STROKE Disease

STROKE Disease

A stroke is when poor blood flow to the brain results in cell death. Prevention includes decreasing risk factors, as well as possibly aspirin, statins, surgery to open up the arteries to the brain in those with problematic narrowing, and warfarin in those with atrial fibrillation. In 2013 approximately 6.9 million people had an ischemic stroke and 3.4 million people had a hemorrhagic stroke. In 2015 there were about 42.4 million people who had previously had a stroke and were still alive.

Classification:

Classification Strokes can be classified into two major categories: ischemic and hemorrhagic. Ischemic strokes are caused by interruption of the blood supply to the brain, while hemorrhagic strokes result from the rupture of a blood vessel or an abnormal vascular structure. About 87% of strokes are ischemic, the rest being hemorrhagic. Bleeding can develop inside areas of ischemia, a condition known as "hemorrhagic transformation." It is unknown how many hemorrhagic strokes actually start as ischemic strokes. 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 24­hour limit divides stroke from transient ischemic attack, which is a related syndrome of stroke symptoms that resolve completely within 24 hours. Ischemic In an 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 # Embolism, # cerebral venous sinus thrombosis. Stroke without an obvious explanation is termed "cryptogenic" ; this constitutes 30­40% of all ischemic strokes. There are various classification systems for acute ischemic stroke. The Oxford Community Stroke Project classification relies primarily on the initial symptoms; based on the extent of the symptoms, the stroke episode is classified as total anterior circulation infarct, partial anterior circulation infarct, lacunar infarct or posterior circulation infarct . 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 classification is based on clinical symptoms as well as results of further investigations; on this basis, a stroke is classified as being due to thrombosis or embolism due to atherosclerosis of a large artery, an embolism originating in the heart, complete blockage of a small blood vessel, other determined cause, undetermined cause . Users of stimulants, such as cocaine and methamphetamine are at a high risk for ischemic strokes. Hemorrhagic There are two main types of hemorrhagic stroke: Cerebral hemorrhage, which is basically bleeding within the brain itself, due to either intraparenchymal hemorrhage or intraventricular hemorrhage . Subarachnoid hemorrhage, which is basically bleeding that occurs outside of the brain tissue but still within the skull, and precisely between the arachnoid mater and pia mater . 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 and subdural hematoma, are not considered "hemorrhagic strokes". Hemorrhagic strokes 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 strokes usually cause specific symptoms or reveal evidence of a previous head injury. Signs and symptoms Stroke symptoms typically start suddenly, over seconds to minutes, and in most cases do not progress further. The symptoms depend on the area of the brain affected. The more extensive the area of the brain affected, the more functions that are likely to be lost. Some forms of stroke can cause additional symptoms. For example, in intracranial hemorrhage, the affected area may compress other structures. Most forms of stroke are not associated with a headache, apart from subarachnoid hemorrhage and cerebral venous thrombosis and occasionally intracerebral hemorrhage. Early recognition Various systems have been proposed to increase recognition of stroke. Different findings are able to predict the presence or absence of stroke to different degrees. Sudden Onset face weakness, arm drift 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 significantly decreased . 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, as advocated by the Department of Health and the Stroke Association, the American Stroke Association, the National Stroke Association, the Los Angeles Prehospital Stroke Screen and the Cincinnati Prehospital Stroke Scale . 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 is recommended for this purpose; it is based on features from the medical history and physical examination. Subtypes If the area of the brain affected contains one of the three prominent central nervous system pathways—the spinothalamic tract, corticospinal tract, and dorsal column, symptoms may include:hemiplegia and muscle weakness of the face numbness reduction in sensory or vibratory sensation initial flaccidity, replaced by spasticity, excessive reflexes, and obligatory synergies. In most cases, the symptoms affect only one side of the body . Depending on the part of the brain affected, 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 a stroke.In addition to the above CNS 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 drooping of eyelid 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 If the cerebral cortex is involved, the CNS pathways can again be affected, but also can produce the following symptoms: aphasia dysarthria apraxia visual field defect memory deficits hemineglect disorganized thinking, confusion, hypersexual gestures 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 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.

Causes:

Causes Thrombotic stroke In thrombotic stroke, a thrombus usually forms around atherosclerotic plaques. Since blockage of the artery is gradual, onset of symptomatic thrombotic strokes is slower than that of a hemorrhagic stroke. A thrombus itself can lead to an embolic stroke 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 : atherosclerosis, vasoconstriction, aortic, carotid or vertebral artery dissection, various inflammatory diseases of the blood vessel wall, noninflammatory vasculopathy, Moyamoya disease and fibromuscular dysplasia. 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 : lipohyalinosis and fibrinoid degeneration and microatheroma . Sickle Cell anemia, which can cause blood cells to clump up and block blood vessels, can also lead to stroke. A stroke is the second leading cause of death in people under 20 with sickle cell anemia. Embolic stroke An embolic stroke refers to an arterial embolism by an embolus, a traveling particle or debris in the arterial bloodstream originating from elsewhere. An embolus is most frequently a thrombus, but it can also be a number of other substances including fat, air, cancer cells or clumps of bacteria . 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 with patent foramen ovale, left ventricular aneurysm without thrombus, isolated left atrial "smoke" on echocardiography, 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. 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 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 than other types of ischemic stroke. intracranial vascular malformations, cerebral amyloid angiopathy, or infarcts into which secondary hemorrhage has occurred. Silent stroke A silent stroke is a stroke that does not have any outward symptoms, and the patients are typically unaware they have had a stroke. Despite not causing identifiable symptoms, a silent stroke still damages the brain, and places the patient at increased risk for both transient ischemic attack and major stroke in the future. Conversely, those who have had a major stroke are also at risk of having silent strokes. In a broad study in 1998, more than 11 million people were estimated to have experienced a stroke in the United States. Approximately 770,000 of these strokes were symptomatic and 11 million were first ever silent MRI infarcts or hemorrhages. Silent strokes typically cause lesions which are detected via the use of neuroimaging such as MRI. Silent strokes are estimated to occur at five times the rate of symptomatic strokes. The risk of silent stroke increases with age, but may also affect younger adults and children, especially those with acute anemia. Pathophysiology Ischemic Ischemic stroke occurs because of a loss of blood supply to part of the brain, initiating the ischemic cascade. Brain tissue ceases to function if deprived of oxygen for more than 60 to 90 seconds, and after approximately three hours will suffer irreversible injury possibly leading to the death of the tissue, i.e., infarction. Atherosclerosis may disrupt the blood supply by narrowing the lumen of blood vessels leading to a reduction of blood flow, by causing the formation of blood clots within the vessel, or by releasing showers of small emboli through the disintegration of atherosclerotic plaques. Embolic infarction occurs when emboli formed elsewhere in the circulatory system, typically in the heart as a consequence of 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 into using anaerobic metabolism within the region of brain tissue affected by ischemia. Anaerobic metabolism produces less adenosine triphosphate but releases a by­product 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". As oxygen or glucose becomes depleted in ischemic brain tissue, the production of high energy phosphate compounds such as adenosine triphosphate fails, leading to failure of energy dependent processes necessary for tissue cell survival. This sets off a series of interrelated events that result in cellular injury and death. 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 so­called uptake carriers, which are powered by the concentration gradients of ions 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, 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 is particularly important. In fact, many antioxidant neuroprotectants such as uric acid and NXY 059 work at the level of the endothelium and not in the brain per se. Free radicals also directly initiate elements of the programmed cell death cascade by means of redox signaling. These processes are the same for any type of ischemic tissue and are referred to collectively as the ischemic cascade. However, brain tissue is especially vulnerable to ischemia since it has a little respiratory reserve and is completely dependent on aerobic metabolism, unlike most other organs. In addition to damaging effects on brain cells, ischemia and infarction can result in loss of structural integrity of brain tissue and blood vessels, partly through the release of matrix metalloproteases, which are zinc­ and calcium dependent enzymes that break down collagen, hyaluronic acid, and other elements of connective tissue. Other proteases also contribute to this process. The loss of vascular structural integrity results in a breakdown of the protective blood brain barrier that contributes to cerebral edema, which can cause secondary progression of the brain injury. Hemorrhagic Hemorrhagic strokes are 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. They result in tissue injury by causing compression of tissue from an expanding hematoma or hematomas. In addition, the pressure may lead to a loss of blood supply to affected tissue with resulting infarction, and the blood released by brain hemorrhage appears to have direct toxic effects on brain tissue and vasculature. Inflammation contributes to the secondary brain injury after hemorrhage. 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 a stroke. It can give a standard score on e.g., the NIH stroke scale. Imaging For diagnosing ischemic stroke in the emergency setting: CT scans MRI scan For diagnosing hemorrhagic stroke in the emergency setting: CT scans MRI scan For detecting chronic hemorrhages, MRI scan is more sensitive. For the assessment of stable stroke, nuclear medicine scans SPECT and PET/CT may be helpful. SPECT documents cerebral blood flow and PET with FDG isotope the metabolic activity of the neurons. Underlying cause When a stroke has been diagnosed, various other studies may be performed to determine the underlying cause. With the current 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 or dissection of the precerebral arteries; an electrocardiogram and echocardiogram ; a Holter monitor study to identify intermittent abnormal heart rhythms; an angiogram of the cerebral vasculature ; 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 strokes, a CT or MRI scan with intravascular contrast may be able to identify abnormalities in the brain arteries 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 strokes 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. Primary prevention is less effective than secondary prevention . In those who are otherwise healthy, aspirin does not appear beneficial and thus is not recommended. In people who have had a myocardial infarction or those with a high cardiovascular risk, it provides some protection against a first stroke. In those who have previously had a stroke, treatment with medications such as aspirin, clopidogrel, and dipyridamole may be beneficial. Risk factors The most important modifiable risk factors for stroke are high blood pressure and atrial fibrillation although the size of the effect is small with 833 people have to be treated for 1 year to prevent one stroke. Other modifiable risk factors include high blood cholesterol levels, diabetes mellitus, cigarette smoking, drinking lots of alcohol and drug use, lack of physical activity, obesity, processed red meat consumption and unhealthy diet. Alcohol use could predispose to ischemic stroke, and intracerebral and subarachnoid hemorrhage via multiple mechanisms . Drugs, most commonly amphetamines and cocaine, can induce stroke through damage to the blood vessels in the brain and acute hypertension. 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. 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 strokes. It 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 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 a stroke or TIA has not been shown to result in benefits. Blood lipids High cholesterol levels have been inconsistently associated with 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. Anticoagulation 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 antiplatelet drugs are highly effective in secondary prevention after a stroke or transient ischemic attack. Thienopyridines might be slightly more effective than aspirin and have a decreased risk of gastrointestinal bleeding, but are more expensive. 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. Except in people with atrial fibrillation, oral anticoagulants are not advised for stroke prevention —any benefit is offset by bleeding risk. 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:

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 patients 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. 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. Previous stroke or TIA Keeping blood pressure below 140/90 mmHg is recommended. Anticoagulation can prevent recurrent ischemic strokes. Among people with nonvalvular atrial fibrillation, anticoagulation can reduce stroke by 60% while antiplatelet agents can reduce stroke by 20%. However, a recent meta­analysis suggests harm from anticoagulation started early after an embolic stroke. Stroke prevention treatment for atrial fibrillation is determined according to the CHA2DS2–VASc score. The most widely used anticoagulant to prevent thromboembolic stroke in patients with nonvalvular atrial fibrillation is the oral agent warfarin while a number of newer agents including dabigatran are alternatives which do not require prothrombin time monitoring. If studies show carotid artery stenosis, and the person has a degree of residual function on the affected side, carotid endarterectomy may decrease the risk of recurrence if performed rapidly after stroke. Management Ischemic stroke Aspirin reduces the overall risk of recurrence by 13% with greater benefit early on. Definitive therapy within the first few hours is aimed at removing the blockage by breaking the clot down, or by removing it mechanically . The philosophical premise underlying the importance of rapid stroke intervention was summed up as Time is Brain! in the early 1990s. Years later, that same idea, that rapid cerebral blood flow restoration results in fewer brain cells dying, has been proved and quantified. Tight blood sugar control in the first few hours does not improve outcomes and may cause harm. High blood pressure is also not typically lowered as this has not been found to be helpful. Cerebrolysin, a mix of pig brain tissue used to treat acute ischemic stroke in many Asian and European countries, does not improve outcomes and may increase the risk of severe adverse events. Thrombolysis Thrombolysis, such as with recombinant tissue plasminogen activator, in acute ischemic stroke, when given within three hours of symptom onset results in an overall benefit of 10% with respect to living without disability. It does not, however, improve chances of survival. A 2014 review found a 5% increase in the number of people living without disability at three to six months; however, there was a 2% increased risk of death in the short term. There is no reliable way to determine who will have an intracranial bleed posttreatment versus who will not. Its use is endorsed by the American Heart Association and the American Academy of Neurology as the recommended treatment for acute stroke within three hours of onset of symptoms as long as there are not other contraindications . This position for tPA is based upon the findings of two studies by one group of investigators which showed that tPA improves the chances for a good neurological outcome. When administered within the first three hours thrombolysis improves functional outcome without affecting mortality. 6.4% of people with large strokes developed substantial brain bleeding as a complication from being given tPA thus part of the reason for increased short term mortality. Additionally, the American Academy of Emergency Medicine states that objective evidence regarding the efficacy, safety, and applicability of tPA for acute ischemic stroke is insufficient to warrant its classification as standard of care. Intra­arterial fibrinolysis, where a catheter is passed up an artery into the brain and the medication is injected at the site of thrombosis, has been found to improve outcomes in people with acute ischemic stroke. Surgery Surgical removal of the blood clot causing the ischemic stroke may improve outcomes if done within 7 hours of the start of symptoms in those with an anterior circulation large artery clot. It however does not change the risk of death. Strokes affecting large portions of the brain can cause significant brain swelling with secondary brain injury in surrounding tissue. This phenomenon is mainly encountered in strokes affecting brain tissue dependent upon the middle cerebral artery for blood supply and is also called "malignant cerebral infarction" because it carries a dismal prognosis. Relief of the pressure may be attempted with medication, but some require hemicraniectomy, the temporary surgical removal of the skull on one side of the head. This decreases the risk of death, although some more people survive with disability who would otherwise have died. Hemorrhagic stroke People with intracerebral hemorrhage require supportive care, including blood pressure control if required. People are monitored for changes in the level of consciousness, and their blood sugar and oxygenation are kept at optimum levels. Anticoagulants and antithrombotics can make bleeding worse and are generally discontinued . A proportion may benefit from neurosurgical intervention to remove the blood and treat the underlying cause, but this depends on the location and the size of the hemorrhage as well as patientrelated factors, and ongoing research is being conducted into the question as to which people with intracerebral hemorrhage may benefit. In subarachnoid hemorrhage, early treatment for underlying cerebral aneurysms may reduce the risk of further hemorrhages. Depending on the site of the aneurysm this may be by surgery that involves opening the skull or endovascularly .Stroke unit Ideally, people who have had a stroke are admitted to a "stroke unit", a ward or dedicated area in a hospital staffed by nurses and therapists with experience in stroke treatment. It has been shown that people admitted to a stroke unit have a higher chance of surviving than those admitted elsewhere in hospital, even if they are being cared for by doctors without experience in stroke. Rehabilitation Stroke rehabilitation is the process by which those with disabling strokes undergo treatment to help them return to normal life as much as possible by regaining and relearning the skills of everyday living. It also aims to help the survivor understand and adapt to difficulties, prevent secondary complications and educate family members to play a supporting role. A rehabilitation team is usually multidisciplinary as it involves staff with different skills working together to help the patient. These include physicians 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, since at least one­third of affected people manifests post stroke depression. Validated instruments such as the Barthel scale may be used to assess the likelihood of a stroke patient being able to manage at home with or without support subsequent to discharge from a hospital. Good nursing care is fundamental in maintaining skin care, feeding, hydration, positioning, and monitoring vital signs such as temperature, pulse, and blood pressure. Stroke rehabilitation begins almost immediately. For most people with stroke, physical therapy, occupational therapy and speech­language pathology are the cornerstones of the rehabilitation process. Often, assistive technology such as wheelchairs, walkers and canes may be beneficial. Many mobility problems can be improved by the use of ankle foot orthoses. PT and OT have overlapping areas of expertise; however, PT focuses on joint range of motion and strength by performing exercises and relearning functional tasks such as bed mobility, transferring, walking and other gross motor functions. Physiotherapists can also work with patients to improve awareness and use of the hemiplegic side. Rehabilitation involves working on the ability to produce strong movements or the ability to perform tasks using normal patterns. Emphasis is often concentrated on functional tasks and patient’s goals. One example physiotherapists employ to promote motor learning involves constraint­induced movement therapy. Through continuous practice the patient relearns to use and adapt the hemiplegic limb during functional activities to create lasting permanent changes. OT is involved in training to help relearn everyday activities known as the activities of daily living such as eating, drinking, dressing, bathing, cooking, reading and writing, and toileting. Speech and language therapy is appropriate for people with the speech production disorders: dysarthria and apraxia of speech, aphasia, cognitive­communication impairments, and problems with swallowing. Patients may have particular problems, such as dysphagia, which can cause swallowed material to pass into the lungs and cause aspiration pneumonia. The condition may improve with time, but in the interim, a nasogastric tube may be inserted, enabling liquid food to be given directly into the stomach. If swallowing is still deemed unsafe, then a percutaneous endoscopic gastrostomy tube is passed and this can remain indefinitely. Treatment of spasticity related to stroke often involves early mobilizations, commonly performed by a physiotherapist, combined with elongation of spastic muscles and sustained stretching through various positionings. Many clinics and hospitals are adopting the use of these off­the­shelf devices for exercise, social interaction, and rehabilitation because they are affordable, accessible and can be used within the clinic and home. and robotic therapies. A stroke can also reduce people's general fitness. Reduced fitness can reduce capacity for rehabilitation as well as general health. A systematic review found that there are inadequate long­term data about the effects of exercise and training on death, dependence and disability after a stroke. Self­management A stroke can affect the ability to live independently and with quality. Depression can reduce motivation and worsen outcome, but can be treated with social and family support, psychotherapy and, in severe cases, antidepressants. Emotional lability, another consequence of stroke, causes the person to switch quickly between emotional highs and lows and to express emotions inappropriately, for instance with an excess of laughing or crying with little or no provocation. While these expressions of emotion usually correspond to the person's actual emotions, a more severe form of emotional lability causes the affected person to laugh and cry pathologically, without regard to context or emotion. Emotional lability occurs in about 20% of those who have had a stroke. Those with a right hemisphere stroke are more likely to have an empathy problems which can make communication harder. Cognitive deficits resulting from stroke include perceptual disorders, aphasia, dementia, and problems with attention and memory. A stroke sufferer may be unaware of his or her own disabilities, a condition called anosognosia. In a condition called hemispatial neglect, the affected person is unable to attend to anything on the side of space opposite to the damaged hemisphere. Cognitive and psychological outcome after a stroke can be affected by the age at which the stroke happened, pre­stroke baseline intellectual functioning, psychiatric history and whether there is pre­existing brain pathology. Up to 10% of people following a stroke develop seizures, most commonly in the week subsequent to the event; the severity of the stroke increases the likelihood of a seizure. Epidemiology Stroke was the second most frequent cause of death worldwide in 2011, accounting for 6.2 million deaths . Approximately 17 million people had a stroke in 2010 and 33 million people have previously had a stroke and were still alive. It is ranked after heart disease and before cancer. Geographic disparities in stroke incidence have been observed, including the existence of a "stroke belt" in the southeastern United States, but causes of these disparities have not been explained. The risk of stroke increases exponentially from 30 years of age, and the cause varies by age. Advanced age is one of the most significant stroke risk factors. 95% of strokes occur in people age 45 and older, and two­thirds of strokes occur in those over the age of 65. The results of this study found that the only significant genetic factor was the person's blood type. Having had a stroke in the past greatly increases one's risk of future strokes. Men are 25% more likely to suffer strokes than women, Hippocrates was first to describe the phenomenon of sudden paralysis that is often associated with ischemia. Apoplexy, from the Greek word meaning "struck down with violence", first appeared in Hippocratic writings to describe this phenomenon. The word stroke was used as a synonym for apoplectic seizure as early as 1599, and is a fairly literal translation of the Greek term. In 1658, in his Apoplexia, Johann Jacob Wepfer identified the cause of hemorrhagic stroke when he suggested that people who had died of apoplexy had bleeding in their brains. The term cerebrovascular accident was introduced in 1927, reflecting a "growing awareness and acceptance of vascular theories and recognition of the consequences of a sudden disruption in the vascular supply of the brain". Its use is now discouraged by a number of neurology textbooks, reasoning that the connotation of fortuitousness carried by the word accident insufficiently highlights the modifiability of the underlying risk factors. Cerebrovascular insult may be used interchangeably. The term brain attack was introduced for use to underline the acute nature of stroke according to the American Stroke Association, and is used colloquially to refer to both ischemic as well as hemorrhagic stroke. Research Angioplasty and stenting Angioplasty and stenting have begun to be looked at as possible viable options in treatment of acute ischemic stroke. Intra­cranial stenting in symptomatic intracranial arterial stenosis, the rate of technical success ranged from 90­98%, and the rate of major periprocedural complications ranged from 4­10%. The rates of restenosis and stroke following the treatment were also favorable. This data suggests that a randomized controlled trial is needed to more completely evaluate the possible therapeutic advantage of this preventative measure. Mechanical thrombectomy Removal of the clot may be attempted in those where it occurs within a large blood vessel and may be an option for those who either are not eligible for or do not improve with intravenous thrombolytics. Significant complications occur in about 7%. Neuroprotection Neuroprotective agents including antioxidants which combat reactive oxygen species, or inhibit programmed cell death, or inhibit excitatory neurotransmitters have been shown experimentally to reduce tissue injury caused by ischemia. Until recently, human clinical trials with neuroprotective agents have failed, with the probable exception of deep barbiturate­induced coma. Disufenton sodium, the disulfonyl derivative of the radical­scavenging phenylbutylnitrone, was reported to be neuroprotective. This agent is thought to work at the level of the blood vessel lining. However the favourable results evidenced from one large­scale trial were not reproduced in a second trial. Hyperbaric oxygen therapy has been studied as a possible protective measure, but as of 2014, while the benefits of this have not been ruled out, further research is said to be needed. See also Dejerine–Roussy syndrome Functional Independence Measure Lipoprotein Weber's syndrome Mechanism of anoxic depolarization in the brain Ultrasound Enhanced systemic thrombolysis References.