Table of Contents StrokeEpidemiology of StrokeTypes of StrokesRisk FactorsModifiable Lifestyle Risk FactorsStroke An Accident Stroke occurs when an artery supplying blood to the brain suddenly becomes blocked or begins to bleed. This can cause part of the brain to die, leading to sudden impairment that can affect a range of activities such as speaking, thinking, movement and communication. Say no to plagiarism. Get a tailor-made essay on “Why violent video games should not be banned”? Get an original essay Symptoms and signs of a stroke include one or more of the following: motor impairments (weakness or paralysis of parts of the body , including the face, on one or both sides) sensory impairments (touch, pain, hot/cold), most often on one side speech difficulties or slurred speech vision difficulties (sudden loss of vision , blurred vision), most often on one side dizziness, loss of balance or unexplained falls severe headaches, difficulty swallowing. Common symptoms of a stroke are the sudden onset of one or more of the following symptoms: loss of strength (paralysis) in the face, arm and/or leg on one side of the body, loss of sensation (including including complete loss of sensation, numbness). or tingling) of the face, an arm and/or a leg on one side of the body; loss of normal speech (for example, difficulty finding correct words); loss of balance; loss of normal vision (for example, double vision, poor vision). , approximately 375,800 Australians have had a stroke at some point in their lives. The majority (70%) were aged 65 and over. It is estimated that just over a third (131,100) of Australians who suffered a stroke had disability due to their stroke. People with disabilities resulting from stroke were significantly more likely to be profoundly limited (always needing assistance) in basic activities (56%) than people with other disabilities. In 2010, stroke was the underlying cause of just over 8,300 deaths in Australia – on average, 23 people died from it every day. The good news is that the death rate has declined by about 70% since 1979. However, although the average rate of decline in stroke death rates has accelerated among people aged 55 and older, it slowed down among those aged 35 to 54. In 2003, stroke accounted for 4.5% of the total burden of disease in Australia. Types of Strokes There are two main types of strokes. An ischemic stroke (brain stroke) is the most common type of stroke caused by a blood clot in an artery that supplies blood to the brain. A clot may form in an artery, in the brain itself, or a clot that has formed in a larger artery in your chest or neck may break loose and be carried by the bloodstream to a smaller artery in your brain where it resides. Clots tend to form in arteries that have narrowed due to the slow buildup of fatty material called “plaque” or “atheroma.” This progressive blockage process is known as "atherosclerosis" and is the same process that causes coronary heart disease. Hemorrhagic strokes occur when an artery in the brain bursts. They cause bleedingin the brain and crushing of tissue around the broken artery. This type of stroke is usually caused by high blood pressure and/or diseases affecting the blood vessels in the brain. Ischemic strokes account for approximately 80% of strokes and hemorrhagic strokes approximately 20%. Risk Factors Non-modifiable risk factors for stroke Modifiable medical risk factors - HTN, AF, coronary heart disease, diabetes, dyslipidemia, asymptomatic carotid stenosis Modifiable lifestyle risk factors - Smoking, alcohol consumption, physical inactivityTable 1 Non-modifiable risk factors for strokeRisk factor Impact on stroke incidenceAge Doubles for each successive decade after age 55Sex 24% to 30% higher in men; However, the absolute annual number of female strokes is higher because females survive longer than males among African Americans and occur at an earlier age rate in the southeastern United States ( so-called “Stroke Belt”), particularly along the coasts of Georgia and the Carolinas (so-called “Stroke Buckle”). Racial ethnicity is 2 times higher among Hispanics and occurs at earlier ages. in Chinesea Heredity Almost 2 times higher in first-degree relatives. Chromosome 9p21 (near the CDKN2A and CDKN2B genes) has been associated with the risk of ischemic stroke. Hypertension is the most important modifiable risk factor for ischemic stroke. Due to its widespread prevalence, depending on age group, the attributable risk of stroke-related hypertension can be as high as 40% in the population and, in the INTERSTROKE study, depending on the definition used, hypertension represented up to 50% of the risk of stroke. stroke. In fact, stroke risk appears to be continually associated with blood pressure down to levels as low as 115/75 mmHg. In light of this, national guidelines have redefined the categories of hypertension such that normal systolic blood pressure is <120 mmHg and normal diastolic blood pressure <80 mmHg. More recently, it has been suggested that variability in blood pressure measurements is associated with a higher risk of stroke. Chronic atrial fibrillation (AF) is a significant risk factor for stroke. In individuals over 65 years of age, the prevalence of AF is approximately 6%. Because the prevalence of AF increases with age, the attributable risk of stroke due to AF is higher in much older age groups. So, for example, AF can account for up to 25% of strokes in people aged 80 to 89. The risk of stroke is approximately 20 times higher in patients with AF with valvular disease and five times higher in patients with AF with non-valvular disease compared to patients without AF. Clinical trials and epidemiological data have been used to develop various stroke risk stratification schemes that can be used in clinical practice for patients with AF. Of note, ongoing monitoring of arrhythmias in the outpatient setting is increasingly showing that AF may actually be responsible for a higher percentage of unexplained strokes than previously thought. People with coronary heart disease have twicegreater risk of stroke than patients without coronary heart disease. The attributable risk of stroke due to coronary heart disease is approximately 12%. Coronary heart disease patients with left ventricular hypertrophy have 3 times the risk of stroke, while coronary heart disease patients with congestive heart failure have 4 times the risk. Within 5 years of a myocardial infarction, the stroke rate is 8.1%, and older patients or those with a cardiac ejection fraction less than 28% are at higher risk of stroke. cerebrovascular. A population study of more than 14,000 subjects observed that the presence of diabetes was independently linked to a higher risk of ischemic stroke. Insulin resistance without overt diabetes is associated with a higher risk of stroke. In the Atherosclerosis Risk in Communities study, high fasting insulin levels in nondiabetics were linked to a higher risk of stroke (relative risk, increase of 1.19 per 50 pmol/L). Additionally, among non-diabetic NOMASS subjects, those with elevated measures of insulin resistance were significantly more likely to have a first ischemic stroke, even after adjusting for other risk factors and the metabolic syndrome. Metabolic syndrome, a constellation of glucose dysmetabolism, obesity, hypertension, and dyslipidemia, has been shown to independently confer a higher risk of first and recurrent stroke. It is not clear whether metabolic syndrome confers a higher risk of first stroke than would be expected for its components. Abnormalities in several serum lipid indices have been linked to symptomatic vascular disease. These associations are particularly strong when it comes to coronary heart disease, but they are sometimes contradictory when it comes to stroke. However, many early studies investigating the relationship between lipids and stroke only examined total serum cholesterol levels and did not include stroke subtyping. Failure to account for heterogeneity in stroke pathophysiology (compared to coronary artery disease) likely contributed to the inconsistent results. Recent studies that have addressed the limitations of previous studies have generally shown an association of elevated serum triglycerides, total cholesterol, low-density lipoprotein cholesterol, and non-high-density lipoprotein cholesterol with the risk of ischemic stroke. , particularly atherosclerotic and lacunar stroke subtypes. High levels of high-density lipoprotein cholesterol have been shown to protect against stroke in the NOMASS study. The prevalence of asymptomatic carotid stenosis increases with age and can be seen in more than 50% of people 65 years or older. Previous studies have shown that the risk of stroke with asymptomatic carotid stenosis is approximately 1.3% per year in patients with 75% or less stenosis, and approximately 3.3% per year. in patients with stenosis greater than 75%. The “best” medical treatment has changed as clinical trial publications have compared carotid endarterectomy to medical treatment of asymptomatic carotid stenosis. The risk of stroke associated with carotid stenosisasymptomatic has decreased significantly over the past 20 years. With contemporary medical treatment, the average annual rate of ipsilateral stroke is estimated to be <1%. and a higher hematocrit. The relative risk of stroke for smokers included in a large meta-analysis was 1.5, and a dose-response association with higher risk of stroke was observed in heavy smokers compared to heavy smokers. light smokers. About 18% of strokes are attributable to active smoking. The risk of stroke associated with former smoking has been shown to decrease significantly over time due to cessation, and the Framingham study found that the risk of stroke was at the level of non -smokers 5 years after stopping. Even passive smoking stimulates the progression of atherosclerosis. Indeed, there is a greater risk of ischemic stroke among female cigarette smokers whose spouse is a smoker than among those whose spouse is not a smoker. Finally, smoking modifies the influence of oral contraceptives on the risk of stroke, as the risk appears to be increased 7-fold in people who smoke and use oral contraceptives. Heavy alcohol consumption is associated with high blood pressure, increased coagulability and cardiac arrhythmias. , and decreased cerebral blood flow. On the other hand, light to moderate consumption has been associated with elevated levels of high-density cholesterol and endogenous tissue plasminogen activators. Increased alcohol consumption is associated with a higher risk of hemorrhagic stroke in a dose-dependent manner. However, studies evaluating the impact of alcohol consumption on ischemic stroke risk have not shown consistent results. Indeed, the majority of published evidence highlights a protective effect of light to moderate drinking (1 to 2 drinks per day) on the risk of ischemic stroke, including data from the Nurses' Health Study and NOMASS (adjusted odds ratio, 0.5). Increased physical activity is associated with reductions in fibrinogen, homocysteine, and platelet activity, as well as increases in high-density lipoprotein cholesterol and plasma plasminogen activator activity. plasma tissues. Observational data shows that physical activity is linked to a lower risk of stroke, while sedentary behavior is linked to a higher risk of stroke. A meta-analysis of 23 studies examining the relationship between physical activity and stroke risk found that highly active subjects had a 27% lower risk of stroke or mortality compared to low-activity subjects. assets. Primary prevention aims to reduce the risk of stroke in asymptomatic people. The most effective prevention involves controlling modifiable risk factors. Adequate reduction of blood pressure, cessation of smoking and the use of antithrombotic therapy in atrial fibrillation are the most effective measures. Carotid endarterectomy may be useful in some patients. Although very useful for general health, strict control of diabetes and high cholesterol, physical exercise and diet have not shown a major influence on the primary prevention of stroke. Aspirin does not appear to be very effective for primary stroke prevention, whereas some ACE inhibitors (e.g. ramipril), ARBs (e.g.example losartan) or statins can have a preventive role beyond their antihypertensive or hypocholesterolemic properties. Secondary stroke prevention aims to reduce the risk. of recurrence after a first stroke or transient ischemic attack. Acting on risk factors is probably as effective as primary prevention. Carotid endarterectomy in cases of symptomatic stenoses > 70% and anticoagulation in patients with atrial fibrillation are by far the most effective measures. Antiplatelet therapy (aspirin, ticlopidine, clopidogrel and long-acting dipyridamole-aspirin combination) significantly reduces stroke recurrence. The most recent data also suggest that perindopril, eprosartan, and some statins are beneficial against stroke recurrence, even in normotensive and normocholesterolemic patients. When used to treat stroke, thrombolysis is described as injecting a chemical agent into the veins, which significantly reduces the risk of stroke. death or complication in patients with ischemic stroke. Patients must meet certain criteria to be eligible for this treatment. These criteria include patient age, time from stroke onset to injection, and type of stroke. Tissue plasminogen activator was licensed in October 2003 by the Australian Therapeutic Good Administration for use within a 3-hour window for ischemic stroke patients, but, based on additional evidence, this window has been extended to 4.5 hours (National Stroke Foundation 2010). Thrombolysis is not comprehensively covered in the NHMD as its collection is not mandatory in the Australian Coding Standard. Additionally, thrombolysis is more likely to be administered in an emergency department before than after hospital admission, and when performed after admission it is not possible to identify when stroke-specific rt-PA was used. In 2009-2010, less than 1% of hospitalizations for stroke required the administration of thrombolytic agents. For many decades, intravenous (IV) thrombolytics have been administered to treat acute thrombosis. Although these drugs were originally effective against coronary thrombosis, their mechanisms have proven beneficial for many other disease processes, including ischemic stroke. Treatment paradigms for acute ischemic stroke have largely followed those of cardiology. More precisely, the objective was to recanalize the occluded artery and restore cerebral perfusion which remains recoverable. To this end, rapid lysis of clots was sought using thrombolytic drugs already effective in the coronary arteries. IV thrombolysis for ischemic stroke began to be widely adopted in the late 1990s, after the publication of the National Institute of Neurological Disorders and Stroke study. Since then, other promising IV thrombolytics have been developed and tested in human trials, but so far none have been shown to be better than a placebo. Adjunctive treatments are also being evaluated. The challenge remains to balance reperfusion and recovery of brain tissue with the potential risks of cerebral hemorrhage. Physiology of thrombolysis The term thrombolytic is generally synonymous with fibrinolytic. In the context of ischemic stroke, this term refersspecifically to the breakdown of fibrin, the tough, net-like backbone of a clot that blocks flow to part of the brain. The clot may form in situ or originate from another source, such as a tight carotid stenosis or the heart. Clinically, a thrombolytic is a drug administered for the purpose of recanalization of the occluded artery and reperfusion of ischemic brain tissue, but still salvageable. If reperfusion is started early enough and the blood supply is renewed in the brain territory deprived of oxygen supply, the tissue can be saved and the resulting damage can be mitigated. Thrombolytic Drugs The effectiveness of thrombolytic drugs depends on a few important factors: 1) the age of the clot can reduce the effectiveness of the thrombolytic, and older clots tend to have more fibrin cross-linking and are more resistant to thrombolytics . 2) the specificity of the lytic for fibrin will determine its activity, and other determinants of effectiveness include half-life and the presence of any neutralizing antibodies. Thrombolytics can be divided into two different categories: 1) fibrin-specific thrombolytics and 2) non-fibrin-specific thrombolytics. thrombolytics. Some examples of fibrin-specific medications are: alteplase, reteplase, and tenecteplase. Non-fibrin-specific drugs include streptokinase or staphylokinase. Alternatively, lytics that convert plasminogen to plasmin can be described as direct or indirect. Direct activators are the same as those previously listed for fibrin-specific drugs. Indirect plasminogen activators include streptokinase, staphylokinase, and desmoteplase (vampire bat plasminogen activator). Direct activators are all serine proteases that cleave a single amino acid bond (arginine-valine) to produce plasmin. Indirect activators are not proteolytic, but rather form a complex with plasminogen which can then convert additional plasminogen to plasmin. More recently, testing of plasmin itself has been under development. The half-life of plasmin is very short; when administered IV, plasmin is rapidly neutralized by α2-anti-plasmin and does not dissolve the thrombus or cause bleeding. Thus, plasmin is better suited as a local agent. IV thrombolysis remains the only medical treatment proven to reduce disability caused by acute ischemic stroke. However, the time window of opportunity for treatment is still narrow because the majority of patients with ischemic stroke do not receive thrombolysis and complete clot lysis occurs in a minority of patients [78]. Ongoing clinical trials aimed at improving recanalization rates are widening the treatment window or expanding eligibility so that more patients can benefit. Regardless of what, if any, new thrombolytic or adjunctive therapy proves effective for future stroke victims, it remains absolutely crucial that patients are transferred promptly to stroke centers. In well-organized stroke centers, it is possible to achieve an IV t-PA injection time of 20 minutes [79]. Stroke is a leading cause of death and disability. Recently, advances have been made in the treatment of acute ischemic stroke, aimed at restoring blood flow to the affected area with the aim of rescuing the ischemic penumbra surrounding the infarct area. This is achieved by the use of thrombolytics by.