A stroke is a medical condition in which poor blood flow to the brain produces cell death. There are two main types of stroke: ischemic, due to lack of blood flow, and hemorrhagic, due to bleeding. They cause the part of the brain to not function properly. Signs and symptoms of a stroke may include an inability to move or feel on one side of the body, problems understanding or speaking, dizziness, or loss of vision to one side. Signs and symptoms often appear as soon as a stroke occurs. If the symptoms last less than an hour or two, this is known as a transient ischemic attack (TIA) or mini stroke. Hemorrhagic stroke can also be associated with severe headaches. The symptoms of a stroke can be permanent. Long-term complications may include pneumonia or loss of bladder control.
The main risk factor for stroke is high blood pressure. Other risk factors include tobacco smoking, obesity, high blood cholesterol, diabetes mellitus, previous TIA, and atrial fibrillation. Ischemic stroke is usually caused by a blockage of blood vessels, although there are also less common causes. Hemorrhagic stroke is caused by direct bleeding into the brain or into the space between the cerebral membranes. Bleeding can occur due to a ruptured brain aneurysm. Diagnosis is usually based on physical examination and is supported by medical imaging such as CT scan or MRI scan. CT scans may exclude bleeding, but do not always rule out ischemia, which initially did not appear on CT scans. Other tests such as electrocardiogram (ECG) and blood tests are performed to determine risk factors and rule out other possible causes. Low blood sugar can cause similar symptoms.
Prevention includes decreased risk factors, as well as the possibility of aspirin, statins, surgery to open arteries to the brain in those with problematic narrowing, and warfarin in those with atrial fibrillation. Stroke or TIA often requires emergency care. An ischemic stroke, if detected within three to four and half hours, can be treated with a drug that can destroy the clot. Aspirin should be used. Some hemorrhagic strokes are beneficial from surgery. Treatment to try to recover a lost function is called stroke rehabilitation and ideally occurs in the stroke unit; However, this is not available in most parts of the world.
In 2013 about 6.9 million people had an ischemic stroke and 3.4 million people had a hemorrhagic stroke. By 2015 there are about 42.4 million people who previously had a stroke and are still alive. Between 1990 and 2010, the annual number of strokes decreased by about 10% in developed countries and increased by 10% in developing countries. By 2015, stroke is the second most common cause of death after coronary artery disease, accounting for 6.3 million deaths (11% of total). Approximately 3.0 million deaths from ischemic stroke while 3.3 million deaths from hemorrhagic stroke. About half of people who have a stroke live less than a year. Overall, two thirds of strokes occur in those over 65 years of age.
Video Stroke
Classification
Stroke can be classified into two main categories: ischemic and haemorrhagic. Ischemic stroke is caused by a disruption of blood supply to the brain, while hemorrhagic stroke results from rupture of blood vessels or abnormal vascular structures. About 87% of strokes are ischemic, the rest are hemorrhagic. Bleeding may develop within the area of ​​ischemia, a condition known as "hemorrhagic transformation." It is not known how many hemorrhagic strokes actually begin as ischemic stroke.
Definition
In the 1970s the World Health Organization defines stroke as "a neurological deficit of cerebrovascular causes that lasts beyond 24 hours or is interrupted by death within 24 hours", although the word "stroke" is centuries old. This definition should reflect the reversibility of network damage and is designed for that purpose, with a 24-hour time period arbitrarily chosen. The 24-hour limit divides the stroke from a transient ischemic attack, which is a syndrome associated with a fully restored stroke within 24 hours. With the availability of treatments that can reduce the severity of strokes when given early, many now prefer alternative terminology, such as brain attack and acute ischemic cerebrovascular syndrome (modeled after heart attack and acute coronary syndrome, respectively), to reflect the urgency of stroke symptoms and the need to act quickly.
Ischemic
In ischemic stroke, blood supply to the brain decreases, causing brain tissue dysfunction in the area. There are four reasons why this can happen:
- Thrombosis (blockage of blood vessels by locally formed blood clots)
- Embolism (obstruction due to embolus from elsewhere in the body),
- Systemic hypoperfusion (general decrease in blood supply, eg, shock)
- Venous cerebral venous thrombosis.
Stroke without clear explanation is called cryptogenic (unknown origin); this constitutes 30-40% of all ischemic strokes.
There are various classification systems for acute ischemic stroke. The Oxford Community Stroke Project Classification (OCSP, also known as the Bamford or Oxford classification) relies heavily on early symptoms; based on the extent of the symptoms, stroke episodes are classified as total anterior circulation infarction (TACI), partial anterior circulation infarction (PACI), lacunar infarction (LACI) or posterior circulating infarction (POCI). These four entities predict stroke rates, affected brain areas, underlying causes, and prognosis. The TOAST (Org Trial 10172 in Acute Stroke Treatment) classification is based on clinical symptoms as well as the results of further investigations; On this basis, a stroke is classified as a result of (1) thrombosis or embolism due to atherosclerosis of the large arteries, (2) emboli originating from the heart, (3) complete blockage of small blood vessels, (4) other causes prescribed, (5) which has not been determined (two possible causes, no identified cause, or incomplete investigation). Users of stimulants, such as cocaine and methamphetamine have a high risk for ischemic stroke.
Hemorrhag
There are two main types of hemorrhagic stroke: Intracerebral hemorrhage, which is essentially bloody in the brain itself (when the artery in the brain breaks, floods the surrounding tissue with blood), due to intraparenchymal bleeding (bleeding in the brain tissue) or intraventricular bleeding (bleeding in the system brain ventricle).
The two main types of hemorrhagic strokes above are also two distinct forms of intracranial hemorrhage, namely the accumulation of blood anywhere within the dome of the skull; but other forms of intracranial hemorrhage, such as epidural hematoma (bleeding between the skull and dura mater, which is the outermost layer of the meninges surrounding the brain) and subdural hematoma (subdural space bleeding), are not considered "strokes hemorrhagic ".
Hemorrhagic stroke can occur in the background of changes in blood vessels in the brain, such as cerebral amyloid angiopathy, cerebral arteriovenous malformations and intracranial aneurysms, which may cause intraparenchymal or subarachnoid hemorrhage.
In addition to neurological disorders, hemorrhagic strokes usually cause specific symptoms (eg, classic subarachnoid hemorrhages causing severe headaches known as thunderclap headaches) or reveal evidence of previous head injuries.
Maps Stroke
Signs and symptoms
Symptoms of a stroke usually start suddenly, in seconds to minutes, and in many cases do not develop further. The symptoms depend on the area of ​​the affected brain. The wider the area of ​​the brain affected, the more functions it will likely lose. Some forms of stroke may cause additional symptoms. For example, in intracranial hemorrhage, the affected area may compress other structures. Most forms of stroke are not associated with headaches, apart from subarachnoid hemorrhage and cerebral vein thrombosis and occasionally intracerebral hemorrhage.
Early recognition
Various systems have been proposed to improve stroke recognition. Different findings can predict the presence or absence of stroke to different degrees. The sudden onset of facial onset, arm flutter (ie, if a person, when asked to raise both arms, unconsciously let one arm flit down) and abnormal speech are the most likely findings to lead to the correct identification of a stroke case that increases the likelihood of 5.5 if at least one of these is present). Similarly, when all three are absent, the likelihood of a stroke decreases significantly (- a likelihood ratio of 0.39). While these findings are not perfect for diagnosing stroke, the fact that they can be evaluated relatively quickly and easily makes it extremely valuable in acute settings.
A mnemonic to remember stroke warning signs is FAST (drooping face, arm weakness, speech impediment, and time to call emergency services), as suggested by the Department of Health and Stroke Association, American Stroke Association, National Stroke Association ( USA), Los Angeles Prehospital Stroke Screen (LAPSS) and Prehospital Cincinnati Stroke Scale (CPSS). Use of this scale is recommended by professional guidelines.
For people referred to the emergency room, early recognition of stroke is important because it can speed diagnostic and treatment tests. A rating system called ROSIER (recognition of stroke in the emergency room) is recommended for this purpose; it is based on features from medical history and physical examination.
Subtype
If the affected area of ​​the brain belongs to one of three prominent central nervous system pathways - the spinothalamic tract, the corticospinal tract, and the medial dorsal-medial line of lemniscus, the symptoms include:
- hemiplegia and facial muscle weakness
- numb
- sensory or vibration sensation reduction
- Initial flexibility (reduced muscle tone), replaced by flexibility (increased muscle tone), excessive reflexes, and mandatory synergy.
In most cases, symptoms affect only one side of the body (unilateral). Depending on the part of the affected brain, defects in the brain are usually on the opposite side of the body. However, since this pathway also runs in the spinal cord and any lesions there can also produce these symptoms, the presence of any of these symptoms does not necessarily indicate a stroke. In addition to the CNS line above, the brain stem causes most of the twelve cranial nerves. Brainstem stroke affects the brainstem and brain, therefore, can produce symptoms associated with deficits in this cranial nerve:
If cerebral cortex is involved, the CNS line may be affected again, but it may also produce the following symptoms:
- aphasia (difficulty with verbal expressions, hearing comprehension, reading and writing; Broca or Wernicke areas are usually involved)
- dysarthria (motor disturbance due to neurological injury)
- apraxia (voluntary movement change)
- visual field defects
- memory deficit (temporal lobe involvement)
- hemineglect (parietal lobe involvement)
- irregular thought, confusion, hypersexual movement (with frontal lobe involvement)
- lack of insight about it, usually related to stroke, disability
If a small brain is involved, ataxia may exist and this includes:
- change how to go
- change in motion coordination
- vertigo and or disequilibrium
Related symptoms
Loss of consciousness, headache, and vomiting are usually more common in hemorrhagic strokes than thrombosis due to increased intracranial pressure from leaking blood suppressing the brain.
If symptoms are maximally at onset, the cause is more likely to be subarachnoid hemorrhage or embolic stroke.
Cause
Thrombotic stroke
In thrombotic strokes, thrombus (blood clots) usually form around atherosclerotic plaques. Due to clogged arteries gradually, the onset of thrombotic stroke is symptomatic at a slower rate than in hemorrhagic stroke. Thrombus itself (even if it does not completely block the blood vessels) can cause embolic stroke (see below) if the thrombus stop and move in the bloodstream, at the point where it is called an embolus. Two types of thrombosis can cause stroke:
- Large vessel disease involves the common and internal carotid artery, the vertebral artery, and the Willis Circle. Diseases that may form thrombi in the large vessels include (in incidence decreases): atherosclerosis, vasoconstriction (tightening of the arteries), arterial dissection of the aorta, carotid or vertebral column, diseases of inflammation in the vessel wall (Takayasu arteritis, giant cell arteritis, vasculitis), vasculopathy noninflammatory, Moyamoya disease and fibromuscular dysplasia.
- small vessel disease involves the smaller arteries in the brain: the branches of the circle of Willis, middle cerebral artery, stem, and arteries arising from the distal vertebral artery and basilar. Diseases that may form thrombi in the small vessels include (in incidence decreases): lipohyalinosis (buildup of material hyaline fat in the blood vessel as a result of high blood pressure and aging) and fibrinoid degeneration (stroke involving these vessels are known as stroke lacunar) and microatheroma (small atherosclerotic plaque).
Sickle cell anemia, which can cause blood cells to clot and block blood vessels, can also cause strokes. Stroke is the second leading cause of death in people under 20 years with sickle cell anemia. Air pollution can also increase the risk of stroke.
Stroke embolik
The embolic stroke refers to arterial embolism (artery blockage) by the embolus, traveling particles or debris in the arterial bloodstream from elsewhere. Embolus is the most common thrombus, but it can also be a number of other substances including fats (eg, from the bone marrow on broken bones), air, cancer cells or bacteria (usually from infective endocarditis).
Because the embolus emerges from elsewhere, local therapy solves the problem only temporarily. Thus, the source of the embolus must be identified. Due to sudden embolism blockage, symptoms are usually maximal at baseline. Also, symptoms may be temporary because the partially absorbed embolus and move to a different location or completely disappear.
Embolism most often arises from the heart (especially in atrial fibrillation) but may originate from elsewhere in the arterial tree. In the paradox embolism, deep vein thrombosis condenses through the atrial or ventricular septum defect in the heart to the brain.
Causes of stroke associated with the heart can be distinguished between high risk and low risk: High risk: atrial fibrillation and paroxysmal atrial fibrillation, rheumatic disease from mitral or aortic valve disease, artificial heart valves, known cardiac thrombus from the atria or ventricle, ailing sinus syndrome, ongoing atrial fluctuations, myocardial infarction recently. chronic myocardial infarction along with ejection fraction & lt; 28 percent, congestive heart failure symptoms with ejection fraction & lt; 30 percent, dilated cardiomyopathy, Libman-Sack Endocarditis, Marantic endocarditis, infective endocarditis, papillary fibroelastoma, left atrial myoma, and coronary artery bypass surgery (CABG). Risk/low potency: mitral valve mitral calsification, patent foramen ovale (PFO), atrial septal aneurysm, aneurysm of the atrium with foramen ovale patent, left ventricular aneurysm without thrombus, isolate " "left atrial smoke in echocardiography (no mitral stenosis or atrial fibrillation), complex atheroma in the rising aorta or proximal.
Among those who have 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 an embolic stroke from an unspecified source (ESUS). This subset of cryptogenic strokes is defined as non-lacunar brain infarction without proximal artery stenosis or cardioembolic source. About one in six ischemic strokes can be classified as ESUS.
Cerebral Hypoperfusion
Cerebral hypoperfusion is the reduction of blood flow to all parts of the brain. The reduction can be to certain parts of the brain depending on the cause. This is most often caused by heart failure from cardiac arrest or arrhythmia, or from decreased cardiac output as a result of myocardial infarction, pulmonary embolism, pericardial effusion, or bleeding. Hypoxemia (low blood oxygen levels) can trigger hypoperfusion. Because the reduction in blood flow is global, all parts of the brain may be affected, especially the vulnerable "DAS" region - the area of ​​the border zone supplied by the main cerebral artery. The watershed stroke refers to the condition when the blood supply to this area is disrupted. Blood flow to these areas does not always stop, but can actually decrease to the point where brain damage can occur.
Venous thrombosis
Cerebral venous sinus thrombosis causes a stroke because of increased local venous pressure, which exceeds the pressure produced by the arteries. Infarction is more likely to undergo bleeding transformation (leaking blood to damaged areas) than other types of ischemic stroke.
Intracerebral hemorrhage
Usually occurs in small arteries or arterioles and is usually caused by hypertension, intracranial vascular malformations (including cavernous angiomas or arteriovenous malformations), cerebral amyloid angiopathy, or infarction where secondary bleeding has occurred. Other potential causes are trauma, bleeding disorders, amyloid angiopathy, use of illegal drugs (eg, amphetamines or cocaine). The hematoma enlarges until the pressure of adjacent tissue restricts its growth, or until its decompression by emptying into the ventricular system, CSF or pial surfaces. One-third of intracerebral hemorrhage is to the ventricle of the brain. ICHs have a 44% mortality rate after 30 days, higher than ischemic stroke or subarachnoid hemorrhage (which technically can be classified as a type of stroke).
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Other causes may include arterial spasm. This may be due to cocaine.
Silent stroke
A silent stroke is a stroke that has no external symptoms, and patients usually do not realize that they have a stroke. Although it does not cause identifiable symptoms, silent strokes still damage the brain, and put the patient at increased risk for both transient ischemic attacks and major strokes in the future. Conversely, those who have a large stroke are also at risk of having a silent stroke. In extensive research in 1998, more than 11 million people were estimated to have suffered a stroke in the United States. About 770,000 of these strokes are symptoms and 11 million are the first silent MRI infarction or bleeding. A silent stroke usually causes lesions detected through the use of neuroimaging such as MRI. Quiet stroke is estimated to occur at five times the rate of stroke symptoms. The risk of silent stroke increases with age, but it can also affect adults and younger children, especially those with acute anemia.
Pathophysiology
Ischemic
Ischemic stroke occurs due to loss of blood supply to the part of the brain, initiating ischemic cascade. Brain tissue ceases to function if oxygen deprivation for more than 60 to 90 seconds, and after about three hours will suffer a permanent injury that may cause tissue death, ie infarction. (This is why fibrinolytics such as alteplase are only given up to three hours since the onset of stroke.) Atherosclerosis may interfere with blood supply by narrowing the lumen of the blood vessels leading to reduced blood flow, by causing the formation of blood clots inside the vessel, or by releasing small embolic rain through disintegration of atherosclerotic plaques. Embryo infarction occurs when emboli forms elsewhere in the circulatory system, usually in the heart as a result of atrial fibrillation, or in the carotid artery, breaks out, enters the cerebral circulation, then inserts and blocks the blood vessels of the brain. Because the blood vessels in the brain are now blocked, the brain becomes low in energy, and thus the resort uses anaerobic metabolism in the area 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 that has the potential to destroy cells because it is acidic and disrupts the normal acid-base balance in the brain. The area of ​​ischemia is referred to as "ischemic penumbra".
As oxygen or glucose becomes depleted in ischemic brain tissue, production of high energy phosphate compounds such as adenosine triphosphate (ATP) fails, leading to energy-dependent process failures (such as ion pumping) required for tissue cell survival. This triggers a series of interrelated events that result in cellular injury and death. The main cause of neuronal injury is the release of stimulation of glutamate neurotransmitters. Glutamate concentrations outside the cells of the nervous system are usually kept low by so-called uptake carriers, which are supported by ion concentration gradients (especially Na ) across the cell membrane. However, a stroke cuts off the supply of oxygen and glucose that drives the ion pump maintaining this gradient. As a result, the transmembrane ion gradient decreases, and the glutamate transporter reverses its direction, releasing glutamate into the extracellular space. Glutamate acts on receptors in nerve cells (especially NMDA receptors), resulting in the inclusion of calcium-activating enzymes that digest cell proteins, lipids, and nuclear materials. The entry of calcium can also cause mitochondrial failure, which can lead further towards energy depletion and can trigger cell death due to programmed cell death.
Ischemia also induces the production of oxygen free radicals and other reactive oxygen species. It reacts with and destroys a number of cellular and extracellular elements. Damage to the lining of the blood vessels or endothelium is very important. In fact, many antioxidant neuroprotectants such as uric acid and NXY-059 work at the endothelium level and not in the brain per se . Free radicals also directly initiate elements of the programmed cell death cascade by redox signaling.
This process is the same for all types of ischemic tissue and collectively referred to as ischemic cascade . However, brain tissue is particularly susceptible to ischemia because it has little respiratory reserves and is entirely dependent on aerobic metabolism, unlike most other organs.
In addition to the damaging effects on brain cells, ischemia and infarction can result in the loss of structural integrity of brain tissue and blood vessels, partly through the release of the metalloprotease matrix, which is an enzyme that depends on zinc and calcium that destroys collagen, hyaluronic acid. , and other elements of connective tissue. Other proteases also contribute to this process. The loss of integrity of the vascular structure results in damage to the protective brain blood barrier that contributes to cerebral edema, which can lead to secondary development of brain injury.
Hemorrhag
Hemorrhagic stroke is classified according to underlying pathology. Some causes of hemorrhagic stroke are hemorrhage hypertension, aneurysm rupture, AV fistula rupture, previous ischemic infarct transformation, and drug induced bleeding. They produce tissue injury by causing tissue compression from a widespread hematoma or hematoma. In addition, pressure can lead to loss of blood supply to the affected tissue with the resulting infarction, and blood released by cerebral hemorrhage appears to have a direct toxic effect on brain tissue and blood vessels. Inflammation contributes to secondary brain injury after bleeding.
Diagnosis
Stroke is diagnosed through several techniques: neurological examination (such as NIHSS), CT scan (most often without contrast enhancement) or MRI scan, Doppler ultrasound, and arteriography. The diagnosis of stroke itself is clinical, with the help of imaging techniques. The imaging technique also helps in determining subtypes and causes of stroke. There is no blood test commonly used for the diagnosis of stroke itself, although blood tests may be helpful in finding possible causes of stroke.
Physical exam
Physical examination, including taking a medical history of symptoms and neurological status, helps provide evaluation of the location and severity of the stroke. This can provide a standard score on eg, NIH stroke scale.
Imaging
To diagnose ischemic stroke (blockage) in emergency settings:
- CT scan ( without contrast enhancement)
- sensitivity = 16% (less than 10% in first 3 hours of symptom onset)
- specificity = 96%
- MRI scan
- sensitivity = 83%
- specificity = 98%
To diagnose a haemorrhagic stroke in emergency settings:
- CT scan ( without contrast enhancement)
- sensitivity = 89%
- specificity = 100%
- MRI scan
- sensitivity = 81%
- specificity = 100%
To detect chronic bleeding, MRI scans are more sensitive.
For a stable stroke assessment, SPECT and PET/CT nuclear drugs scans may be helpful. SPECT documented cerebral blood flow and PET with FDG isotopic metabolic activity of neurons.
A CT scan can not detect an ischemic stroke, especially if small, recent onset, or in the brainstem or cerebellum area. CT scans more to override certain stroke mimics and detect bleeding.
Underlying cause
When a stroke has been diagnosed, various other studies can be done to determine the underlying cause. With the current treatment and diagnostic options available, it is crucial to determine whether there is a peripheral source of embolism. Selection of tests may vary because the causes of stroke vary with age, comorbidity and clinical presentation. Here is a commonly used technique:
- an ultrasound/doppler study of the carotid artery (for detecting carotid stenosis) or precerebral artery dissection;
- electrocardiogram (EKG) and echocardiogram (to identify arrhythmias and heart-induced clots that can spread to the brain vessels through the bloodstream);
- a Holter monitor study to identify abnormal heart rhythms,
- an angiogram of the cerebral blood vessels (if bleeding is suspected to be from aneurysms or arteriovenous malformations);
- Blood tests to determine whether high blood cholesterol, if there is an abnormal tendency to bleed, and if some more rare process such as homocystinuria may be involved.
For a haemorrhagic stroke, a CT scan or MRI with intravascular contrast may be able to identify abnormalities in the cerebral artery (such as aneurysm) or other sources of bleeding, and structural MRI if this does not indicate a cause. If this also does not identify the underlying reasons for bleeding, cerebral invasive angiography may be performed but this requires access to the bloodstream with intravascular catheters and may lead to further strokes as well as complications at these insertion sites and investigations because it is reserved for special situations. If there are symptoms suggesting that bleeding may occur as a result of venous thrombosis, CT or MRI venography may be used to examine the cerebral veins.
Misdiagnosis
Among people with ischemic stroke, misdiagnosis occurs 2 to 26% of the time. A "chameleon stroke" (SC) is a stroke that is diagnosed as something else.
People who do not have a stroke can also be misdiagnosed as a stroke. Giving thrombolytics (freezing of blood clots) in such cases causes intracerebral hemorrhage 1 to 2% of the time, which is less than a person with a stroke. This unnecessary treatment adds health care costs. However, AHA/ASA guidelines state that starting an intravenous tPA in imitation probability is preferred to delay treatment for additional testing.
Women, African-Americans, Hispanics-Americans, Asians and Pacific Islanders are more often misdiagnosed for conditions other than strokes when actually having a stroke. In addition, adults under the age of 44 are seven times more likely to have missed strokes than adults over age 75. This is especially true in younger people with posterior circulatory infarction. Some medical centers have used hyperacute MRI in experimental studies for people initially thought to have a low probability of stroke. And in some of these people, strokes have been found which are then treated with thrombolytic drugs.
Prevention
Given the burden of stroke, prevention is an important public health problem. Primary prevention is less effective than secondary prevention (as assessed by the amount needed to treat to prevent one stroke per year). The latest guidelines detail the evidence for primary prevention in stroke. In those who are healthy, aspirin does not appear to be beneficial and thus is not recommended. In people who have had myocardial infarction or those with high cardiovascular risk, this provides protection against the first stroke. In those who previously had a stroke, treatment with drugs such as aspirin, clopidogrel, and dipyridamole may be beneficial. The US Preventive Services Task Force (USPSTF) recommends not to screen for carotid artery stenosis in those without symptoms.
Risk factors
The most modifiable risk factors for stroke are high blood pressure and atrial fibrillation although the effect size is small with 833 people should be treated for 1 year to prevent a stroke. Other modifiable risk factors include high blood cholesterol, diabetes mellitus, smoking (active and passive), heavy alcohol use, drug use, lack of physical activity, obesity, consumption of processed red meat, and unhealthy diet. Smoking just one cigarette per day increases the risk by more than 30%. Alcohol use may predispose to ischemic stroke, and intracerebral and subarachnoid hemorrhage via multiple mechanisms (eg via hypertension, atrial fibrillation, thrombocytosis rebound and platelet aggregation and clotting disorders). Drugs, most commonly amphetamines and cocaine, can induce a stroke through damage to 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 a cause of stroke, in both children and adults.
A high level of physical activity reduces the risk of stroke by about 26%. There is a lack of high quality studies that see promotional efforts to improve lifestyle factors. Nonetheless, given the large amount of indirect evidence, the 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 may be a useful surgical method to prevent stroke.
Blood pressure
High blood pressure accounts for 35-50% of stroke risk. Reduction of systolic blood pressure of 10 mmHg or diastolic 5 mmHg reduces the risk of stroke by ~ 40%. Lowering blood pressure has been proven conclusively to prevent ischemic and hemorrhagic strokes. This is equally important in secondary prevention. Even patients older than 80 years and those with isolated systolic hypertension benefit from antihypertensive therapy. The available evidence does not indicate a major difference in stroke prevention between antihypertensive drugs - therefore, other factors such as protection against other forms of cardiovascular disease and costs should be considered. Regular use of beta-blockers after a stroke or TIA has not been shown to result in benefits.
Lipid blood
High cholesterol levels have been inconsistently associated with stroke (ischemic). Statins have been shown to reduce the risk of stroke by about 15%. Since previous meta-analyzes of other lipid-lowering drugs showed no decreased risk, statins could use their effects through mechanisms other than their lipid-lowering effects.
Diabetes mellitus
Diabetes mellitus increases the risk of stroke by 2 to 3 times. While intensive blood sugar control has been shown to reduce the complications of small blood vessels such as kidney damage and damage to the retina of the eye has not been proven to reduce complications of major blood vessels such as stroke.
Anticoagulation drugs
Oral anticoagulants such as warfarin have been a mainstay of stroke prevention for over 50 years. However, some studies have shown that aspirin and other antiplatelets are very effective in secondary prevention after stroke or transient ischemic attacks. Low dose aspirin (eg 75-150 mg) is as effective as high doses but has fewer side effects; the lowest effective dose is still unknown. Thienopyridines (clopidogrel, ticlopidine) may be slightly more effective than aspirin and have a reduced risk of gastrointestinal bleeding, but are more expensive. Clopidogrel has fewer side effects than ticlopidine. Dipyridamole may be added to aspirin therapy to provide a small additional benefit, although headache is a common side effect. Low-dose aspirin is also effective for stroke prevention after myocardial infarction.
Those with atrial fibrillation had a 5% stroke risk per year, and this risk was higher in those with valvular atrial fibrillation. Depending on the risk of stroke, anticoagulation with drugs such as warfarin or aspirin is useful for prevention. Except in people with atrial fibrillation, oral anticoagulation is not recommended for stroke prevention - many benefits are offset by the risk of bleeding.
However, in primary prevention, antiplatelet drugs do not reduce the risk of ischemic stroke but increase the risk of major bleeding. Further research is needed to investigate the possible effects of aspirin protection against ischemic stroke in women.
Surgery
Carotid endarterectomy or carotid angioplasty can be used to eliminate atherosclerotic narrowing of the carotid artery. There is evidence to support this procedure in certain cases. Endarterectomy for significant stenosis has been shown to be useful in preventing further stroke in those who already have it. Stenting of the carotid artery has not proven to be equally useful. People are selected for surgery by age, sex, stenosis level, time since symptoms and preferences of people. Surgery is most efficient if not delayed too long - the risk of recurrent stroke in patients with stenosis 50% or greater up to 20% after 5 years, but endarterectomy reduces this risk to about 5%. The number of procedures needed to cure one patient is 5 for the initial surgery (within two weeks after the initial stroke), but 125 if delayed more than 12 weeks.
Screening for carotid artery narrowing has not proven to be a useful test in the general population. The study of surgical intervention for asymptomatic carotid artery stenosis showed only a slight decrease in the risk of stroke. To be useful, the degree of surgical complication should be kept below 4%. Even then, for 100 operations, 5 patients will benefit by avoiding a stroke, 3 will develop a stroke despite surgery, 3 will develop a stroke or die from the operation itself, and 89 will remain stroke free but will also do so without intervention.
Diet
Nutrition, particularly Mediterranean-style diets, has the potential to reduce the risk of stroke by more than half. It does not seem to decrease the level of homocysteine ​​â € <â €
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 mmph systolic or greater than 100 mmHg Diastolic. In those who previously had preeclampsia, other risk factors should be treated more aggressively.
Previous stroke or TIA
Keeping blood pressure below 140/90 mmHg is recommended. Anticoagulation may prevent recurrent ischemic stroke. Among people with nonvalvular atrial fibrillation, anticoagulation can reduce stroke by up to 60% while antiplatelet agents can reduce stroke by 20%. However, a recent meta-analysis shows the dangers of anticoagulation that started early after an embolic stroke. The treatment of stroke prevention for atrial fibrillation was determined according to the CHA2DS2-VASc score. The most widely used anticoagulants to prevent thromboembolic stroke in patients with nonvalvular atrial fibrillation are oral warfarin agents while a number of new agents including dabigatrants are alternatives that do not require prothrombin time monitoring.
Anticoagulants, when used after a stroke, should not be discontinued for dental procedures.
If the study shows carotid artery stenosis, and the person has a residual function level on the affected side, carotid endarterectomy (surgical removal of stenosis) may decrease the risk of recurrence if performed rapidly after a stroke.
Management
Ischemic stroke
Aspirin reduces the risk of recurrence as a whole by 13% with greater benefit early on. The definitive therapy in the first few hours is aimed at removing blockages by breaking down the lumps (thrombolysis), or by throwing them away mechanically (thrombectomy). The philosophical premise underlying the importance of rapid stroke intervention is concluded as Time is the Brain! in the early 1990s. Years later, the same idea, that the rapid recovery of cerebral blood flow produces fewer dying brain cells, has been proven and quantified.
A tight blood sugar control within the first few hours does not improve results and can cause damage. High blood pressure is also usually not lowered because this has not been found to help. Cerebrolysin, a mixture of pig brain tissue used to treat acute ischemic stroke in many Asian and European countries, does not improve yield and may increase the risk of severe side effects.
thrombolysis
Thrombolysis, such as with recombinant tissue plasminogen activator (rtPA), in acute ischemic stroke, when administered within three hours of symptom onset produces an overall benefit of 10% with respect to life without disability. However, it does not increase the chances of survival. The benefits are greater than ever used. Between three and four and a half hours, the effect is less clear. The 2014 review found a 5% increase in the number of people living without disabilities at three to six months; However, there is a 2% increased risk of death in the short term. After four and a half hours, thrombolysis worsens results. This benefit or lack of benefits occurs regardless of the age of the person being treated. There is no reliable way to determine who will undergo post-intracranial hemorrhagic treatment than those who do not.
Its use is supported by the American Heart Association and the American Academy of Neurology as the recommended treatment for acute stroke within three hours of symptom onset as long as there are no other contraindications (such as abnormal laboratory values, high blood pressure, or more recently). operation). This position for landfill is based on the findings of two studies by one group of researchers showing that tPA increases the chances for good neurological outcomes. When administered within the first three hours, thrombolysis improves functional outcomes without affecting mortality. 6.4% of people with large strokes have substantial cerebral hemorrhage as a complication of a given tPA so that part of the reason for the short-term mortality increase. In addition, the American Academy of Emergency Medicine states that objective evidence on the efficacy, safety, and application of landfills for acute ischemic stroke is not sufficient to ensure classification as a standard of care. Intra-arterial fibrinolysis, in which the catheter is passed arteries to the brain and drugs injected at the site of thrombosis, has been found to improve outcomes in people with acute ischemic stroke.
Surgery
Surgical removal of blood clots causing ischemic stroke can improve results if done within 7 hours of starting symptoms in those with large anterior artery clots. But that does not change the risk of death. Significant complications occur in about 7%. Intravenous thrombolysis is generally used in eligible people even if they are considered for mechanical thrombectomy. Certain cases may benefit from thrombectomy up to 24 hours after onset of symptoms.
Stroke that affects most of the brain can cause significant brain swelling with secondary brain injury in surrounding tissues. This phenomenon is especially found in strokes that affect brain tissue that depends on the cerebral artery of the media for blood supply and is also called "malignant cerebral infarction" because it brings a bleak prognosis. Relief pressure may be tried with medication, but some require hemikraniektomi, temporary skull removal on one side of the head. This reduces the risk of death, although some people survive with disabilities that should die.
Hemorrhagic stroke
People with intracerebral hemorrhage require supportive care, including blood pressure control if necessary. People are monitored for altered levels of consciousness, and their blood sugar and oxygenation are kept at optimal levels. Anticoagulants and antithrombots can worsen bleeding and are generally discontinued (and reversed if possible). A proportion may benefit from neurosurgical intervention to elevate the blood and treat the underlying cause, but this depends on the location and size of the bleeding and the factors associated with the patient, and ongoing research is being done into the question for people which with intracerebral hemorrhage can be beneficial.
In subarachnoid hemorrhage, early treatment for underlying cerebral aneurysms may reduce the risk of further bleeding. Depending on the location of the aneurysm this may be by surgery involving opening the skull or endovascular (through a blood vessel).
Unit stroke
Ideally, people who have had a stroke are treated in "stroke units", wards or special areas in hospitals run by nurses and therapists with experience in stroke treatment. It has been shown that people treated in stroke units have a higher chance of survival than those treated elsewhere in the hospital, even if they are treated by a doctor without experience in stroke.
Rehabilitation
Stroke rehabilitation is a process whereby people with crippling strokes undergo treatment to help them return to normal life as much as possible by regaining and re-learning daily life skills. It also aims to help victims understand and adapt to adversity, prevent secondary complications and educate family members to play a supporting role.
The rehabilitation team is usually multidisciplinary because it involves staff with different skills that work together to help the patient. These include doctors trained in rehabilitation medicine, clinical pharmacists, nursing staff, physiotherapists, occupational therapists, speech and language therapists, and orthotists. Some teams may also include psychologists and social workers, because at least one-third of affected people manifest post-stroke depression. Validated instruments such as the Barthel scale can be used to assess the likelihood a stroke patient can manage at home with or without support after being discharged from the hospital.
Good care is essential in maintaining skin care, feeding, hydration, positioning, and monitoring vital signs such as temperature, pulse, and blood pressure. Stroke rehabilitation begins immediately.
For most people with stroke, physical therapy (PT), occupational therapy (OT) and pathology talk language (SLP) is the cornerstone of the rehabilitation process. Often, auxiliary technologies such as wheelchairs, walkers and sticks can be useful. Many mobility problems can be increased with the use of foot ank orthosis. PT and OT have overlapping areas of expertise; However, the PT focuses on the range of motion and strength by exercising and re-learning functional tasks such as bed mobility, transfer, walking and other gross motor functions. Physiotherapists can also work with patients to raise awareness and use of the hemiplegia side. Rehabilitation involves working on the ability to produce strong movements or the ability to perform tasks using a normal pattern. Emphasis is often concentrated on the functional tasks and goals of the patient. One example of a physiotherapist used to promote motor learning involves constrained movement therapy induced by constraints. Through the patient's continuous practice of re-learning to use and adjust the hemiplegia branch during functional activities to create lasting permanent changes. The PL is involved in training to help relearn the daily activities known as daily life activities (ADL) such as eating, drinking, dressing, bathing, cooking, reading and writing, and spraying. Speech and language therapy is suitable for people with speech production disorders: dysarthria and apraxia speak, aphasia, cognitive-communication disorder, and swallowing problems.
Patients may have specific problems, such as dysphagia, which can cause ingested material into the lungs and cause aspiration pneumonia. This condition may improve over time, but for a while, a nasogastric tube can be inserted, allowing liquid food to be administered directly to the stomach. If swallowing is still considered unsafe, the percussion endoscopic gastrostomy (PEG) tube is passed and this can remain indefinitely.
Treatment of stroke-related flexibility often involves early mobilization, commonly performed by physiotherapists, combined with elongation of seizure muscles and sustained stretching through various positions. Getting an initial increase in range of motion is often achieved through rhythmic rotation patterns associated with affected limbs. Once full coverage has been achieved by the therapist, the extremity should be positioned in an extended position to prevent further contractures, skin damage, and not using limbs with the use of splints or other means to stabilize the joints. Cold in the form of ice packs or ice packs has been proven to briefly reduce the flexibility by dampening the rate of temporary nerve shooting. Electrical stimulation to the muscle or antagonistic vibration has also been used with some success.
Stroke rehabilitation should begin as soon as possible and can last from a few days to over a year. Most functional returns are seen in the first few months, and then the increase falls with the "windows" officially considered by US and other state rehabilitation units to be closed after six months, with little chance for further improvements. However, patients have been known to continue improving for years, regaining and strengthening abilities such as writing, walking, running, and speaking. Daily rehabilitation exercises should continue to be part of the stroke patient's routine. Total recovery is unusual but not impossible and most patients will improve to some extent: proper diet and exercise are known to help the brain to recover.
Several current and future therapeutic methods include the use of virtual reality and video games for rehabilitation. These rehabilitation forms offer the potential to motivate patients to perform specific therapeutic tasks that many other forms do not. Many clinics and hospitals adopt the use of these tools for exercise, social interaction, and rehabilitation as they are affordable, accessible and can be used in clinics and homes. Mirror therapy is associated with an increase in upper limb motor function in patients with stroke. Other non-invasive rehabilitation methods used to improve physical therapy of motor function in stroke patients include transcranial magnetic stimulation and direct transcranial flow stimulation. and robotic therapy.
Stroke can also reduce the general fitness of people. Reduced fitness can reduce the capacity for rehabilitation and general health. Physical exercise as part of a rehabilitation program after a stroke appears safe. Cardiorespiratory fitness exercises that involve walking in rehabilitation can improve speed, tolerance and independence while walking, and can improve balance. There is inadequate long-term data about the effects of exercise and training on death, dependency and disability after a stroke. Future research fields can concentrate on optimal sports recipes and long-term health benefits of exercise. The effect of physical exercise on cognition can also be studied further.
The ability to walk independently in their community, indoors or outdoors, is essential following a stroke. Although no negative effects were reported, it is unclear whether the results could improve with this walking program when compared to usual care.
Self-management
Stroke can affect the ability to live independently and qualified. The self-management program is a specialized training that educates stroke victims about stroke and its consequences, helping them acquire skills to overcome their challenges, and help them organize and fulfill their own goals during their recovery process. These programs are tailored to the target audience, and are led by someone trained and skilled in stroke and its consequences (most often professional, but also stroke and peers). The 2016 review reports that these programs improve the quality of life after a stroke, with no negative effects. People with strokes feel more empowered, happy and satisfied with life after this training.
Prognosis
Defects affect 75% of sufferers sufficient stroke to reduce their work ability. Stroke can affect people physically, mentally, emotionally, or a combination of all three. The results of stroke vary greatly depending on the size and location of the lesion. Dysfunction corresponds to areas of the brain that have been damaged.
Some of the physical defects that can occur due to a stroke include muscle weakness, numbness, pressure sores, pneumonia, incontinence, apraxia (inability to perform learning movements), difficulty performing daily activities, loss of appetite, loss of speech, vision loss and pain. If the stroke is severe enough, or at a specific location such as the brain stem, coma or death can occur.
Emotional problems after a stroke can be caused by direct damage to the emotional center in the brain or from frustration and difficulty adapting to new limitations. Post-stroke emotional difficulties include anxiety, panic attacks, flat effects (failure to express emotions), mania, apathy, and psychosis. Other difficulties may include a decrease in the ability to communicate emotions through facial expressions, body language and sound.
Disorders in self-identity, relationships with others, and emotional well-being can cause social consequences after a stroke due to a lack of ability to communicate. Many people who experience communication disorders after a stroke find it more difficult to cope with social problems rather than physical disorders. The wider aspect of care should address speech impairment of emotional impact on those who have difficulty speaking after a stroke. Those who experience a stroke are at risk of paralysis which can lead to an image of a disturbed body that can also cause other social problems.
30 to 50% of stroke suffer from post-stroke depression, characterized by lethargy, irritability, sleep disturbances, lower self-esteem and withdrawal. Depression can reduce motivation and worsen outcomes, but can be treated with social and family support, psychotherapy and, in severe cases, antidepressants.
Emotional lability, another consequence of stroke, causes people to switch quickly between emotional highs and lows and to express emotions inappropriately, for example by over laughing or crying with little or no provocation. While this emotional expression usually corresponds to the actual emotion of a person, the more severe form of emotional liability causes the affected person to laugh and cry pathologically, regardless of context or emotion. Some people show the opposite of what they feel, like crying when they are happy. Emotional lability occurs in about 20% of those who have a stroke. Those with right hemisphere stroke are more likely to have empathy problems that can make communication more difficult.
Cognitive deficits due to stroke include perceptual disorders, aphasia, dementia, and problems with attention and memory. Stroke patients may not be aware of their own disability, a condition called anosognosia. In a condition called hemispasial neglect, the affected person can not attend anything on the opposite side of the room with a broken hemisphere.
Cognitive and psychological outcomes after a stroke can be affected by age at which a stroke occurs, pre-stroke intellectual function, psychiatric history and whether there is a pre-existing brain pathology.
Up to 10% of people who follow a stroke develop seizures, most often within the week after the event; stroke severity increases the likelihood of seizure.
Epidemiology
Stroke is the second most common cause of death in the world in 2011, accounting for 6.2 million deaths (~ 11% of total). Approximately 17 million people suffered a stroke in 2010 and 33 million people previously had a stroke and are still alive. Between 1990 and 2010 stroke numbers declined by about 10% in developed countries and increased by 10% in developing countries. Overall, two thirds of strokes occur in those over 65 years of age. South Asians are at very high risk of stroke, accounting for 40% of global stroke deaths.
It ranks after heart disease and before cancer. In the United States stroke is the leading cause of disability, and recently declined from the third leading to the fourth leading cause of death. Geographical disparities in stroke incidence have been observed, including the presence of a "stroke belt" in the southeastern United States, but the cause of this gap has not been explained.
The risk of stroke increases exponentially from the age of 30, and the cause varies with age. Old age is one of the most significant stroke risk factors. 95% of strokes occur in people aged 45 years and over, and two thirds of strokes occur in those over the age of 65 years. The risk of a person who dies if he has a stroke also increases with age. However, stroke can occur at any age, including in childhood.
Family members may have a genetic predisposition to stroke or share a lifestyle that contributes to stroke. Higher levels of the Von Willebrand factor are more common among people who have an ischemic stroke for the first time. The results of this study found that the only significant genetic factor was the person's blood group. Having had a stroke in the past greatly increases a person's future stroke risk.
Men are 25% more likely to suffer a stroke than women, but 60% of deaths from strokes occur in women. Because women live longer, they are older on average when they have a stroke and are thus more likely to be killed. Some stroke risk factors apply only to women. The main ones include pregnancy, labor, menopause, and treatment (HRT).
History
Episodes of stroke and family stroke have been reported since the 2nd millennium BC and beyond in ancient Mesopotamia and Persia. Hippocrates (460 to 370 BC) is the first to describe the phenomenon of sudden paralysis often associated with ischemia. Apoplexy, from the Greek word for "violent beating," first appeared in the writings of Hippocrates to describe this phenomenon. The word stroke is used as a synonym for apoplectic seizures as early as 1599, and is a fairly literal translation of the Greek term.
In 1658, in his book Apoplexia , Johann Jacob Wepfer (1620-1695) identifies the cause of hemorrhagic stroke when he suggests that people who die from apoplexy bleed in their brains. Wepfer also identifies the major arteries supplying the brain, the vertebral and carotid arteries, and identifies the cause of the type of ischemic stroke known as cerebral infarction when it suggests that apoplexy may be caused by a blockage into the vessel. Rudolf Virchow first described the mechanism of thromboembolism as a major factor.
The term "cerebrovascular accident" was introduced in 1927, reflecting "increased awareness and acceptance of vascular theory and (...) recognition of the consequences of abrupt interruption in the brain's vascular supply". Its use is now blocked by a number of neurological textbooks, the reason that the accidental connotations brought by the word accident are not enough to highlight the alteration of underlying risk factors. Cerebrovascular Insults can be used interchangeably.
The term "brain attack" was introduced for use to underline the acute nature of stroke according to the American Stroke Association, which since 1990 has used the term, and used everyday language to refer both ischemic and haemorrhagic. blow.
Research
Angioplasty and stenting
Angioplasty and stenting have begun to be seen as a possible viable option in the treatment of acute ischemic stroke. Intra-cranial stenting in symptomatic intracranial artery stenosis, the technical success rate (decreased stenosis & lt; 50%) ranges from 90-98%, and the major peri-procedural complication rate ranges from 4-10%. The rate of restenosis and stroke after treatment is also beneficial. These data suggest that randomized controlled trials are needed to more fully evaluate the possible therapeutic benefits of these precautions.
Neuroprotection
Neuroprotective agents include antioxidants that fight reactive oxygen species, or inhibit the death of programmed cells, or inhibit excitatory neurotransmitters have been shown experimentally to reduce tissue injury caused by ischemia. To date, clinical trials in humans with neuroprotective agents have failed, with the possibility of induced deep barbiturate induced coma. Disufenton sodium, a disulfonyl derivative of a radical phenylbutylnitrone, reported as neuro
Source of the article : Wikipedia
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