cerebral stroke

脳卒中

WordNet

1. treat gingerly or carefully; "You have to stroke the boss"
2. a sudden loss of consciousness resulting when the rupture or occlusion of a blood vessel leads to oxygen lack in the brain (同)apoplexy, cerebrovascular_accident, CVA
3. (golf) the unit of scoring in golf is the act of hitting the ball with a club; "Nicklaus won by three strokes"
4. (sports) the act of swinging or striking at a ball with a club or racket or bat or cue or hand; "it took two strokes to get out of the bunker"; "a good shot requires good balance and tempo"; "he left me an almost impossible shot" (同)shot
5. a light touch with the hands (同)stroking
6. a single complete movement
7. any one of the repeated movements of the limbs and body used for locomotion in swimming or rowing
8. a light touch
9. a mark made on a surface by a pen, pencil, or paintbrush; "she applied the paint in careful strokes"
10. the oarsman nearest the stern of the shell who sets the pace for the rest of the crew
11. row at a particular rate
12. strike a ball with a smooth blow
13. touch lightly and repeatedly, as with brushing motions; "He stroked his long beard"
14. of or relating to the cerebrum or brain; "cerebral hemisphere"; "cerebral activity"
15. involving intelligence rather than emotions or instinct; "a cerebral approach to the problem"; "cerebral drama" (同)intellectual

PrepTutorEJDIC

1. 脳卒中
2. (こぶし・武器・金づちなどの)『一打ち』,一撃,打告《+of+名》 / 《単数形で》(運の)巡り合わせ《+of+名》 / 《単数形で》(…の)ひと仕事,ひと働き;みごとな成果《+of+名》 / (鐘・時計などの)『打つ音』《+of+名》 / (時計などが打って示す)時刻 / (繰り返される動作・運動の)『一動作』,一行程 / (ペン・鉛筆・筆などの)ひと筆,ひとなで;筆の運び,筆致 / 卒中 / (ゴルフ・テニスなどの)一打ち,ストローク / (心臓などの)一打ち,鼓動,脈搏 / (ボートの)整調[手] / 〈ボート〉‘の'整調をこぐ / 《副詞[句]を伴って》〈ボール〉‘を'打つ
3. 〈髪・動物など〉‘を'なでる,さする / 〈人〉‘を'なだめる《+名+down, down+名》 / 一なで,一さすり
4. 大脳の,脳の / 頭脳的な,知的な

Wikipedia preview

出典(authority):フリー百科事典『ウィキペディア（Wikipedia）』「2013/02/25 17:11:19」(JST)

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For other uses, see Stroke (disambiguation).

Stroke
Classification and external resources
CT scan slice of the brain showing a right-hemispheric ischemic stroke.
ICD-10	I61-I64ner
ICD-9	434.91
OMIM	601367
DiseasesDB	2247
MedlinePlus	000726
eMedicine	neuro/9 emerg/558 emerg/557 pmr/187
MeSH	D020521

A stroke, or cerebrovascular accident (CVA), is the rapid loss of brain function due to disturbance in the blood supply to the brain. This can be due to ischemia (lack of blood flow) caused by blockage (thrombosis, arterial embolism), or a hemorrhage. As a result, the affected area of the brain cannot function, which might result in an inability to move one or more limbs on one side of the body, inability to understand or formulate speech, or an inability to see one side of the visual field.

A stroke is a medical emergency and can cause permanent neurological damage and death. Risk factors for stroke include old age, high blood pressure, previous stroke or transient ischemic attack (TIA), diabetes, high cholesterol, tobacco smoking and atrial fibrillation. High blood pressure is the most important modifiable risk factor of stroke. It is the second leading cause of death worldwide.

An ischemic stroke is occasionally treated in a hospital with thrombolysis (also known as a "clot buster"), and some hemorrhagic strokes benefit from neurosurgery. Treatment to recover any lost function is termed stroke rehabilitation, ideally in a stroke unit and involving health professions such as speech and language therapy, physical therapy and occupational therapy. Prevention of recurrence may involve the administration of antiplatelet drugs such as aspirin and dipyridamole, control and reduction of high blood pressure, and the use of statins. Selected patients may benefit from carotid endarterectomy and the use of anticoagulants.

Classification

A slice of brain from the autopsy of a person who suffered an acute middle cerebral artery (MCA) stroke

Strokes can be classified into two major categories: ischemic and hemorrhagic. Ischemic strokes are those that are caused by interruption of the blood supply, while hemorrhagic strokes are the ones which result from rupture of a blood vessel or an abnormal vascular structure. About 87% of strokes are caused by ischemia, and the remainder by hemorrhage. Some hemorrhages develop inside areas of ischemia ("hemorrhagic transformation"). It is unknown how many hemorrhages actually start as ischemic stroke.

Ischemic

Main articles: Cerebral infarction and Brain ischemia

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:

1. Thrombosis (obstruction of a blood vessel by a blood clot forming locally)
2. Embolism (obstruction due to an embolus from elsewhere in the body, see below),
3. Systemic hypoperfusion (general decrease in blood supply, e.g., in shock)
4. Venous thrombosis.

Stroke without an obvious explanation is termed "cryptogenic" (of 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 primarily on the initial symptoms; based on the extent of the symptoms, the stroke episode is classified as total anterior circulation infarct (TACI), partial anterior circulation infarct (PACI), lacunar infarct (LACI) or posterior circulation infarct (POCI). These four entities predict the extent of the stroke, the area of the brain affected, the underlying cause, and the prognosis. The TOAST (Trial of Org 10172 in Acute Stroke Treatment) classification is based on clinical symptoms as well as results of further investigations; on this basis, a stroke is classified as being due to (1) thrombosis or embolism due to atherosclerosis of a large artery, (2) embolism of cardiac origin, (3) occlusion of a small blood vessel, (4) other determined cause, (5) undetermined cause (two possible causes, no cause identified, or incomplete investigation).

Hemorrhagic

Main articles: Intracranial hemorrhage and intracerebral hemorrhage

An intraparenchymal bleed (bottom arrow) with surrounding edema (top arrow)

Intracranial hemorrhage is the accumulation of blood anywhere within the skull vault. A distinction is made between intra-axial hemorrhage (blood inside the brain) and extra-axial hemorrhage (blood inside the skull but outside the brain). Intra-axial hemorrhage is due to intraparenchymal hemorrhage or intraventricular hemorrhage (blood in the ventricular system). The main types of extra-axial hemorrhage are epidural hematoma (bleeding between the dura mater and the skull), subdural hematoma (in the subdural space) and subarachnoid hemorrhage (between the arachnoid mater and pia mater). Most of the hemorrhagic stroke syndromes have specific symptoms (e.g., headache, 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 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 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 (i.e., if a person, when asked to raise both arms, involuntarily lets one arm drift downward) and abnormal speech are the findings most likely to lead to the correct identification of a case of stroke increasing the likelihood by 5.5 when at least one of these is present). Similarly, when all three of these are absent, the likelihood of stroke is significantly decreased (– likelihood ratio of 0.39). While these findings are not perfect for diagnosing stroke, the fact that they can be evaluated relatively rapidly and easily make them very valuable in the acute setting.

Proposed systems include FAST (face, arm, speech, and time), as advocated by the Department of Health (United Kingdom) and the Stroke Association, the American Stroke Association, the National Stroke Association (US), the Los Angeles Prehospital Stroke Screen (LAPSS) and the Cincinnati Prehospital Stroke Scale (CPSS). Use of these scales is recommended by professional guidelines.

For people referred to the emergency room, early recognition of stroke is deemed important as this can expedite diagnostic tests and treatments. A scoring system called ROSIER (recognition of stroke in the emergency room) is recommended for this purpose; it is based on features from the medical history and physical examination.

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 (medial lemniscus), symptoms may include:

• hemiplegia and muscle weakness of the face
• numbness
• reduction in sensory or vibratory sensation
• initial flaccidity (hypotonicity), replaced by spasticity (hypertonicity), hyperreflexia, and obligatory synergies.

In most cases, the symptoms affect only one side of the body (unilateral). 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 stroke affecting the brain stem and brain therefore can produce symptoms relating to deficits in these cranial nerves:

• altered smell, taste, hearing, or vision (total or partial)
• drooping of eyelid (ptosis) and weakness of ocular muscles
• decreased reflexes: gag, swallow, pupil reactivity to light
• decreased sensation and muscle weakness of the face
• balance problems and nystagmus
• altered breathing and heart rate
• weakness in sternocleidomastoid muscle with inability to turn head to one side
• weakness in tongue (inability to protrude and/or move from side to side)

If the cerebral cortex is involved, the CNS pathways can again be affected, but also can produce the following symptoms:

• aphasia (difficulty with verbal expression, auditory comprehension, reading and/or writing Broca's or Wernicke's area typically involved)
• dysarthria (motor speech disorder resulting from neurological injury)
• apraxia (altered voluntary movements)
• visual field defect
• memory deficits (involvement of temporal lobe)
• hemineglect (involvement of parietal lobe)
• disorganized thinking, confusion, hypersexual gestures (with involvement of frontal lobe)
• lack of insight of his or her, usually stroke-related, disability

If the cerebellum is involved, the patient may have the following:

• altered walking gait
• altered movement coordination
• vertigo and or disequilibrium

Associated symptoms

Loss of consciousness, headache, and vomiting usually occurs 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

Thrombotic stroke

In thrombotic stroke a thrombus (blood clot) usually forms around atherosclerotic plaques. Since blockage of the artery is gradual, onset of symptomatic thrombotic strokes is slower. A thrombus itself (even if non-occluding) can lead to an embolic stroke (see below) if the thrombus breaks off, at which point it is called an "embolus." Two types of thrombosis can cause stroke:

• 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): atherosclerosis, vasoconstriction (tightening of the artery), aortic, carotid or vertebral artery dissection, various inflammatory diseases of the blood vessel wall (Takayasu arteritis, giant cell arteritis, vasculitis), 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 (in descending incidence): lipohyalinosis (build-up of fatty hyaline matter in the blood vessel as a result of high blood pressure and aging) and fibrinoid degeneration (stroke involving these vessels are known as lacunar infarcts) and microatheroma (small atherosclerotic plaques).

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 killer of people under 20 who suffer from sickle-cell anemia.

Embolic stroke

An embolic stroke refers to the blockage of an artery by an arterial embolus, a travelling 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 (e.g., from bone marrow in a broken bone), air, cancer cells or clumps of bacteria (usually from infectious endocarditis).^{[citation needed]}

Because an embolus arises from elsewhere, local therapy solves the problem only temporarily. Thus, the source of the embolus must be identified. Because the embolic blockage is sudden in onset, symptoms usually are maximal at start. Also, symptoms may be transient as the embolus is partially resorbed and moves to a different location or dissipates altogether.

Emboli most commonly arise from the heart (especially in atrial fibrillation) but may originate from elsewhere in the arterial tree. In paradoxical embolism, a deep vein thrombosis embolises through an atrial or ventricular septal defect in the heart into the brain.^{[citation needed]}

Cardiac causes can be distinguished between high and low-risk:

• High risk: atrial fibrillation and paroxysmal atrial fibrillation, rheumatic disease of the mitral or aortic valve disease, artificial heart valves, known cardiac thrombus of the atrium or ventricle, sick sinus syndrome, sustained atrial flutter, recent myocardial infarction, chronic myocardial infarction together with ejection fraction <28 percent, symptomatic congestive heart failure with ejection fraction <30 percent, dilated cardiomyopathy, Libman-Sacks endocarditis, Marantic endocarditis, infective endocarditis, papillary fibroelastoma, left atrial myxoma and coronary artery bypass graft (CABG) surgery.
• Low risk/potential: calcification of the annulus (ring) of the mitral valve, patent foramen ovale (PFO), atrial septal aneurysm, atrial septal aneurysm with patent foramen ovale, left ventricular aneurysm without thrombus, isolated left atrial "smoke" on echocardiography (no mitral stenosis or atrial fibrillation), complex atheroma in the ascending aorta or proximal arch.

Systemic hypoperfusion

Systemic hypoperfusion is the reduction of blood flow to all parts of the body. 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.^{[citation needed]} Hypoxemia (low blood oxygen content) may precipitate the hypoperfusion. Because the reduction in blood flow is global, all parts of the brain may be affected, especially "watershed" areas - border zone regions supplied by the major cerebral arteries. A watershed stroke refers to the condition when blood supply to these areas is compromised. Blood flow to these areas does not necessarily stop, but instead it may lessen to the point where brain damage can occur.

Venous thrombosis

Cerebral venous sinus thrombosis leads to stroke due to locally increased venous pressure, which exceeds the pressure generated by the arteries. Infarcts are more likely to undergo hemorrhagic transformation (leaking of blood into the damaged area) than other types of ischemic stroke.

Intracerebral hemorrhage

It generally occurs in small arteries or arterioles and is commonly due to hypertension, intracranial vascular malformations (including cavernous angiomas or arteriovenous malformations), cerebral amyloid angiopathy, or infarcts into which secondary haemorrhage has occurred. Other potential causes are trauma, bleeding disorders, amyloid angiopathy, illicit drug use (e.g., amphetamines or cocaine). The hematoma enlarges until pressure from surrounding tissue limits its growth, or until it decompresses by emptying into the ventricular system, CSF or the pial surface. A third of intracerebral bleed is into the brain's ventricles. ICH has a mortality rate of 44 percent after 30 days, higher than ischemic stroke or subarachnoid hemorrhage (which technically may also be classified as a type of stroke).

Silent stroke

A silent stroke is a stroke that does not have any outward symptoms, and the patients are typically unaware they have suffered a stroke. Despite not causing identifiable symptoms, a silent stroke still causes damage to the brain, and places the patient at increased risk for both transient ischemic attack and major stroke in the future. Conversely, those who have suffered 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

Micrograph showing cortical pseudolaminar necrosis, a finding seen in strokes on medical imaging and at autopsy. H&E-LFB stain.

Micrograph of the superficial cerebral cortex showing neuron loss and reactive astrocytes in a person that suffered a stroke. H&E-LFB stain.

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 death of the tissue, i.e., infarction. (This is why fibrinolytics such as alteplase are given only until three hours since the onset of the stroke.) 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 occlude brain blood vessels. Since blood vessels in the brain are now occluded, the brain becomes low in energy, and thus it resorts into using anaerobic metabolism within the region of brain tissue affected by ischemia. Unfortunately, this kind of metabolism produces less adenosine triphosphate (ATP) but releases a by-product called lactic acid. Lactic acid is an irritant which could potentially destroy cells since it is an acid and disrupts the normal acid-base balance in the brain. The ischemia area is referred to as the "ischemic penumbra".

Then, as oxygen or glucose becomes depleted in ischemic brain tissue, the production of high energy phosphate compounds such as adenosine triphosphate (ATP) fails, leading to failure of energy-dependent processes (such as ion pumping) necessary for tissue cell survival. This sets off a series of interrelated events that result in cellular injury and death. A major cause of neuronal injury is release of the excitatory neurotransmitter glutamate. The concentration of glutamate outside the cells of the nervous system is normally kept low by so-called uptake carriers, which are powered by the concentration gradients of ions (mainly Na⁺) across the cell membrane. However, stroke cuts off the supply of oxygen and glucose which powers the ion pumps maintaining these gradients. As a result the transmembrane ion gradients run down, and glutamate transporters reverse their direction, releasing glutamate into the extracellular space. Glutamate acts on receptors in nerve cells (especially NMDA receptors), producing an influx of calcium which activates enzymes that digest the cells' proteins, lipids and nuclear material. Calcium influx can also lead to the failure of mitochondria, which can lead further toward energy depletion and may trigger cell death due to apoptosis.^{[citation needed]}

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 apoptosis cascade by means of redox signaling.^{[citation needed]}

These processes are the same for any type of ischemic tissue and are referred to collectively as the ischemic cascade. However, brain tissue is especially vulnerable to ischemia since it has little respiratory reserve and is completely dependent on aerobic metabolism, unlike most other organs.

In addition to injurious 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.^{[citation needed]}

Hemorrhagic

Hemorrhagic strokes result in tissue injury by causing compression of tissue from an expanding hematoma or hematomas. This can distort and injure tissue. 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.

Diagnosis

A CT showing early signs of a middle cerebral artery stroke with loss of definition of the gyri and grey white boundary

Stroke is diagnosed through several techniques: a neurological examination (such as the NIHSS), CT scans (most often without contrast enhancements) or MRI scans, Doppler ultrasound, and arteriography. The diagnosis of stroke itself is clinical, with assistance from the imaging techniques. Imaging techniques also assist in determining the subtypes and cause of stroke. There is yet no commonly used blood test for the stroke diagnosis itself, though blood tests may be of help in finding out the likely cause of stroke.

Definition

The traditional definition of stroke, devised by the World Health Organization in the 1970s, is a "neurological deficit of cerebrovascular cause that persists beyond 24 hours or is interrupted by death within 24 hours". This definition was supposed to reflect the reversibility of tissue damage and was devised for the purpose, with the time frame of 24 hours being chosen arbitrarily. The 24-hour limit divides stroke from transient ischemic attack, which is a related syndrome of stroke symptoms that resolve completely within 24 hours. With the availability of treatments that, when given early, can reduce stroke severity, many now prefer alternative concepts, such as brain attack and acute ischemic cerebrovascular syndrome (modeled after heart attack and acute coronary syndrome, respectively), that reflect the urgency of stroke symptoms and the need to act swiftly.

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 (without contrast enhancements)

sensitivity= 16%

specificity= 96%

• MRI scan

sensitivity= 83%

specificity= 98%

For diagnosing hemorrhagic stroke in the emergency setting:

• CT scans (without contrast enhancements)

sensitivity= 89%

specificity= 100%

• MRI scan

sensitivity= 81%

specificity= 100%

For detecting chronic hemorrhages, 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

12-lead ECG of a patient with a stroke, showing large deeply inverted T-waves. Various ECG changes may occur in people with strokes and other brain disorders.

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. Commonly used techniques include:

• an ultrasound/doppler study of the carotid arteries (to detect carotid stenosis) or dissection of the precerebral arteries;
• an electrocardiogram (ECG) and echocardiogram (to identify arrhythmias and resultant clots in the heart which may spread to the brain vessels through the bloodstream);
• a Holter monitor study to identify intermittent arrhythmias;
• an angiogram of the cerebral vasculature (if a bleed is thought to have originated from an aneurysm or arteriovenous malformation);
• blood tests to determine hypercholesterolemia, bleeding diathesis and some rarer causes such as homocysteinuria.

Prevention

Given the disease burden of strokes, prevention is an important public health concern. Primary prevention is less effective than secondary prevention (as judged by the number needed to treat to prevent one stroke per year). Recent guidelines detail the evidence for primary prevention in stroke. Because stroke may indicate underlying atherosclerosis, it is important to determine the patient's risk for other cardiovascular diseases such as coronary heart disease. Conversely, aspirin confers some protection against first stroke in people who have had a myocardial infarction or those with a high cardiovascular risk. In those who have previously had a stroke, treatment with medications such as aspirin, clopidogrel and dipyridamole may be given to prevent platelets from aggregating.

Risk factors

The most important modifiable risk factors for stroke are high blood pressure and atrial fibrillation (although magnitude of this effect is small: the evidence from the Medical Research Council trials is that 833 patients have to be treated for 1 year to prevent one stroke). Other modifiable risk factors include high blood cholesterol levels, diabetes, cigarette smoking (active and passive), heavy alcohol consumption 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 (for example via hypertension, atrial fibrillation, rebound thrombocytosis and platelet aggregation and clotting disturbances). The drugs most commonly associated with stroke are cocaine, amphetamines causing hemorrhagic stroke, but also over-the-counter cough and cold drugs containing sympathomimetics.

No high quality studies have shown the effectiveness of interventions aimed at weight reduction, promotion of regular exercise, reducing alcohol consumption or smoking cessation. Nonetheless, given the large body of circumstantial evidence, best medical management for stroke includes advice on diet, exercise, smoking and alcohol use. Medication or drug therapy is the most common method of stroke prevention; carotid endarterectomy can be a useful surgical method of preventing stroke.

Blood pressure

Hypertension (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 should be considered and cost.

Atrial fibrillation

Those with atrial fibrillation have a 5% a year risk of stroke, and this risk is higher in those with valvular atrial fibrillation. Depending on the stroke risk, anticoagulation with medications such as warfarin or aspirin is warranted for stroke prevention.

Blood lipids

High cholesterol levels have been inconsistently associated with (ischemic) stroke. Statins have been shown to reduce the risk of stroke by about 15%. Since earlier meta-analyses of other lipid-lowering drugs did not show a decreased risk, statins might exert their effect through mechanisms other than their lipid-lowering effects.

Diabetes mellitus

Diabetes mellitus increases the risk of stroke by 2 to 3 times. While intensive control of blood sugar has been shown to reduce microvascular complications such as nephropathy and retinopathy it has not been shown to reduce macrovascular complications such as stroke.

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. Low doses of aspirin (for example 75–150 mg) are as effective as high doses but have fewer side effects; the lowest effective dose remains unknown. Thienopyridines (clopidogrel, ticlopidine) "might be slightly more effective" than aspirin and have a decreased risk of gastrointestinal bleeding, but they are more expensive. Their exact role remains controversial. Ticlopidine has more skin rash, diarrhea, neutropenia and thrombotic thrombocytopenic purpura. Dipyridamole can be added to aspirin therapy to provide a small additional benefit, even though headache is a common side effect. Low-dose aspirin is also effective for stroke prevention after sustaining a myocardial infarction. Except for in 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 while increasing the risk of major bleeding. Further studies are needed to investigate a possible protective effect of aspirin against ischemic stroke in women.

Surgery

Carotid endarterectomy or carotid angioplasty can be used to remove atherosclerotic narrowing (stenosis) of the carotid artery. There is evidence supporting this procedure in selected cases. Endarterectomy for a significant stenosis has been shown to be useful in the secondary prevention after a previous stroke. Carotid artery stenting has not been shown to be equally useful. Patients are selected for surgery based on age, gender, degree of stenosis, time since symptoms and patients' preferences. Surgery is most efficient when not delayed too long —the risk of recurrent stroke in a patient who has a 50% or greater stenosis is up to 20% after 5 years, but endarterectomy reduces this risk to around 5%. The number of procedures needed to cure one patient was 5 for early surgery (within two weeks after the initial stroke), but 125 if delayed longer than 12 weeks.

Screening for carotid artery narrowing has not been shown to be a useful screening 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.

Diet

Nutrition, specifically the Mediterranean-style diet, has the potential for decreasing the risk of having a stroke by more than half. It does not appear that lowering levels of homocysteine with folic acid affects the risk of stroke.

Secondary prevention of ischemic stroke

Anticoagulation can prevent recurrent stroke. Among patients with nonvalvular atrial fibrillation, anticoagulation can reduce stroke by 60% while antiplatelet agents can reduce stroke by 20%. However, a recent meta-analysis suggests harm from anti-coagulation started early after an embolic stroke. Stroke prevention treatment for atrial fibrillation is determined according to the CHADS/CHADS2 system. The most widely used anticoagulant to prevent thromboembolic stroke in patients with nonvalvular atrial fibrillation is the oral agent warfarin while dabigatran is a new alternative which does not require prothrombin time monitoring.

If studies show carotid stenosis, and the patient has residual function in the affected side, carotid endarterectomy (surgical removal of the stenosis) may decrease the risk of recurrence if performed rapidly after stroke.

Management

Ischemic stroke

Definitive therapy is aimed at removing the blockage by breaking the clot down (thrombolysis), or by removing it mechanically (thrombectomy). The more rapidly blood flow is restored to the brain, the fewer brain cells die.

Tight control of blood sugars 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.

Thrombolysis

Thrombolysis with recombinant tissue plasminogen activator (rtPA) in acute ischemic stroke, when given before three hours of symptom onset increases the risk of death in the short term but in the long term improves the rate of independence and late mortality; the increase in long term mortality is not significant. When broken down by time to treatment it increases the chance of being alive and living independently by 9% in those treated within three hours, however the benefit for those treated between three and six hours is not significant. These benefits or lack of benefits occurred regardless of the age of the person treated. There is no realiable way to determine who will have an intracranial hemorrhage post treatment versus who will not.

It 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 (such as abnormal lab values, high blood pressure, or recent surgery). 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 hemorrhage as a complication from being given tPA thus part of the reason for increased short term mortality. Additionally, it is the position of the American Academy of Emergency Medicine 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.Intra-arterial 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.

Mechanical thrombectomy

Merci Retriever L5.

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%. A randomized control trial of these procedures has not been done as of 2011.

Hemicraniectomy

Large territory strokes can cause significant edema of the brain with secondary brain injury in surrounding tissue. This phenomenon is mainly encountered in strokes of the middle cerebral artery territory, and is also called "malignant cerebral infaction" 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 neurosurgical evaluation to detect and treat the cause of the bleeding, although many may not need surgery. Anticoagulants and antithrombotics, key in treating ischemic stroke, can make bleeding worse. People are monitored for changes in the level of consciousness, and their blood pressure, blood sugar, and oxygenation are kept at optimum levels.^{[citation needed]}

Stroke unit

Ideally, people who have had a stroke are admitted to a "stroke unit", a ward or dedicated area in 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.

When an acute stroke is suspected by history and physical examination, the goal of early assessment is to determine the cause. Treatment varies according to the underlying cause of the stroke, thromboembolic (ischemic) or hemorrhagic.

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 person. These include nursing staff, physiotherapists, occupational therapists, speech and language therapists, orthotists and usually a physician trained in rehabilitation medicine. Some teams may also include psychologists, social workers, and pharmacists since at least one third of the people manifest 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 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 (PT), occupational therapy (OT) and speech-language pathology (SLP) 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 re-learning 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 constraint-induced 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 (ADLs) such as eating, drinking, dressing, bathing, cooking, reading and writing, and toileting. Speech and language therapy is appropriate for patients with the speech production disorders: dysarthria and apraxia of speech, aphasia, cognitive-communication impairments and/or dysphagia (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 (PEG) tube is passed and this can remain indefinitely.

Treatment of spasticity related to stroke often involves early mobilisations, commonly performed by a physiotherapist, combined with elongation of spastic muscles and sustained stretching through various positioning. Gaining initial improvements in range of motion is often achieved through rhythmic rotational patterns associated with the affected limb. After full range has been achieved by the therapist, the limb should be positioned in the lengthened positions to prevent against further contractures, skin breakdown, and disuse of the limb with the use of splints or other tools to stabilize the joint. Cold in the form of ice wraps or ice packs have been proven to briefly reduce spasticity by temporarily dampening neural firing rates. Electrical stimulation to the antagonist muscles or vibrations has also been used with some success.

Stroke rehabilitation should be started as quickly as possible and can last anywhere from a few days to over a year. Most return of function is seen in the first few months, and then improvement falls off with the "window" considered officially by U.S. state rehabilitation units and others to be closed after six months, with little chance of further improvement. However, patients have been known to continue to improve for years, regaining and strengthening abilities like writing, walking, running, and talking. Daily rehabilitation exercises should continue to be part of the stroke patient's routine. Complete 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.

Some current and future therapy methods include the use of virtual reality and video games for rehabilitation. These forms of rehabilitation offer potential for motivating patients to perform specific therapy tasks that many other forms do not. Many clinics and hospitals are adopting the use of these off-the-shelf devices for exercise, social interaction and rehabilitation because they are affordable, accessible and can be used within the clinic and home.

Other novel non-invasive rehabilitation methods are currently being developed to augment physical therapy to improve motor function of stroke patients, such as transcranial magnetic stimulation (TMS) and transcranial direct-current stimulation (tDCS) and robotic therapies.

Prognosis

Disability affects 75% of stroke survivors enough to decrease their employability. Stroke can affect peoples physically, mentally, emotionally, or a combination of the three. The results of stroke vary widely depending on size and location of the lesion. Dysfunctions correspond to areas in the brain that have been damaged.

Some of the physical disabilities that can result from stroke include muscle weakness, numbness, pressure sores, pneumonia, incontinence, apraxia (inability to perform learned movements), difficulties carrying out daily activities, appetite loss, speech loss, vision loss, and pain. If the stroke is severe enough, or in a certain location such as parts of the brainstem, coma or death can result.

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. Post-stroke emotional difficulties include anxiety, panic attacks, flat affect (failure to express emotions), mania, apathy, and psychosis.

30 to 50% of stroke survivors suffer post stroke depression, which is characterized by lethargy, irritability, sleep disturbances, lowered self esteem, and withdrawal. Depression can reduce motivation and worsen outcome, but can be treated with antidepressants.

Emotional lability, another consequence of stroke, causes the patient 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 patient's actual emotions, a more severe form of emotional lability causes patients to laugh and cry pathologically, without regard to context or emotion. Some patients show the opposite of what they feel, for example crying when they are happy. Emotional lability occurs in about 20% of stroke patients.

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, a patient is unable to attend to anything on the side of space opposite to the damaged hemisphere.

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

Disability-adjusted life year for cerebral vascular disease per 100,000 inhabitants in 2004.

no data   <250   250-425   425-600   600-775   775-950   950-1125

1125-1300   1300-1475   1475-1650   1650-1825   1825-2000   >2000

Stroke was the second most common cause of death worldwide in 2004, resulting in 5.7 million deaths (~10% of the total). Approximately 9 million people had a stroke in 2008 and 30 million people have previously had a stroke and are 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 incidence of stroke increases exponentially from 30 years of age, and etiology 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 two-thirds of strokes occur in those over the age of 65. A person's risk of dying if he or she does have a stroke also increases with age. However, stroke can occur at any age, including in childhood.

Family members may have a genetic tendency for stroke or share a lifestyle that contributes to stroke. Higher levels of Von Willebrand factor are more common amongst people who have had ischemic stroke for the first time. 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, yet 60% of deaths from stroke occur in women. Since women live longer, they are older on average when they have their strokes and thus more often killed (NIMH 2002). Some risk factors for stroke apply only to women. Primary among these are pregnancy, childbirth, menopause and the treatment thereof (HRT).

History

Hippocrates first described the sudden paralysis that is often associated with stroke.

Episodes of stroke and familial stroke have been reported from the 2nd millennium BC onward in ancient Mesopotamia and Persia. Hippocrates (460 to 370 BC) 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 (1620–1695) identified the cause of hemorrhagic stroke when he suggested that people who had died of apoplexy had bleeding in their brains. Wepfer also identified the main arteries supplying the brain, the vertebral and carotid arteries, and identified the cause of ischemic stroke [also known as cerebral infarction] when he suggested that apoplexy might be caused by a blockage to those vessels.

Rudolf Virchow first described the mechanism of thromboembolism as a major factor.

Research

Angioplasty and stenting

Angioplasty and stenting have begun to be looked at as possible viable options in treatment of acute ischemic stroke. Intra-cranial stenting in symptomatic intracranial arterial stenosis, the rate of technical success (reduction to stenosis of <50%) ranged from 90-98%, and the rate of major peri-procedural complications ranged from 4-10%. The rates of restenosis and/or 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.

Neuroprotection

Brain tissue survival can be improved to some extent if one or more of these processes is inhibited. Drugs that scavenge reactive oxygen species, inhibit apoptosis, or inhibit excitatory neurotransmitters, for example, have been shown experimentally to reduce tissue injury caused by ischemia. Agents that work in this way are referred to as being neuroprotective. Until recently, human clinical trials with neuroprotective agents have failed, with the probable exception of deep barbiturate coma. However, more recently NXY-059, the disulfonyl derivative of the radical-scavengin phenylbutylnitrone, is reported to be neuroprotective in stroke. This agent appears to work at the level of the blood vessel lining or endothelium. Unfortunately, after producing favorable results in one large-scale clinical trial, a second trial failed to show favorable results. Benefit of NXY-059 is questionable.

References

Further reading

• J. P. Mohr, Dennis Choi, James Grotta, Philip Wolf (2004). Stroke: Pathophysiology, Diagnosis, and Management. New York: Churchill Livingstone. ISBN 0-443-06600-0. OCLC 52990861 50477349 52990861.
• Charles P. Warlow, Jan van Gijn, Martin S. Dennis, Joanna M. Wardlaw, John M. Bamford, Graeme J. Hankey, Peter A. G. Sandercock, Gabriel Rinkel, Peter Langhorne, Cathie Sudlow, Peter Rothwell (2008). Stroke: Practical Management (3rd ed.). Wiley-Blackwell. ISBN 1-4051-2766-X.

External links

• Stroke at the Open Directory Project

UpToDate Contents

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• 1. 急性脳卒中の初期評価およびマネージメント initial assessment and management of acute stroke
• 2. 脳卒中サブタイプの臨床診断 clinical diagnosis of stroke subtypes
• 3. 成人における脳卒中の予後 stroke prognosis in adults
• 4. 脳卒中評価の概要 overview of the evaluation of stroke
• 5. 脳卒中の病因および分類 etiology and classification of stroke

English Journal

• Effects of moderate-intensity aerobic cycling and swim exercise on post-exertional blood pressure in healthy young untrained and triathlon-trained men and women.

• Lakin R, Notarius C, Thomas S, Goodman J.Source*Department of Exercise Sciences, University of Toronto, Toronto, Canada.
• Clinical science (London, England : 1979).Clin Sci (Lond).2013 Dec 1;125(12):543-53. doi: 10.1042/CS20120508.
• Aerobic exercises such as running, walking and cycling are known to elicit a PEH (post-exercise hypotensive) response in both trained and UT (untrained) subjects. However, it is not known whether swim exercise produces a similar effect in normotensive individuals. The complex acute physiological res
• PMID 23763298

• Effects of Fuel Temperature on Injection Process and Combustion of Dimethyl Ether Engine.

• Guangxin G, Zhulin Y, Apeng Z, Shenghua L, Yanju W.SourceXi'an Jiaotong University , No. 28, Xianning Road , Xi'an, 710049 , P.R. China.
• Journal of energy resources technology.J Energy Resour Technol.2013 Dec;135(4):422021-422025. Epub 2013 May 31.
• To investigate the effects of fuel temperature on the injection process in the fuel-injection pipe and the combustion characteristics of compression ignition (CI) engine, tests on a four stroke, direct injection dimethyl ether (DME) engine were conducted. Experimental results show that as the fuel t
• PMID 23918238

• Polymorphisms in migraine-associated gene, atp1a2, and ischemic stroke risk in a biracial population: the genetics of early onset stroke study.

• Harriott AM, Dueker N, Cheng YC, Ryan KA, O'Connell JR, Stine OC, McArdle PF, Wozniak MA, Stern BJ, Mitchell BD, Kittner SJ, Cole JW.SourceSchool of Medicine, University of Maryland, Baltimore, 655 W. Baltimore St, Baltimore, MD 21201 USA.
• SpringerPlus.Springerplus.2013 Dec;2(1):46. Epub 2013 Feb 11.
• In a recent meta-analysis migraine was associated with a two-fold increase in stroke risk. While the mechanism driving this association is unknown, one intriguing hypothesis is that migraineurs are genetically predisposed to developing ischemic stroke. Mutations in the ATP1A2 gene are implicated in
• PMID 23459313

Japanese Journal

• Impact of polyvascular disease on clinical outcomes in patients undergoing coronary revascularization: An observation from the CREDO-Kyoto Registry Cohort-2.

• Morikami Yuko,Natsuaki Masahiro,Morimoto Takeshi,Ono Koh,Nakagawa Yoshihisa,Furukawa Yutaka,Sakata Ryuzo,Aota Masaki,Okada Yukikatsu,Onoe Masahiko,Kawasuji Michio,Koshiji Takaaki,Nakajima Hiroyuki,Nishizawa Junichiro,Yamanaka Kazuo,Yamamoto Hiroyuki,Kimura Takeshi
• Atherosclerosis 228(2), 426-431, 2013-06-00
• … [Objective]Patients with coronary artery disease (CAD) often have prior stroke or concomitant extra-cardiac vascular disease (EVD) such as cerebral, aortic, or peripheral vascular disease. …
• NAID 120005293576

• 内科的治療を受ける高齢脳梗塞患者のせん妄状態出現に関連する入院初日の因子と入院3日間のせん妄状態の変化に影響する因子

• 菅原 峰子
• 老年看護学 : 日本老年看護学会誌 17(2), 28-37, 2013-03-20
• 目的:高齢脳梗塞患者におけるせん妄状態出現と入院初日の因子の関連および3日間のせん妄状態の変化への影響を明らかにした.方法:対象者は5医療施設で脳梗塞の内科的治療を受ける65歳以上の患者50人であった.選定条件は,脳梗塞症状出現後1週間以内に入院し,入院時の意識レベルが清明からJapan Coma Scale I-3の範囲で,失語症がなく,情報提供に同意した者である.せん妄の評価には日本語版NEE …
• NAID 110009594835

• ワルファリン内服中の頭蓋内出血症例に対する第Ⅸ因子複合体投与の経験

• 田村 洋行,岡島 真里,山岸 利暢,八坂 剛一,坪井 謙,藤原 俊文
• 自治医科大学紀要 = Jichi Medical University Journal 35, 71-75, 2013-03-00
• … 来院時modified NIH Stroke Scale（NIHSS）は中央値12（0-40）であった。 … In one patient with cerebral subcortical hemorrhage, a hematoma enlarged after administration, and 3 patients with non-traumatic hemorrhage died（ 17.6%）. … The median NIH Stroke Scale（ NIHSS） result was 12（ 0-40）. …
• NAID 120005295167

Related Links

• www.jstage.jst.go.jp

詳細の表示を試みましたが、サイトのオーナーによって制限されているため表示できません。

• Stroke

Good Outcome Rate of 35% in IV-tPA–Treated Patients With Computed Tomography Angiography Confirmed Severe Anterior Circulation Occlusive Stroke

• Cerebral Stroke - EzineArticles Submission - Submit Your ...

Every year around 1 % of people within the age group of 60 years to 65 years suffer from Paralysis because of Cerebral stroke. Below the age of 40 years occurrence of Cerebral stroke is negligible. Every year around 1 % ...

Related Pictures

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★リンクテーブル★

リンク元	「脳卒中」「apoplexy」「acute stroke」「apoplexia cerebri」「脳卒中発作」
関連記事	「cerebral」「stroke」

「脳卒中」

　　[★]

英

cerebral stroke, cerebral apoplexy,stroke

ラ

apoplexia cerebri

関

卒中、脳血管障害 cerebrovascular disorders, cerebrovascular diseases

概念

• 突発的に出現する精神症状・神経症状であり、脳血管の病的状態に起因するもの
• 脳梗塞(血栓症、塞栓症)
• 脳出血(実質内の出血)、クモ膜下出血

疫学

参考1

• 死因：第3位
• 全国の寝たきり患者の原因疾患の第1位
• 病型別頻度：()

• 一過性脳虚血発作：5.8％
• アテローム血栓性梗塞：24.1％
• ラクナ梗塞：22.7％
• 心原性脳塞栓症：19.2％
• その他の脳梗塞：5.1％
• 高血圧性脳出血：13.7％
• 脳出血(その他)：3.0％
• クモ膜下出血：6.4％

• 厚労省の患者調査 傷病分類はこれ　→　[[1]]

リスク因子

参考1

• 最大のリスク因子は高血圧
• 年齢、男性、高血圧、糖尿病、脂質異常症、喫煙、心房細動、大量飲酒

参考

• 1. 脳卒中治療ガイドライン2009

http://www.jsts.gr.jp/jss08.html

-stroke

「apoplexy」

　　[★]

• n.

• (医)卒中、卒中発作

関

acute stroke、apoplectic、apoplectic stroke、apoplexia、apoplexia cerebri、cerebral apoplexy、cerebral stroke、cerebrovascular accident、cerebrovascular stroke、CVA、extravasation、stroke

同

apoplexia

　

「acute stroke」

　　[★]

脳卒中急性期、急性脳卒中

関

apoplexy、cerebral stroke、cerebrovascular accident、cerebrovascular stroke、CVA、stroke

「apoplexia cerebri」

　　[★]

脳卒中

関

apoplexy、cerebral apoplexy、cerebral stroke、stroke

「脳卒中発作」

　　[★]

英

cerebral stroke

関

脳卒中

「cerebral」

　　[★]

• adj.

• 大脳の、大脳性の、脳性の、脳の

関

brain、cerebri、cerebro、cerebrum、encephalic、encephalo、encephalon

　 　 　

「stroke」

　　[★] 脳卒中