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brain is interrupted. That is, a stroke involves the sudden loss of neuronal function due to disturbance in cerebral perfusion. This disturbance in perfusion is commonly arterial, but can be venous. The part of the brain with disturbed perfusion no longer receives adequate oxygen. This initiates the ischemic cascade which causes brain cells to die or be seriously damaged, impairing local brain function. Stroke is a medical emergency and can cause permanent neurologic damage or even death if not promptly diagnosed and treated. It is the third leading cause of death and the leading cause of adult disability in the United States and industrialized European nations. On average, a stroke occurs every 45 seconds and someone dies every 3 minutes. Of every 5 deaths from stroke, 2 occur in men and 3 in women. Risk factors include advanced age, hypertension (high blood pressure), diabetes mellitus, high cholesterol, and cigarette smoking. Cigarette smoking is the most important modifiable risk factor of stroke. The term "brain attack" is starting to come into use in the United States for stroke, just as the term "heart attack" is used for myocardial infarction, where a cutoff of blood causes necrosis to the tissue of the heart. Many hospitals have "brain attack" teams within their neurology departments specifically for swift treatment of stroke. Types of stroke Strokes can be classified into two major categories: ischemic and hemorrhagic. Ischemia can be due to thrombosis, embolism, or systemic hypoperfusion. Hemorrhage can be due to intracerebral hemorrhage or subarachnoid hemorrhage. ~80% of strokes are due to ischemia. Ischemic stroke In an ischemic stroke, which is the cause of approximately 85-90% of strokes, a blood vessel becomes occluded and the blood supply to part of the brain is totally or partially blocked. Ischemic stroke is commonly divided into thrombotic stroke, embolic stroke, systemic hypoperfusion (Watershed or Border Zone stroke), or venous thrombosis. Thrombotic stroke In thrombotic stroke, a thrombus-forming process develops in the affected artery. The thrombus — a built up clot — gradually narrows the lumen of the artery and impedes blood flow to distal tissue. These clots usually form around atherosclerotic plaques. Since blockage of the artery is gradual, onset of symptomatic thrombotic strokes is slower. A thrombus itself (even if nonoccluding) can lead to an embolic stroke (see below) if the thrombus breaks off—at which point it is then called an "embolus." Thrombotic stroke can be divided into two types depending on the type of vessel the thrombus is formed on:
Large vessel disease involves the common and internal carotids, vertebral, and the Circle of Willis. Diseases that may form thrombi in the large vessels include (in descending incidence): o Atherosclerosis o Vasoconstriction
but it can also be a plaque broken off from an atherosclerotic blood vessel or a number of other substances including fat (e. the source of the embolus must be identified. Diseases that may form thrombi in the small vessels include (in descending incidence): o Lipohyalinosis (lipid hyaline build-up secondary to hypertension and aging) and fibrinoid degeneration (stroke involving these vessels are known as lacunar infarcts) o Microatheromas from larger arteries that extend into the smaller arteries (atheromatous branch disease) o o o o o o o  Embolic stroke Embolic stroke refers to the blockage of arterial access to a part of the brain by an embolus -. Embolic stroke can be divided into four categories: • • • • those with known cardiac source those with potential cardiac or aortic source (from transthoracic or transesophageal echocardiogram) those with an arterial source those with unknown source High risk cardiac causes include: • • • • • • • • • • Atrial fibrillation and paroxysmal atrial fibrillation Rheumatic mitral or aortic valve disease Bioprosthetic and mechanical heart valves Atrial or ventricular thrombus Sick sinus syndrome Sustained atrial flutter Recent myocardial infarction (within one month) Chronic myocardial infarction together with ejection fraction <28 percent Symptomatic congestive heart failure with ejection fraction <30 percent Dilated cardiomyopathy . and even cancerous cells. air. and arteries arising from the distal vertebral and basilar artery. local therapy only solves the problem temporarily. middle cerebral artery. Because an embolus arises from elsewhere.• Dissection Takayasu arteritis Giant cell arteritis Arteritis/vasculitis Noninflammatory vasculopathy Moyamoya syndrome Fibromuscular dysplasia Small vessel disease involves the intracerebral arteries. Also. An embolus is most frequently a blood clot.g. Thus. from bone marrow in a broken bone). stem. symptoms usually are maximal at start. Because the embolic blockage is sudden in onset. branches of the Circle of Willis. symptoms may be transient as the embolus lyses and moves to a different location or dissipates altogether. Another cause is bacterial emboli released in infectious endocarditis..a traveling particle or debris in the arterial bloodstream originating from elsewhere.
border zone regions supplied by the major cerebral arteries. it can cause increased intracranial pressure which physically impinges on brain tissue and restricts blood flow into the brain.• • • • • • • Libman-Sacks endocarditis Antiphospholipid syndrome Marantic endocarditis from cancer Infective endocarditis Papillary fibroelastoma Left atrial myxoma Coronary artery bypass graft (CABG) surgery Potential cardiac causes include: • • • • • • • Mitral annular calcification Patent foramen ovale Atrial septal aneurysm Atrial septal aneurysm with patent foramen ovale Left ventricular aneurysm without thrombus Isolated left atrial smoke on echocardiography (no mitral stenosis or atrial fibrillation) Complex atheroma in the ascending aorta or proximal arch Systemic hypoperfusion (Watershed stroke) Systemic hypoperfusion is the reduction of blood flow to all parts of the body. amyloid angiopathy. Because the reduction in blood flow is global. ischemic strokes. but instead it may lessen to the point where brain damage can occur. or from reduced cardiac output as a result of myocardial infarction. blood irritates brain tissue. all parts of the brain may be affected. Hypoxemia (low blood oxygen content) may precipitate the hypoperfusion. forming a gradually enlarging hematoma (pooling of blood). pericardial effusion. hemorrhagic strokes interrupt the brain's blood supply because the bleeding vessel can no longer carry the blood to its target tissue. A third of intracerebral bleed is into the brain's . if the bleeding continues. Blood flow to these areas does not necessarily stop.. pulmonary embolism. Hemorrhagic stroke A hemorrhagic stroke.g. There are two types of hemorrhagic stroke: intracerebral hemorrhage. CSF or the pial surface. illicit drug use (e. or cerebral hemorrhage. and. In addition. In this respect. and vascular malformations. Like ischemic strokes. disrupting the delicate chemical balance. or bleeding. or until it decompresses by emptying into the ventricular system. bleeding disorders. It is most commonly due to cardiac pump failure from cardiac arrest or arrhythmias. is a form of stroke that occurs when a blood vessel in the brain ruptures or bleeds. trauma. It generally occurs in small arteries or arterioles and is commonly due to hypertension. and subarachnoid hemorrhage. amphetamines or cocaine). hemorrhagic strokes are more dangerous than their more common counterpart. The hematoma enlarges until pressure from surrounding tissue limits its growth. Intracerebral hemorrhage Main article: intracerebral hemorrhage Intracerebral hemorrhage (ICH) is bleeding directly into the brain tissue. especially "watershed" areas --.
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 (SCM) with inability to turn head to one side weakness in tongue (inability to protrude and/or move from side to side) . SAH has a 40% mortality over 30 day period. ICH has a mortality rate of 44 percent after 30 days. However. Death or deep coma ensues if the bleeding continues. Bleeding into the CSF from a ruptured aneurysm occurs very quickly. symptoms may include: • • • muscle weakness (hemiplegia) numbness reduction in sensory or vibratory sensation In most cases. taste. The defect in the brain is usually on the opposite side of the body (depending on which part of the brain is affected). since these pathways also travel in the spinal cord and any lesion there can also produce these symptoms. Subarachnoid hemorrhage Main article: subarachnoid hemorrhage Subarachnoid hemorrhage (SAH) is bleeding into the cerebrospinal fluid (CSF) of the subarachnoid space surrounding the brain. Hemorrhage from other sources is less abrupt and may continue for a longer period of time. Ischemic strokes usually only affect regional areas of the brain perfused by the blocked artery. the presence of any one of these symptoms does not necessarily suggest a stroke. but often can also cause more global symptoms due to bleeding and increased intracranial pressure. Hemorrhagic strokes can affect local areas.ventricles. In addition to the above CNS pathways.the spinothalamic tract. hearing. corticospinal tract. A stroke affecting the brainstem therefore can produce symptoms relating to deficits in these cranial nerves: • • • • • • • • altered smell. the brainstem also consists of the 12 cranial nerves. and dorsal column (medial lemniscus). higher than ischemic stroke or even the very deadly subarachnoid hemorrhage. causing rapidly increased intracranial pressure. The two most common causes of SAH are rupture of aneurysms from the base of the brain and bleeding from vascular malformations near the pial surface. The bleeding usually only lasts a few seconds but rebleeding is common. or vision (total or partial) drooping of eyelid (ptosis) and weakness of ocular muscles decreased reflexes: gag. the symptoms affect only one side of the body. swallow. If the area of the brain affected contains one of the three prominent Central nervous system pathways -. Signs and symptoms The symptoms of stroke depend on the type of stroke and the area of the brain affected.
Recent data indicate that there is about a ten to fifteen percent chance of suffering a stroke in the year following a TIA. with half of that risk manifest in the first month. the cause is more likely to be a subarachnoid hemorrhage or an embolic stroke.meaning no deficits can be identified that attributes to certain areas of the brain -. If symptoms are maximal at onset. but. patients complain of a sudden. further. but also can produce the following symptoms: • • • • • • aphasia (inability to speak or understand language from involvement of Broca's or Wernicke's area) apraxia (altered voluntary movements) visual field cut(involvement of occipital lobe) memory deficits (involvement of temporal lobe) hemineglect (involvement of parietal lobe) disorganized thinking. and a large proportion of patients develop strokes in the future. the diagnosis is transient ischemic attack (TIA). The pain may or may not radiate down into neck and legs. Vomiting may occur soon after the onset of headache. confusion. the patient may have the following: • • • trouble walking altered movement coordination vertigo and or disequilibrium Loss of consciousness. or maximum 24 hours. The combination of headache and vomiting is uncommon in ischemic stroke. Subarachnoid hemorrhage Main article: subarachnoid hemorrhage The symptoms of SAH occur abruptly due to the sudden onset of increased intracranial pressure. Usually the neurologic exam is nonfocal -. for the same reason. This syndrome may be a warning sign. with much of that risk manifest in the first 48 hours. such treatments (slightly) increase the likelihood and effects of hemorrhagic stroke since they impair clotting. the CNS pathways can again be affected. hypersexual gestures (with involvement of frontal lobe) If the cerebellum is involved. and vomiting usually occurs more often in hemorrhagic stroke than in thrombosis because of the increased intracranial pressure from the leaking blood compressing on the brain. The chances of suffering an ischemic stroke can be reduced by using aspirin or related compounds such as clopidogrel. [Diagnosis . which inhibit platelets from aggregating and forming obstructive clots. Transient ischemic attack (TIA) If the symptoms resolve within an hour. which is in essence a mini or brief stroke. Often.If the cerebral cortex is involved. and.unless the bleeding also occurs into the brain. headache. extremely severe and widespread headache.
. various other studies may be performed to determine whether there is a peripheral source of emboli: • • • • an ultrasound/doppler study of the carotid arteries (to detect carotid stenosis) an electrocardiogram (ECG) and echocardiogram (to identify arrhythmias and resultant clots in the heart which may spread to the brain vessels through the bloodstream) a Holter monitor study to identify intermittent arrhythmias an angiogram of the cerebral vasculature (if a bleed is thought to have originated from an aneurysm or arteriovenous malformation) Treatment Early assessment It is important to identify a stroke as early as possible because patients who are treated earlier are more likely to survive and have better recoveries.Stroke is diagnosed through several techniques: a neurological examination. and extent of stroke. or anticoagulant medication (warfarin). The patient should be transported to the nearest hospital that can provide a rapid evaluation and treatment with the latest available therapies targeted to the type of stroke." If the person has difficulty performing any of these tasks. Hemorrhagic stroke must be ruled out with medical imaging. The faster these therapies are started for hemorrhagic and ischemic stroke. emergency medical services should be contacted immediately. dipyridamole). These are: • • • Ask the individual to smile. dependent on the cause. Doppler ultrasound. a patient is given antiplatelet medication (aspirin. A simple set of tasks has been put forward by physicians to help those without medical training help to identify someone who is having a stroke. Ask the individual to raise both arms and keep them raised. Ask the individual to speak a simple sentence (coherently). and arteriography. the chances for recovery from each type improves greatly. and the person's symptoms described. If a stroke is confirmed on imaging. blood tests. "It is sunny out today. Only detailed physical examination and medical imaging provide information on the presence. type. clopidogrel. when this type of stroke has been found. Quick decisions about medication and the need for surgery have been shown to improve outcome. For example. since this therapy would be harmful to patients with that type of stroke. CT scans (without contrast enhancements) or MRI scans. Studies show that patients treated in hospitals with a dedicated Stroke Team or Stroke Unit and a specialized care program for stroke patients have improved odds of recovery.  Ischemic stroke As ischemic stroke is due to a thrombus (blood clot) occluding a cerebral artery.
Thrombolysis In increasing numbers of primary stroke centers. It is common for the blood pressure to be elevated immediately following a stroke. and the patient has residual function in the affected side. 55% of patients with large strokes developed substantial brain hemorrhage as a complication from being given tPA. 1742-1744. Additional therapies for ischemic stroke include aspirin (50 to 325 mg daily). 39% of all patients who were treated with tPA had a good outcome at three months. liver function tests and glucose levels are carried out. The latter is used by emergency medical technicians (EMTs) to determine whether a patient needs transport to a stroke center. However. If studies show carotid stenosis. abnormal lab values. However. since studies have shown that this increases blood flow to the brain... often using scoring systems such as the National Institutes of Health Stroke Scale. carotid endarterectomy (surgical removal of the stenosis) may decrease the risk of recurrence. tPA. physicians are advised to use their discretion when considering its . The patient may be positioned so that his or her head is flat on the stretcher. Until additional evidence clarifies such controversies. renal function. it is the position of the American Academy of Emergency Medicine that objective evidence regarding the efficacy. and combined aspirin and dipyridamole extended release (25/200 mg twice daily).Whether thrombolysis is performed or not. and that the stroke patient is receiving adequate oxygen and intravenous fluids. clopidogrel (75 mg daily). Studies indicated that while high blood pressure causes stroke. pharmacologic thrombolysis ("clot busting") with the drug Tissue plasminogen activator. it is actually beneficial in the emergency period to allow better blood flow to the brain. rather than sitting up. N Engl J Med 1995. When administered within the first 3 hours. This position for tPA is based upon the findings of one study (NINDS. high blood pressure. some of the data were flawed and the safety and efficacy of tPA is controversial. and applicability of tPA for acute ischemic stroke is insufficient to warrant its classification as standard of care.). and the Los Angeles Prehospital Stroke Screen. treatment of the arrhythmia and anticoagulation with warfarin or high-dose aspirin may decrease the risk of recurrence.) which showed that tPA improves the chances for a good neurological outcome. the following investigations are required: • • • Stroke symptoms are documented. Additionally. it 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 (eg. the use of tPA in acute stroke is controversial. only 26% of placebo controlled patients had a good functional outcome. If the stroke has been the result of cardiac arrhythmia (such as atrial fibrillation) with cardiogenic emboli. tPA is often misconstrued in the news as a "magic bullet" and it is important for patients to be aware that despite the study that supports its use. recent surgery. A recent study (Neurology 2006:66. Other immediate strategies to protect the brain during stroke include ensuring that blood sugar is as normal as possible (such as commencement of an insulin sliding scale in known diabetics). On one hand. A CT scan is performed to rule out hemorrhagic stroke Blood tests. coagulation studies (PT/INR and APTT). and tests of electrolytes. safety. such as a full blood count. is used to dissolve the clot and unblock the artery.) found the mortality to be higher among patients receiving tPA versus those who did not. the Cincinnati Stroke Scale.333:1581-1587.
These include nursing staff. In August 2004. AAEM believes it is inappropriate to claim that either use or non-use of intravenous thrombolytic therapy constitutes a standard of care issue in the treatment of stroke. blood sugar. and deploying a corkscrew-like device to ensnare the clot. speech and language therapy. Anticoagulants and antithrombotics. bathing. Often. called the Merci Retriever. For most stroke patients. and oxygenation are kept at optimum levels. such as complete or partial inability to swallow. occupational therapy. hydration. can make bleeding worse and cannot be used in intracerebral hemorrhage. OT involves exercise and training to help the stroke patient relearn everyday activities sometimes called the Activities of daily living (ADLs) such as eating.use. This is accomplished by inserting a catheter into the femoral artery. dressing. or problems forming speech. social workers. physical therapy is the cornerstone of the rehabilitation process. cooking. assistive technology such as a wheelchair and standing frame may be beneficial. which is then withdrawn from the body. Speech and language therapy is appropriate for patients with problems understanding speech or written words. Some teams may also include psychologists. which can cause swallowed material to pass into the lungs and cause aspiration pneumonia. Mechanical Thrombectomy Another intervention for acute ischemic stroke is removal of the offending thrombus directly. key in treating ischemic stroke. Already newer generation devices are being tested in the Multi MERCI trial. the FDA cleared one such device. pulse. Given the cited absence of definitive evidence. A rehabilitation team is usually multidisciplinary as it involves staff with different skills working together to help the patient. Stroke rehabilitation begins almost immediately. drinking and swallowing. The . require neurosurgical evaluation to detect and treat the cause of the bleeding. and blood pressure. Patients may have particular problems. and pharmacists since at least one third of the patients manifest post stroke depression. reading and writing. physiotherapy. based on data from the MERCI (Mechanical Embolus Removal in Cerebral Ischemia) Trial. and toileting. and usually a physician trained in rehabilitation medicine. Both the MERCI and Multi MERCI trials evaluated the use of mechanical thrombectomy up to 8 hours after onset of symptoms. directing it up into the cerebral circulation. Patients are monitored and their blood pressure. Care and rehabilitation Stroke rehabilitation is the process by which patients 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. prevent secondary complications and educate family members to play a supporting role. It also aims to help the survivor understand and adapt to difficulties. Good nursing care is fundamental in maintaining skin care. Another type of therapy involving relearning daily activities is occupational therapy (OT). Hemorrhagic stroke Patients with bleeding into (intracerebral hemorrhage) or around the brain (subarachnoid hemorrhage). and monitoring vital signs such as temperature. feeding. positioning.
In a condition called hemispatial neglect. emotionally. Emotional problems resulting from stroke can result from direct damage to emotional centers in the brain or from frustration and difficulty adapting to new limitations. then a percutaneous endoscopic gastrostomy (PEG) tube is passed and this can remain indefinitely. Some of the physical disabilities that can result from stroke include paralysis. which is characterized by lethargy. However. enabling liquid food to be given directly into the stomach. Some patients show the opposite of what they feel. apraxia (inability to perform learned movements). causes the patient to switch quickly between emotional highs and lows and to express emotions inappropriately. without regard to context or emotion. If swallowing is still unsafe after a week. walking. Emotional lability occurs in about 20% of stroke patients. but can be treated with antidepressants. The results of stroke vary widely depending on size and location of the lesion. irritability. most commonly in the week subsequent to the event. running. a nasogastric tube may be inserted. lowered self esteem. patients may continue to improve for years. coma or death can result. the severity of the stroke increases the likelihood of a seizure. and pain. pneumonia. flat affect (failure to express emotions). Risk factors and prevention Prevention of stroke can work at various levels including: . apathy. Stroke rehabilitation can last anywhere from a few days to several months. panic attacks. Post-stroke emotional difficulties include anxiety. but in the interim. While these expressions of emotion usually correspond to the patient's actual emotions. vision loss. pressure sores. difficulties carrying out daily activities. Prognosis Disability affects 75% of stroke survivors enough to decrease their employability. mentally. mania. Cognitive deficits resulting from stroke include perceptual disorders. Emotional lability.condition may improve with time. Most return of function is seen in the first few days and weeks. Depression can reduce motivation and worsen outcome. another consequence of stroke. and withdrawal. Complete recovery is unusual but not impossible. a more severe form of emotional lability causes patients to laugh and cry pathologically. If the stroke is severe enough. and problems with attention and memory. 30 to 50% of stroke survivors suffer post stroke depression (Post stroke depression). a condition called anosognosia. numbness. Stroke can affect patients physically. regaining and strengthening abilities like writing. sleep disturbances. for example crying when they are happy. incontinence. a patient is unable to attend to anything on the side of space opposite to the damaged hemisphere. dementia. A stroke sufferer may be unaware of his or her own disabilities. for instance with an excess of laughing or crying with little or no provocation. Most patients will improve to some extent. or a combination of the three. and talking. and psychosis. Up to 10% of all stroke patients develop seizures. Dysfunctions correspond to areas in the brain that have been damaged. speech problems. appetite loss. and then improvement falls off.
which can cause blood cells to clump up and block blood vessels. menopause and the treatment thereof (HRT). In patients who have strokes due to abnormalities of the heart. and cigarette smoking. Primary among these are pregnancy. diabetes. tertiary prevention . Since women live longer. 2. Also see Antiplatelet drug treatment. including in fetuses. 95% of strokes occur in people age 45 and older. and genetic or congenital conditions. Sickle cell anemia. high blood cholesterol levels. The results of this study found that the only significant genetic factor was the person's blood type. Treatment of risk factors in patients who have already had strokes (secondary prevention) is also very important as they are at high risk of subsequent events compared with those who have never had a stroke. However. Medication or drug therapy is the most common method of stroke prevention. Stroke is the second leading killer of people under 20 who suffer from sickle-cell anemia. by public health measures such as reducing smoking and the other behaviours that increase risk. which supplies blood to the brain. Procedures such as carotid endarterectomy or carotid angioplasty can be used to remove significant atherosclerotic narrowing (stenosis) of the carotid artery. yet 60% of deaths from stroke occur in women. heart disease. physical exercise. and avoidance of illicit drugs and excessive alcohol consumption are all recommended ways of reducing the risk of stroke. secondary prevention . Having had a stroke in the past greatly increases one's risk of future strokes. and two-thirds of strokes occur in those over the age of 65. Some risk factors for stroke apply only to women. illicit drug use. Family members may have a genetic tendency for stroke or share a lifestyle that contributes to stroke. The most important modifiable risk factors for stroke are hypertension. Identification of patients with treatable risk factors for stroke is paramount. control of hypercholesterolemia. diabetes mellitus. Prevention is an important public health concern. Men are 1. (The value and role of carotid artery ultrasound scanning in screening has yet to be established.actions taken to reduce the risk in those who already have disease or risk factors that may have been identified through screening. smoking cessation.) .the reduction of risk factors across the board. they are older on average when they have their strokes and thus more often killed (NIMH 2002). anticoagulation with medications such as warfarin is often necessary for stroke prevention. These procedures have been shown to prevent stroke in certain patients. stroke can occur at any age. Higher levels of Von Willebrand factor are more common amongst people who have had ischemic stroke for the first time. A person's risk of dying if he or she does have a stroke also increases with age.25 times more likely to suffer CVAs than women. Stroke seems to run in some families. primary prevention . such as atrial fibrillation. One of the most significant stroke risk factors is advanced age. Treating hypertension.actions taken to reduce the risk of complications (including further strokes) in people who have already had a stroke. childbirth. Other risks include heavy alcohol consumption (see Alcohol consumption and health).1. also increases stroke risk. especially where carotid stenosis leads to ischemic events such as transient ischemic attack. and 3. Aspirin (usually at a low dose of 75 mg) is recommended for the primary and secondary prevention of stroke.
In fact. These break off. These include the failure of mitochondria. or by releasing showers of small emboli through the disintegration of atherosclerotic plaques. which have toxic effects in excessive concentrations. is reported be neuroprotective in stroke. initiating the Ischemic cascade. partly through the release of matrix . Brain tissue ceases to function if deprived of oxygen for more than 60 to 90 seconds and after a few hours will suffer irreversible injury possibly leading to death of the tissue.. after producing favorable results in one large-scale clinical trial. Free radicals also directly initiate elements of the apoptosis cascade by means of redox signaling . a second trial failed to show favorable results. The ischemia area where tissue might recover is referred to as the ischemic penumbra. Brain tissue survival can be improved to some extent if one or more of these processes is inhibited. Drugs that scavenge Reactive oxygen species. human clinical trials with neuroprotective agents have failed. Ischaemia also induces production of oxygen free radicals and other reactive oxygen species. Damage to the blood vessel lining or endothelium is particularly important. However. However. Other processes include the loss of membrane ion pump function leading to electrolyte imbalances in brain cells. Agents that work in this way are referred to as being neuroprotective. As oxygen or glucose becomes depleted in ischemic brain tissue. This sets off a series of interrelated events that result in cellular injury and death. by causing the formation of blood clots within the vessel. unlike most other organs. Atherosclerosis may disrupt the blood supply by narrowing the lumen of blood vessels leading to a reduction of blood flow. enter the cerebral circulation.  In addition to injurious effects on brain cells. This agent appears to work at the level of the blood vessel lining or endothelium. within the region of brain tissue affected by ischemia there is a spectrum of severity. then lodge in and occlude brain blood vessels. or inhibit excitotoxic neurotransmitters. have been shown experimentally to reduce tissue injury due to ischemia.e. There is also the release of excitatory neurotransmitters. Unfortunately. i. many antioxidant neuroprotectants such as uric acid and NXY-059 work at the level of the endothelium and not in the brain per se. more recently NXY-059. ischemia and infarction can result in loss of structural integrity of brain tissue and blood vessels. with the probable exception of deep barbiturate coma. the production of high energy phosphate compounds such as adenine triphosphate (ATP) fails leading to failure of energy dependent processes necessary for tissue cell survival. These react with and damage a number of cellular and extracellular elements. brain tissue is especially vulnerable to ischemia since it has little respiratory reserve and is completely dependent on aerobic metabolism. part of the tissue may immediately die while other parts may only be injured and could potentially recover. for example. Thus. or in the carotid arteries. infarction. inhibit apoptosis. These processes are the same for any type of ischemic tissue and are referred to collectively as the ischemic cascade. which can lead further toward energy depletion and may trigger cell death due to apoptosis. Embolic infarction occurs when emboli formed elsewhere in the circulatory system.Pathophysiology Ischemic stroke occurs due to a loss of blood supply to part of the brain. the disulfonyl derivative of the radicalscavenging spintrap phenylbutylnitrone. Due to collateral circulation. Until recently. typically in the heart as a consequence of atria fibriliation.
metalloproteases. and identified the cause of ischemic stroke when he suggested that apoplexy might be caused by a blockage to those vessels. As is the case with any type of brain injury. hyaluronic acid. and causes 10% of worldwide deaths  The incidence of stroke increases exponentially from 30 years of age . Wepfer also identified the main arteries supplying the brain. Johann Jacob Wepfer (1620-1695) identified the cause of hemorrhagic stroke when he suggested that people who had died of apoplexy had bleeding in their brains. in his Apoplexia. . Inhibition of the inflammatory response has been shown experimentally to reduce tissue injury due to cerebral infarction. which can cause secondary progression of the brain injury. Stroke is the third leading cause of death in the Western world. In 1658.” first appeared in Hippocratic writings to describe stroke symptoms. and other elements of connective tissue. Hippocrates (460 to 370 BC) was first to describe the phenomenon of sudden paralysis. the immune system is activated by cerebral infarction and may under some circumstances exacerbate the injury caused by the infarction. which we now know is caused by stroke. Apoplexy. This can distort and injure tissue. which are zinc. In addition. Other proteases also contribute to this process. after heart disease and cancer. the pressure may lead to a loss of blood supply to affected tissue with resulting infarction. the vertebral and carotid arteries.  Epidemiology Stroke will soon be the most common cause of death worldwide.and calcium-dependent enzymes that break down collagen. Hemorrhagic strokes result in tissue injury by causing compression of tissue from an expanding hematoma or hematomas. from the Greek word meaning "struck down with violence.400 years ago. and the blood released by brain hemorrhage appears to have direct toxic effects on brain tissue and vasculature. and etiology varies by age History Over 2. but this has not proved out in clinical studies. The loss of vascular structural integrity results in a breakdown of the protective blood brain barrier that contributes to cerebral edema.
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