vessels (vasculitis).
Heart attack.
Low blood pressure (hypotension) may also cause an ischemic stroke, although less commonly. Low blood pressure results in reduced blood flow to the brain and may develop as a result of narrowed or diseased arteries, a heart attack, a large loss of blood, or a severe infection.
Some surgeries (such as endarterectomy) or other procedures (such as angioplasty) that are used to treat narrowed carotid arteries may ultimately cause a blood clot to break loose, resulting in a stroke.
Causes of hemorrhagic stroke
A hemorrhagic stroke is caused by bleeding inside the brain (called intracerebral hemorrhage) or bleeding in the space around the brain (called subarachnoid hemorrhage). Bleeding inside the brain may be a result of long-standing high blood pressure. Bleeding in the space around the brain may be caused by a ruptured aneurysm or uncontrolled high blood pressure.
Other causes of hemorrhagic stroke are less common but include:
Inflammation in the blood vessels, which may develop from conditions such as syphilis or tuberculosis.
Blood-clotting disorders, such as hemophilia.
Head or neck injuries that result in damage to blood vessels in the head or neck.
Radiation treatment for cancer in the neck or brain.
Cerebral amyloid angiopathy (a degenerative blood vessel disorder).
2006-09-27 20:39:00
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answer #4
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answered by Anonymous
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