Stroke

stroke Stroke can be classified into two major categories: ischemic and hemorrhagic. Ischemic stroke is caused by interruption of the blood supply to the brain, while hemorrhagic stroke results from the rupture of a blood vessel or an abnormal vascular structure. About 87% of stroke is ischemic, with the rest being hemorrhagic. Bleeding can develop inside areas of ischemia, a condition known as "hemorrhagic transformation." It is unknown how many cases of hemorrhagic stroke actually start as ischemic stroke. 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. Ischemic During 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: • Thrombosis (obstruction of a blood vessel by a blood clot forming locally) • Embolism (obstruction due to an embolus from elsewhere in the body), • Cerebral venous sinus thrombosis. Stroke without an obvious explanation is termed cryptogenic stroke (idiopathic); this constitutes 30–40% of all cases of ischemic stroke. There are 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 total anterior circulation infarct (TACI), partial anterior circulation infarct (PACI), lacunar infarct (LACI) or posterior circulation infarct (POCI). These four entities predict the extent of the stroke, the area of the brain that is affected, the underlying cause, and the prognosis. The TOAST (Trial of Org 10172 in Acute Stroke Treatment) classification is based on clinical symptoms as well as results of further investigations; on this basis, stroke is classified as being due to (1) thrombosis or embolism due to atherosclerosis of a large artery, (2) an embolism originating in the heart, (3) complete blockage of a small blood vessel, (4) other determined cause, (5) undetermined cause (two possible causes, no cause identified, or incomplete investigation). Users of stimulants such as cocaine and methamphetamine are at a high risk for ischemic stroke. Hemorrhagic of an intraparenchymal bleed (bottom arrow) with surrounding edema (top arrow) There are two main types of hemorrhagic stroke: • Intracerebral hemorrhage, which is bleeding within the brain itself (when an artery in the brain bursts, flooding the surrounding tissue with blood), due to either intraparenchymal hemorrhage (bleeding within the brain tissue) or intraventricular hemorrhage (bleeding within the brain's ventricular system). • Subarachnoid hemorrhage, which is bleeding that occurs outside of the brain tissue but still within the skull, and precisely between the arachnoid mater and pia mater (the delicate innermost layer of the three layers of the meninges that surround the brain). The above two main types of hemorrhagic stroke are also two different forms of intracranial hemorrhage, which is the accumulation of blood anywhere within the cranial vault; but the other forms of intracranial hemorrhage, such as epidural hematoma (bleeding between the skull and the dura mater, which is the thick outermost layer of the meninges that surround the brain) and subdural hematoma (bleeding in the subdural space), are not considered "hemorrhagic stroke". Hemorrhagic stroke may occur on the background of alterations to the blood vessels in the brain, such as cerebral amyloid angiopathy, cerebral arteriovenous malformation and an intracranial aneurysm, which can cause intraparenchymal or subarachnoid hemorrhage. In addition to neurological impairment, hemorrhagic stroke usually causes specific symptoms (for instance, subarachnoid hemorrhage classically causes a severe headache known as a thunderclap headache) or reveal evidence of a previous head injury. ==Signs and symptoms==

Early recognition infographic describing the FAST mnemonic for early recognition of stroke Systems have been proposed to increase recognition of stroke. 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 decreased (– likelihood ratio of 0.39). 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. A mnemonic to remember the warning signs of stroke is FAST (facial droop, arm weakness, speech difficulty, and time to call emergency services), as advocated by the Department of Health (United Kingdom) and the Stroke Association, the American Stroke Association, and the National Stroke Association (US). FAST is less reliable in the recognition of posterior circulation stroke. The revised mnemonic BE FAST, which adds balance (sudden trouble keeping balance while walking or standing) and eyesight (new onset of blurry or double vision or sudden, painless loss of sight) to the assessment, has been proposed to address this shortcoming and improve early detection of stroke even further. Other scales for prehospital detection of stroke include the Los Angeles Prehospital Stroke Screen (LAPSS) and the Cincinnati Prehospital Stroke Scale (CPSS), on which the FAST method was based. Use of these scales is recommended by professional guidelines. For people referred to the emergency room, early recognition of stroke is deemed important as this can expedite diagnostic tests and treatments. A scoring system called ROSIER (recognition of stroke in the emergency room) is recommended for this purpose; it is based on features from the medical history and physical examination. Associated symptoms Loss of consciousness, headache, and vomiting usually occur 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. Subtypes If the area of the brain affected includes one of the three prominent central nervous system pathways—the spinothalamic tract, corticospinal tract, and the dorsal column–medial lemniscus pathway, symptoms may include: • hemiplegia and muscle weakness of the face • numbness • reduction in sensory or vibratory sensation • initial flaccidity (reduced muscle tone), replaced by spasticity (increased muscle tone), excessive reflexes, and obligatory synergies. In most cases, the symptoms affect only one side of the body (unilateral). The defect in the brain is usually on the opposite side of the body. However, since these pathways also travel in the spinal cord and any lesion there can also produce these symptoms, the presence of any one of these symptoms does not necessarily indicate stroke. In addition to the above central nervous system pathways, the brainstem gives rise to most of the twelve cranial nerves. A brainstem stroke affecting the brainstem 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 stick out the tongue or move it from side to side) If the cerebral cortex is involved, the central nervous system pathways can again be affected, but can also produce the following symptoms: • aphasia (difficulty with verbal expression, auditory comprehension, reading and 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, ataxia might be present and this includes: • altered walking gait • altered movement coordination • vertigo and or disequilibrium Preceding signs and symptoms In the days before a stroke (generally in the previous 7 days, even the previous one), a considerable proportion of patients have a "sentinel headache": a severe and unusual headache that indicates a problem. Its appearance makes it advisable to seek medical review and to consider prevention against stroke. ==Causes==

Thrombotic stroke In thrombotic stroke, a thrombus (blood clot) usually forms around atherosclerotic plaques. Since blockage of the artery is gradual, onset of symptomatic thrombotic stroke is slower than that of hemorrhagic stroke. A thrombus itself (even if it does not completely block the blood vessel) can lead to an embolic stroke (see below) if the thrombus breaks off and travels in the bloodstream, at which point it is called an embolus. Two types of thrombosis can cause stroke: • Large vessel disease involves the common and internal carotid arteries, the vertebral artery, and the Circle of Willis. Diseases that may form thrombi in the large vessels include (in descending incidence): atherosclerosis, vasoconstriction (tightening of the artery), aortic, carotid or vertebral artery dissection, inflammatory diseases of the blood vessel wall (Takayasu arteritis, giant cell arteritis, vasculitis), noninflammatory vasculopathy, Moyamoya disease and fibromuscular dysplasia. Strokes caused by artery dissections are in the strictest sense not always caused by a 'defined disease state', such events can occur in very young people and can be caused by physical injury such as hyperextension of the neck area or often by other forms of trauma. • Small vessel disease involves the smaller arteries inside the brain: branches of the circle of Willis, middle cerebral artery, stem, and arteries arising from the distal vertebral and basilar artery. Diseases that may form thrombi in the small vessels include (in descending incidence): lipohyalinosis (build-up of fatty hyaline matter in the blood vessel as a result of high blood pressure and aging) and fibrinoid degeneration (stroke involving these vessels is known as a lacunar stroke) and microatheroma (small atherosclerotic plaques). Anemia causes increased blood flow in the blood circulatory system. This causes the endothelial cells of the blood vessels to express adhesion factors which encourages the clotting of blood and formation of thrombus. Sickle-cell anemia, which can cause blood cells to clump up and block blood vessels, can also lead to stroke. Stroke is the second leading cause of death in people under 20 with sickle-cell anemia. Causes of stroke related to the heart can be distinguished between high- and low-risk: • High risk: atrial fibrillation and paroxysmal atrial fibrillation, rheumatic disease of the mitral or aortic valve disease, artificial heart valves, known cardiac thrombus of the atrium or ventricle, sick sinus syndrome, sustained atrial flutter, recent myocardial infarction, chronic myocardial infarction together with ejection fraction <28 percent, symptomatic congestive heart failure with ejection fraction <30 percent, dilated cardiomyopathy, Libman-Sacks endocarditis, Marantic endocarditis, infective endocarditis, papillary fibroelastoma, left atrial myxoma, 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), and complex atheroma in the ascending aorta or proximal arch Among those who have a complete blockage of one of the carotid arteries, the risk of stroke on that side is about one percent per year. A special form of embolic stroke is the embolic stroke of undetermined source (ESUS). This subset of cryptogenic stroke is defined as a non-lacunar brain infarct without proximal arterial stenosis or cardioembolic sources. About one out of six cases of ischemic stroke could be classified as ESUS. Cerebral hypoperfusion Cerebral hypoperfusion is the reduction of blood flow to all parts of the brain. The reduction could be to a particular part of the brain depending on the cause. It is most commonly due to heart failure from cardiac arrest or arrhythmias, or from reduced cardiac output as a result of myocardial infarction, pulmonary embolism, pericardial effusion, or bleeding. Hypoxemia (low blood oxygen content) may precipitate the hypoperfusion. Because the reduction in blood flow is global, all parts of the brain may be affected, especially vulnerable "watershed" areas—border zone regions supplied by the major cerebral arteries. A watershed stroke refers to the condition when the blood supply to these areas is compromised. Blood flow to these areas does not necessarily stop, but instead it may lessen to the point where brain damage can occur. Venous thrombosis 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. intracranial vascular malformations (including cavernous angiomas or arteriovenous malformations), cerebral amyloid angiopathy, or infarcts into which secondary hemorrhage has occurred. Cancer is also another well recognized potential cause of stroke. Although, malignancy in general can increase the risk of stroke, certain types of cancer such as pancreatic, lung and gastric are typically associated with a higher thromboembolism risk. The mechanism with which cancer increases stroke risk is thought to be secondary to an acquired hypercoagulability. Air pollution is responsible for around 27% of deaths from strokes worldwide, according to the Global Burden of Disease Study. Silent stroke Silent stroke is stroke that does not have any outward symptoms, and people are typically unaware they had experienced stroke. Despite not causing identifiable symptoms, silent stroke still damages the brain and places the person at increased risk for both transient ischemic attack and major stroke in the future. Conversely, those who have had major stroke are also at risk of having silent stroke. In a broad study in 1998, more than 11 million people were estimated to have experienced stroke in the United States. Approximately 770,000 of these were symptomatic and 11 million were first-ever silent MRI infarcts or hemorrhages. Silent stroke typically causes lesions which are detected via the use of neuroimaging such as MRI. Silent stroke is estimated to occur at five times the rate of symptomatic stroke. The risk of silent stroke increases with age, but they may also affect younger adults and children, especially those with acute anemia. ==Pathophysiology==

Ischemic : The neurons become hypereosinophilic and there is an infiltrate of neutrophils. There is slight edema and loss of normal architecture in the surrounding neuropil. Ischemic stroke occurs because of a loss of blood supply to part of the brain, initiating the ischemic cascade. 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 atrial fibrillation, or in the carotid arteries, break off, enter the cerebral circulation, then lodge in and block brain blood vessels. Since blood vessels in the brain are now blocked, the brain becomes low in energy, and thus it resorts to using anaerobic metabolism within the region of brain tissue affected by ischemia. Anaerobic metabolism produces less adenosine triphosphate (ATP) but releases a by-product called lactic acid. Lactic acid is an irritant which could potentially destroy cells since it is an acid and disrupts the normal acid-base balance in the brain. The ischemia area is referred to as the "ischemic penumbra". After the initial ischemic event the penumbra transitions from a tissue remodeling characterized by damage to a remodeling characterized by repair. As oxygen or glucose becomes depleted in ischemic brain tissue, the production of high energy phosphate compounds such as adenosine triphosphate (ATP) fails, leading to failure of energy-dependent processes (such as ion pumping) necessary for tissue cell survival. This sets off a series of interrelated events that result in cellular injury and death. A major cause of neuronal injury is the release of the excitatory neurotransmitter glutamate. The concentration of glutamate outside the cells of the nervous system is normally kept low by so-called uptake carriers, which are powered by the concentration gradients of ions (mainly Na+) across the cell membrane. However, stroke cuts off the supply of oxygen and glucose which powers the ion pumps maintaining these gradients. As a result, the transmembrane ion gradients run down, and glutamate transporters reverse their direction, releasing glutamate into the extracellular space. Glutamate acts on receptors in nerve cells (especially NMDA receptors), producing an influx of calcium which activates enzymes that digest the cells' proteins, lipids, and nuclear material. Calcium influx can also lead to the failure of mitochondria, which can lead further toward energy depletion and may trigger cell death due to programmed cell death. Ischemia 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 may occur. 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. Collateral flow and reperfusion The brain can compensate inadequate blood flow in a single artery by the collateral system. This system relies on the efficient connection between the carotid and vertebral arteries through the circle of Willis and, to a lesser extent, the major arteries supplying the cerebral hemispheres. However, variations in the circle of Willis, caliber of collateral vessels, and acquired arterial lesions such as atherosclerosis can disrupt this compensatory mechanism, increasing the risk of brain ischemia resulting from artery blockage. The extent of damage depends on the duration and severity of the ischemia. If ischemia persists for more than 5 minutes with perfusion below 5% of normal, some neurons will die. However, if ischemia is mild, the damage will occur slowly and may take up to 6 hours to completely destroy the brain tissue. In case of severe ischemia lasting more than 15 to 30 minutes, all of the affected tissue will die, leading to infarction. The rate of damage is affected by temperature, with hyperthermia accelerating damage and hypothermia slowing it down and other factors. Prompt restoration of blood flow to ischemic tissues can reduce or reverse injury, especially if the tissues are not yet irreversibly damaged. This is particularly important for the moderately ischemic areas (penumbras) surrounding areas of severe ischemia, which may still be salvageable due to collateral flow. Hemorrhagic Hemorrhagic stroke is classified based on their underlying pathology. Some causes of hemorrhagic stroke are hypertensive hemorrhage, ruptured aneurysm, ruptured AV fistula, transformation of prior ischemic infarction, and drug-induced bleeding. Inflammation contributes to the secondary brain injury after hemorrhage. ==Diagnosis==

infarction shown on the left. Right image after 7 hours. Stroke is diagnosed through several techniques: a neurological examination (such as the NIHSS), CT scans (most often without contrast enhancements) or MRI scans, Doppler ultrasound, and arteriography. The diagnosis of stroke itself is clinical, with assistance from the imaging techniques. Imaging techniques also assist in determining the subtypes and cause of stroke. There is yet no commonly used blood test for the stroke diagnosis itself, though blood tests may be of help in finding out the likely cause of stroke. In deceased people, an autopsy of stroke may help establishing the time between stroke onset and death. Physical examination A physical examination, including taking a medical history of the symptoms and a neurological status, helps giving an evaluation of the location and severity of stroke. It can give a standard score on e.g., the NIH stroke scale. Imaging For diagnosing ischemic (blockage) stroke in the emergency setting: • CT scans (without contrast enhancements) • sensitivity= 16% (less than 10% within first 3 hours of symptom onset) • 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, an MRI scan is more sensitive. For the assessment of stable stroke, nuclear medicine scans such as single-photon emission computed tomography (SPECT) and positron emission tomography–computed tomography (PET/CT) may be helpful. SPECT documents cerebral blood flow, whereas PET with an FDG isotope shows cerebral glucose metabolism. CT scans may not detect ischemic stroke, especially if it is small, of recent onset, A CT scan is used more to rule out certain stroke mimics and detect bleeding. Cerebrovascular reserve capacity is another factor that affects stroke outcome it is the amount of increase in cerebral blood flow after a purposeful stimulation of blood flow by the physician, such as by giving inhaled carbon dioxide or intravenous acetazolamide. The increase in blood flow can be measured by PET scan or transcranial doppler sonography. However, in people with obstruction of the internal carotid artery of one side, the presence of leptomeningeal collateral circulation is associated with reduced cerebral reserve capacity. Underlying cause . ECG changes may occur in people with stroke and other brain disorders. When stroke has been diagnosed, other studies may be performed to determine the underlying cause. With the 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. The following are commonly used techniques: • an ultrasound/doppler study of the carotid arteries (to detect carotid stenosis) or dissection of the precerebral arteries; • an electrocardiogram (ECG) and echocardiogram (to identify arrhythmias and resultant clots in the heart which may spread to the brain vessels through the bloodstream); • a Holter monitor study to identify intermittent abnormal heart rhythms; • an angiogram of the cerebral vasculature (if a bleed is thought to have originated from an aneurysm or arteriovenous malformation); • blood tests to determine if blood cholesterol is high, if there is an abnormal tendency to bleed, and if some rarer processes such as homocystinuria might be involved. For hemorrhagic stroke, a CT or MRI scan with intravascular contrast may be able to identify abnormalities in the brain arteries (such as aneurysms) or other sources of bleeding, and structural MRI if this shows no cause. If this too does not identify an underlying reason for the bleeding, invasive cerebral angiography could be performed but this requires access to the bloodstream with an intravascular catheter and can cause further stroke as well as complications at the insertion site and this investigation is therefore reserved for specific situations. If there are symptoms suggesting that the hemorrhage might have occurred as a result of venous thrombosis, CT or MRI venography can be used to examine the cerebral veins. Misdiagnosis Among people with ischemic stroke, misdiagnosis occurs 2 to 26% of the time. People not having stroke may also be misdiagnosed with the condition. Giving thrombolytics (clot-busting) in such cases causes intracerebral bleeding 1 to 2% of the time, which is less than that of people with stroke. This unnecessary treatment adds to health care costs. Even so, the AHA/ASA guidelines state that starting intravenous tPA in possible mimics is preferred to delaying treatment for additional testing. Women, African-Americans, Hispanic-Americans, Asian and Pacific Islanders are more often misdiagnosed for a condition other than stroke when in fact having stroke. In addition, adults under 44 years of age are seven times more likely to have stroke missed than are adults over 75 years of age. This is especially the case for younger people with posterior circulation infarcts. Some medical centers have used hyperacute MRI in experimental studies for people initially thought to have a low likelihood of stroke, and in some of these people, stroke has been found which were then treated with thrombolytic medication. ==Prevention==

Given the disease burden of stroke, prevention is an important public health concern. Primary prevention is less effective than secondary prevention (as judged by the number needed to treat to prevent one stroke per year). About the use of aspirin as a preventive medication for stroke, in healthy people aspirin does not appear beneficial and thus is not recommended, but in people with high cardiovascular risk, or those who have had a myocardial infarction, it provides some protection against a first stroke. In those who have previously had stroke, treatment with medications such as aspirin, clopidogrel, and dipyridamole may be beneficial. Risk factors The most important modifiable risk factors for stroke are chronic uncontrolled hypertension and atrial fibrillation, although the size of the effect is small; 833 people have to be treated for 1 year to prevent one stroke. Other modifiable risk factors include high blood cholesterol levels, diabetes mellitus, end-stage kidney disease, (active and passive), heavy alcohol use, drug use, lack of physical activity, obesity, processed red meat consumption, and unhealthy diet. Smoking just one cigarette per day increases the risk more than 30%. Alcohol use could predispose to ischemic stroke, as well as intracerebral and subarachnoid hemorrhage via multiple mechanisms (for example, via hypertension, atrial fibrillation, rebound thrombocytosis and platelet aggregation and clotting disturbances). Drugs, most commonly amphetamines and cocaine, can induce stroke through damage to the blood vessels in the brain and acute hypertension. Migraine with aura doubles a person's risk for ischemic stroke. Untreated, celiac disease regardless of the presence of symptoms can be an underlying cause of stroke, both in children and adults. According to a 2021 WHO study, working 55+ hours a week raises the risk of stroke by 35% and the risk of dying from heart conditions by 17%, when compared to a 35-40-hour week. High levels of physical activity reduce the risk of stroke by about 26%. There is a lack of high quality studies looking at promotional efforts to improve lifestyle factors. Nonetheless, given the large body of circumstantial evidence, best medical management for stroke includes advice on diet, exercise, smoking and alcohol use. Medication is the most common method of stroke prevention; carotid endarterectomy can be a useful surgical method of preventing stroke. A recent 2025 reports that women under 50 with a history of pregnancy complications face a higher risk of ischemic stroke. Conditions such as hypertensive disorders of pregnancy, gestational diabetes, preterm birth, small-for-gestational-age infants, stillbirth, and miscarriage were more common among stroke patients than those without stroke. The risk was especially elevated for strokes linked to large artery disease in women with prior hypertensive disorders, preterm births or small-for-gestational-age deliveries. Blood pressure High blood pressure accounts for 35–50% of stroke risk. Blood pressure reduction of 10 mmHg systolic or 5 mmHg diastolic reduces the risk of stroke by ~40%. Lowering blood pressure has been conclusively shown to prevent both ischemic and hemorrhagic stroke. It is equally important in secondary prevention. Even people older than 80 years and those with isolated systolic hypertension benefit from antihypertensive therapy. The available evidence does not show large differences in stroke prevention between antihypertensive drugs—therefore, other factors such as protection against other forms of cardiovascular disease and cost should be considered. The routine use of beta-blockers following stroke or TIA has not been shown to result in benefits. Blood lipids High cholesterol levels have been inconsistently associated with (ischemic) stroke. Statins have been shown to reduce the risk of stroke by about 15%. Since earlier meta-analyses of other lipid-lowering drugs did not show a decreased risk, statins might exert their effect through mechanisms other than their lipid-lowering effects. Anticoagulant drugs Oral anticoagulants such as warfarin have been the mainstay of stroke prevention for over 50 years. However, several studies have shown that aspirin and other antiplatelets are highly effective in secondary prevention after stroke or transient ischemic attack. Thienopyridines (clopidogrel, ticlopidine) might be slightly more effective than aspirin and have a decreased risk of gastrointestinal bleeding but are more expensive. Both aspirin and clopidogrel may be useful in the first few weeks after a minor stroke or high-risk TIA. Clopidogrel has less side effects than ticlopidine. Low-dose aspirin is also effective for stroke prevention after having a myocardial infarction. Depending on the stroke risk, anticoagulation with medications such as warfarin or aspirin is useful for prevention with various levels of comparative effectiveness depending on the type of treatment used. Oral anticoagulants, especially Xa (apixaban) and thrombin (dabigatran) inhibitors, have been shown to be superior to warfarin in stroke reduction and have a lower or similar bleeding risk in patients with atrial fibrillation. In primary prevention, however, antiplatelet drugs did not reduce the risk of ischemic stroke but increased the risk of major bleeding. Further studies are needed to investigate a possible protective effect of aspirin against ischemic stroke in women. Surgery Carotid endarterectomy or carotid angioplasty can be used to remove atherosclerotic narrowing of the carotid artery. There is evidence supporting this procedure in selected cases. Carotid artery stenting has not been shown to be equally useful. People are selected for surgery based on age, gender, degree of stenosis, time since symptoms and the person's preferences. Screening for carotid artery narrowing has not been shown to be a useful test in the general population. Studies of surgical intervention for carotid artery stenosis without symptoms have shown only a small decrease in the risk of stroke. To be beneficial, the complication rate of the surgery should be kept below 4%. Even then, for 100 surgeries, 5 people 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. It does not appear that lowering levels of homocysteine with folic acid affects the risk of stroke. public service announcement about a woman who had stroke after pregnancy Women A number of specific recommendations have been made for women including taking aspirin after the 11th week of pregnancy if there is a history of previous chronic high blood pressure and taking blood pressure medications during pregnancy if the blood pressure is greater than 150 mmHg systolic or greater than 100 mmHg diastolic.