脳卒中　　　　　　　　　　　　　　　

WordNet

treat gingerly or carefully; "You have to stroke the boss"
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
(golf) the unit of scoring in golf is the act of hitting the ball with a club; "Nicklaus won by three strokes"
(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
a light touch with the hands (同)stroking
a single complete movement
any one of the repeated movements of the limbs and body used for locomotion in swimming or rowing
a light touch
a mark made on a surface by a pen, pencil, or paintbrush; "she applied the paint in careful strokes"
the oarsman nearest the stern of the shell who sets the pace for the rest of the crew
row at a particular rate
strike a ball with a smooth blow
touch lightly and repeatedly, as with brushing motions; "He stroked his long beard"
the act of attacking; "attacks on women increased last year"; "they made an attempt on his life" (同)attempt
(military) an offensive against an enemy (using weapons); "the attack began at dawn" (同)onslaught, onset, onrush
a decisive manner of beginning a musical tone or phrase (同)tone-beginning
an offensive move in a sport or game; "they won the game with a 10-hit attack in the 9th inning"
strong criticism; "he published an unexpected attack on my work"
a sudden occurrence of an uncontrollable condition; "an attack of diarrhea"
begin to injure; "The cancer cells are attacking his liver"; "Rust is attacking the metal"
set to work upon; turn ones energies vigorously to a task; "I attacked the problem as soon as I got out of bed"
the onset of a corrosive or destructive process (as by a chemical agent); "the film was sensitive to attack by acids"; "open to attack by the elements"
attack in speech or writing; "The editors of the left-leaning paper attacked the new House Speaker" (同)round, assail, lash out, snipe, assault
take the initiative and go on the offensive; "The Serbs attacked the village at night"; "The visiting team started to attack" (同)aggress
launch an attack or assault on; begin hostilities or start warfare with; "Hitler attacked Poland on September 1, 1939 and started World War II"; "Serbian forces assailed Bosnian towns all week" (同)assail
learn or discover with certainty
a deliberately offensive act or something producing the effect of deliberate disrespect; "turning his back on me was a deliberate insult" (同)affront
a swimming stroke in which the arms move forward and backward while the legs do a scissors kick
a method of moving the arms and legs to push against the water and propel the swimmer forward
the act of hitting a tennis ball with a tennis racket (同)tennis shot

PrepTutorEJDIC

(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
〈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
…'を'『襲う』,『攻撃する』;(ゲームで)…'を'攻める / (演説・文書などで)…'を'『非難する』,攻撃する / 〈病気・不運などが〉…'を'襲う,冒す / 〈仕事など〉‘に'勢いよく取りかかる,着手する / 『攻撃をする』 / 〈U〉〈C〉(…に対する)『攻撃』;(ゲームの)攻め;非難《+『on』(『upon, against』)+『名』》 / 〈C〉発病,発作 / 〈U〉(仕事への)着手,開始
〈事実など〉'を'『確かめる』,つきとめる
〈人・物など〉‘を'『侮辱する』,はずかしめる / (…に対する)『侮辱』,侮辱的な言動《+『to』+『名』》
横泳ぎ

Wikipedia preview

出典(authority):フリー百科事典『ウィキペディア（Wikipedia）』「2015/09/25 22:31:28」(JST)

Stroke, also known as cerebrovascular accident (CVA), cerebrovascular insult (CVI), or brain attack, is when poor blood flow to the brain results in cell death. There are two main types of stroke: ischemic, due to lack of blood flow, and hemorrhagic due to bleeding. They result in part of the brain not functioning properly.^[1] Signs and symptoms of a stroke may include an inability to move or feel on one side of the body, problems understanding or speaking, feeling like the world is spinning, or loss of vision to one side among others.^[2]^[3] Signs and symptoms often appear soon after the stroke has occurred. If symptoms last less than one or two hours it is known as a transient ischemic attack (TIA).^[3] Hemorrhagic strokes may also be associated with a severe headache.^[3] The symptoms of a stroke can be permanent.^[1] Long term complications may include pneumonia or loss of bladder control.^[3]

The main risk factor for stroke is high blood pressure.^[4] Other risk factors include tobacco smoking, obesity, high blood cholesterol, diabetes mellitus, previous TIA, and atrial fibrillation among others.^[2]^[4] An ischemic stroke is typically caused by blockage of a blood vessel.^[5] A hemorrhagic stroke is caused by bleeding either directly into the brain or into the space surrounding the brain.^[5]^[6] Bleeding may occur due to a brain aneurysm.^[5] Diagnosis is typically with medical imaging such as a CT scan or MRI scan along with a physical exam. Other tests such as an electrocardiogram (ECG) and blood tests are done to determine risk factors and rule out other possible causes. Low blood sugar may cause similar symptoms.^[7]

Prevention includes decreasing risk factors as well as possibly aspirin, statins, surgery to open up the arteries to the brain in those with problematic narrowing, and warfarin in those with atrial fibrillation.^[2] A stroke often requires emergency care.^[1] An ischemic stroke, if detected within three to four and half hours, may be treatable with a medication that can break down the clot. Aspirin should be used. Some hemorrhagic strokes benefit from surgery. Treatment to try recover lost function is called stroke rehabilitation and ideally takes place in a stroke unit; however, these are not available in much of the world.^[2]

In 2010 approximately 17 million people had a stroke and 33 million people had previously had a stroke and were still alive. Between 1990 and 2010 the number of strokes which occurred each year decreased by approximately 10% in the developed world and increased by 10% in the developing world.^[8] In 2013, stroke was the second most frequent cause of death after coronary artery disease, accounting for 6.4 million deaths (12% of the total).^[9] About 3.3 million deaths resulted from ischemic stroke while 3.2 million deaths resulted from hemorrhagic stroke.^[9] About half of people who have had a stroke live less than one year.^[2] Overall, two thirds of strokes occurred in those over 65 years old.^[8]

1 Classification
- 1.1 Definition
- 1.2 Ischemic
- 1.3 Hemorrhagic
2 Signs and symptoms
- 2.1 Early recognition
- 2.2 Subtypes
- 2.3 Associated symptoms
3 Causes
- 3.1 Thrombotic stroke
- 3.2 Embolic stroke
- 3.3 Cerebral hypoperfusion
- 3.4 Venous thrombosis
- 3.5 Intracerebral hemorrhage
- 3.6 Silent stroke
4 Pathophysiology
- 4.1 Ischemic
- 4.2 Hemorrhagic
5 Diagnosis
- 5.1 Physical examination
- 5.2 Imaging
- 5.3 Underlying cause
6 Prevention
- 6.1 Risk factors
  - 6.1.1 Blood pressure
  - 6.1.2 Blood lipids
  - 6.1.3 Diabetes mellitus
  - 6.1.4 Anticoagulation drugs
  - 6.1.5 Surgery
  - 6.1.6 Diet
- 6.2 Women
- 6.3 Previous stroke or TIA
7 Management
- 7.1 Ischemic stroke
  - 7.1.1 Thrombolysis
  - 7.1.2 Surgery
- 7.2 Hemorrhagic stroke
- 7.3 Stroke unit
- 7.4 Rehabilitation
8 Prognosis
9 Epidemiology
10 History
11 Research
- 11.1 Angioplasty and stenting
- 11.2 Mechanical thrombectomy
- 11.3 Neuroprotection
12 See also
13 References
14 Further reading
15 External links

Classification

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

Strokes can be classified into two major categories: ischemic and hemorrhagic.^[10] Ischemic strokes are caused by interruption of the blood supply to the brain, while hemorrhagic strokes result from the rupture of a blood vessel or an abnormal vascular structure. About 87% of strokes are ischemic, the rest being hemorrhagic. Bleeding can develop inside areas of ischemia, a condition known as "hemorrhagic transformation." It is unknown how many hemorrhagic strokes actually start as ischemic strokes.^[2]

Definition

In the 1970s the World Health Organization defined stroke as a "neurological deficit of cerebrovascular cause that persists beyond 24 hours or is interrupted by death within 24 hours",^[11] although the word "stroke" is centuries old. This definition was supposed to reflect the reversibility of tissue damage and was devised for the purpose, with the time frame of 24 hours being chosen arbitrarily. The 24-hour limit divides stroke from transient ischemic attack, which is a related syndrome of stroke symptoms that resolve completely within 24 hours.^[2] With the availability of treatments which can reduce stroke severity when given early, many now prefer alternative terminology, such as brain attack and acute ischemic cerebrovascular syndrome (modeled after heart attack and acute coronary syndrome, respectively), to reflect the urgency of stroke symptoms and the need to act swiftly.^[12]

Ischemic

In an ischemic stroke, blood supply to part of the brain is decreased, leading to dysfunction of the brain tissue in that area. There are four reasons why this might happen:

Thrombosis (obstruction of a blood vessel by a blood clot forming locally)
Embolism (obstruction due to an embolus from elsewhere in the body, see below),^[2]
Systemic hypoperfusion (general decrease in blood supply, e.g., in shock)^[13]
Venous thrombosis.^[14]

Stroke without an obvious explanation is termed "cryptogenic" (of unknown origin); this constitutes 30-40% of all ischemic strokes.^[2]^[15]

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 that is affected, the underlying cause, and the prognosis.^[16]^[17] 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) an embolism originating in the heart, (3) complete blockage of a small blood vessel, (4) other determined cause, (5) undetermined cause (two possible causes, no cause identified, or incomplete investigation).^[18] Users of stimulant drugs such as cocaine and methamphetamine are at a high risk for ischemic strokes.^[19]

Hemorrhagic

CT scan of an intraparenchymal bleed (bottom arrow) with surrounding edema (top arrow)

An intracranial hemorrhage is the accumulation of blood anywhere within the cranial vault. The main types of intracranial 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).

A cerebral hemorrhage is bleeding within the brain tissue. A cerebral hemorrhage can be due to either intraparenchymal hemorrhage or intraventricular hemorrhage (blood in the ventricular system). Most of the hemorrhagic stroke syndromes have specific symptoms particularly headaches, or have evidence of a previous head injury).

Signs and symptoms

Stroke symptoms typically start suddenly, over seconds to minutes, and in most cases do not progress further. The symptoms depend on the area of the brain affected. The more extensive the area of 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).^[20] 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),^[21] 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)^[22] and the Cincinnati Prehospital Stroke Scale (CPSS).^[23] Use of these scales is recommended by professional guidelines.^[24]

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.^[24]^[25]

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 (reduced muscle tone), replaced by spasticity (increased muscle tone), excessive reflexes, and obligatory synergies.^[26]

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 brainstem 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 stick out the tongue and/or move it 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

Illustration of an embolic stroke, showing a blockage lodged in a blood vessel.

In thrombotic stroke a thrombus^[27] (blood clot) usually forms around atherosclerotic plaques. Since blockage of the artery is gradual, onset of symptomatic thrombotic strokes is slower than that of a hemorrhagic stroke. A thrombus itself (even if it does not completely block the blood vessel) can lead to an embolic stroke (see below) if the thrombus breaks off and travels in the bloodstream, at which point it is called an embolus. Two types of thrombosis can cause stroke:

Large vessel disease involves the common and internal carotid arteries, the vertebral artery, and the Circle of Willis.^[28] 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.^[29] 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 (a stroke involving these vessels are known as a lacunar stroke) and microatheroma (small atherosclerotic plaques).^[30]

Sickle-cell anemia, which can cause blood cells to clump up and block blood vessels, can also lead to stroke. A stroke is the second leading cause of death in people under 20 with sickle-cell anemia.^[31] Air pollution may also increase stroke risk.^[32]

Embolic stroke

An embolic stroke refers to an arterial embolism (a blockage of an artery) by an embolus, a traveling particle or debris in the arterial bloodstream originating from elsewhere. An embolus is most frequently a thrombus, but it can also be a number of other substances including fat (e.g., from bone marrow in a broken bone), air, cancer cells or clumps of bacteria (usually from infectious endocarditis).^[33]

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 embolizes through an atrial or ventricular septal defect in the heart into the brain.^[33]

Causes of stroke related to the heart can be distinguished between high and low-risk:^[34]

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.

Cerebral hypoperfusion

Cerebral 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 vulnerable "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.^[14]

Intracerebral hemorrhage

It generally occurs in small arteries or arterioles and is commonly due to hypertension,^[35] intracranial vascular malformations (including cavernous angiomas or arteriovenous malformations), cerebral amyloid angiopathy, or infarcts into which secondary hemorrhage has occurred.^[2] 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^[2]).

Silent stroke

A silent stroke is a stroke that does not have any outward symptoms, and the patients are typically unaware they have had a stroke. Despite not causing identifiable symptoms, a silent stroke still damages the brain, and places the patient at increased risk for both transient ischemic attack and major stroke in the future. Conversely, those who have had a major stroke are also at risk of having silent strokes.^[36] 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.^[37]^[38] The risk of silent stroke increases with age, but may also affect younger adults and children, especially those with acute anemia.^[37]^[39]

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 has had 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.^[40] 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.^[41] Embolic infarction occurs when emboli formed elsewhere in the circulatory system, typically in the heart as a consequence of atrial fibrillation, or in the carotid arteries, break off, enter the cerebral circulation, then lodge in and block brain blood vessels. Since blood vessels in the brain are now blocked, the brain becomes low in energy, and thus it resorts into using anaerobic metabolism within the region of brain tissue affected by ischemia. Anaerobic metabolism produces less adenosine triphosphate (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".^[42]

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 programmed cell death.^[43]

Ischemia also induces production of oxygen free radicals and other reactive oxygen species. These react with and damage a number of cellular and extracellular elements. Damage to the blood vessel lining or endothelium is particularly important. In fact, many antioxidant neuroprotectants such as uric acid and NXY-059 work at the level of the endothelium and not in the brain per se. Free radicals also directly initiate elements of the programmed cell death cascade by means of redox signaling.^[44]

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 damaging effects on brain cells, ischemia and infarction can result in loss of structural integrity of brain tissue and blood vessels, partly through the release of matrix metalloproteases, which are zinc- and calcium-dependent enzymes that break down collagen, hyaluronic acid, and other elements of connective tissue. Other proteases also contribute to this process. The loss of vascular structural integrity results in a breakdown of the protective blood brain barrier that contributes to cerebral edema, which can cause secondary progression of the brain injury.^{[citation needed]}

Hemorrhagic

Bleeding within the skull cavity can occur from various causes. Subdural and epidural bleeding mostly are the result of trauma.^[45] Hemorrhagic strokes arise from bleeding within the brain parenchyma or intraventricular spaces, and are classified based on their underlying pathology. Some examples of hemorrhagic stroke are hypertensive hemorrhage, ruptured aneurysm, ruptured AV fistula, transformation of prior ischemic infarction, and drug induced bleeding.^[46] They 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.^[31]^[47] Inflammation contributes to the secondary brain injury after hemorrhage.^[47]

Diagnosis

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

Dens media sign in a patient with middle cerebral artery infarction shown on the left. Right image after 7 hours.

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.^[48]

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:^[49]

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.^[50]

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. The following are commonly used techniques:

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 abnormal heart rhythms;
an angiogram of the cerebral vasculature (if a bleed is thought to have originated from an aneurysm or arteriovenous malformation);
blood tests to determine if blood cholesterol is high, if there is an abnormal tendency to bleed, and if some rarer processes such as homocysteinuria might be involved.

Prevention

Given the disease burden of strokes, prevention is an important public health concern.^[51] Primary prevention is less effective than secondary prevention (as judged by the number needed to treat to prevent one stroke per year).^[51] Recent guidelines detail the evidence for primary prevention in stroke.^[52] In those who are otherwise healthy, aspirin does not appear beneficial and thus is not recommended.^[53] In people who have had a myocardial infarction or those with a high cardiovascular risk, it provides some protection against a first stroke.^[54]^[55] In those who have previously had a stroke, treatment with medications such as aspirin, clopidogrel and dipyridamole may be beneficial.^[54] The U.S. Preventive Services Task Force (USPSTF) recommends against screening for carotid artery stenosis in those without symptoms.^[56]

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^[57]^[58]). Other modifiable risk factors include high blood cholesterol levels, diabetes mellitus, cigarette smoking^[59]^[60] (active and passive), heavy alcohol consumption^[61] and drug use,^[62] lack of physical activity, obesity, processed red meat consumption^[63] and unhealthy diet.^[64] 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).^[65] Drugs, most commonly amphetamines and cocaine, can induce stroke through damage to the blood vessels in the brain and/or acute hypertension.^[66]^[67]

No high-quality studies have shown the effectiveness of interventions aimed at weight reduction, promotion of regular exercise, reducing alcohol consumption or smoking cessation.^[68] Nonetheless, given the large body of circumstantial evidence, best medical management for stroke includes advice on diet, exercise, smoking and alcohol use.^[69] 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.^[70] Blood pressure reduction of 10 mmHg systolic or 5 mmHg diastolic reduces the risk of stroke by ~40%.^[71] Lowering blood pressure has been conclusively shown to prevent both ischemic and hemorrhagic strokes.^[72]^[73] It is equally important in secondary prevention.^[74] Even patients older than 80 years and those with isolated systolic hypertension benefit from antihypertensive therapy.^[75]^[76]^[77] The available evidence does not show large differences in stroke prevention between antihypertensive drugs —therefore, other factors such as protection against other forms of cardiovascular disease and cost should be considered.^[78]^[79] The routine use of beta-blockers following a stroke or TIA has not been shown to result in benefits.^[80]

Blood lipids

High cholesterol levels have been inconsistently associated with (ischemic) stroke.^[73]^[81] Statins have been shown to reduce the risk of stroke by about 15%.^[82] Since earlier meta-analyses of other lipid-lowering drugs did not show a decreased risk,^[83] statins might exert their effect through mechanisms other than their lipid-lowering effects.^[82]

Diabetes mellitus

Diabetes mellitus increases the risk of stroke by 2 to 3 times. While intensive blood sugar control has been shown to reduce small blood vessel complications such as kidney damage and damage to the retina of the eye it has not been shown to reduce large blood vessel complications such as stroke.^[84]^[85]

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.^[54] 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.^[86] Thienopyridines (clopidogrel, ticlopidine) "might be slightly more effective" than aspirin and have a decreased risk of gastrointestinal bleeding, but are more expensive.^[87]^{[needs update]} Their exact role remains controversial. Ticlopidine is associated with higher rates of skin rash, diarrhea, low blood neutrophil count and thrombotic thrombocytopenic purpura.^[87] Dipyridamole can be added to aspirin therapy to provide a small additional benefit, even though headache is a common side effect.^[88] Low-dose aspirin is also effective for stroke prevention after having a myocardial infarction.^[55]

Those with atrial fibrillation have a 5% a year risk of stroke, and this risk is higher in those with valvular atrial fibrillation.^[89] Depending on the stroke risk, anticoagulation with medications such as warfarin or aspirin is useful for prevention.^[90] Except in people with atrial fibrillation, oral anticoagulants are not advised for stroke prevention —any benefit is offset by bleeding risk.^[91]

In primary prevention however, antiplatelet drugs did not reduce the risk of ischemic stroke but increased the risk of major bleeding.^[92]^[93] Further studies are needed to investigate a possible protective effect of aspirin against ischemic stroke in women.^[94]^[95]

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.^[69] Endarterectomy for a significant stenosis has been shown to be useful in the prevention of further strokes in those who have already had one.^[96] Carotid artery stenting has not been shown to be equally useful.^[97]^[98]^{[needs update]} Patients are selected for surgery based on age, gender, degree of stenosis, time since symptoms and patients' preferences.^[69] 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.^[99]^[100]

Screening for carotid artery narrowing has not been shown to be a useful screening test in the general population.^[101] Studies of surgical intervention for carotid artery stenosis without symptoms have shown only a small decrease in the risk of stroke.^[102]^[103] 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.^[69]

Diet

Nutrition, specifically the Mediterranean-style diet, has the potential for decreasing the risk of having a stroke by more than half.^[104] It does not appear that lowering levels of homocysteine with folic acid affects the risk of stroke.^[105]^[106]

Women

A number of specific recommendations have been made for women including taking aspirin after the 11th week of pregnancy if there is a history of previous chronic high blood pressure and taking blood pressure medications during pregnancy if the blood pressure is greater than 150 mmHg systolic or greater than 100 mmHg diastolic. In those who have previously had preeclampsia other risk factors should be treated more aggressively.^[107]

Previous stroke or TIA

Keeping blood pressure below 140/90 mmHg is recommended.^[108] Anticoagulation can prevent recurrent ischemic strokes. Among people with nonvalvular atrial fibrillation, anticoagulation can reduce stroke by 60% while antiplatelet agents can reduce stroke by 20%.^[109] However, a recent meta-analysis suggests harm from anti-coagulation started early after an embolic stroke.^[110] 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 a number of newer agents including dabigatran are alternatives which do not require prothrombin time monitoring.^[108]

Anticoagulants, when used following stroke, should not be stopped for dental procedures.^[111]

If studies show carotid stenosis, and the person 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 philosophical premise underlying the importance of rapid stroke intervention was summed up as Time is Brain! in the early 1990s.^[112] Years later, that same idea, that rapid cerebral blood flow restoration results in fewer brain cells dying, has been proved and quantified.^[113]

Tight blood sugar control in the first few hours does not improve outcomes and may cause harm.^[114]^{[needs update]} High blood pressure is also not typically lowered as this has not been found to be helpful.^[115]^[116]

Thrombolysis

Thrombolysis, such as with recombinant tissue plasminogen activator (rtPA), in acute ischemic stroke, when given within three hours of symptom onset results in an overall benefit of 10% with respect to living without disability.^[117]^[118] It does not, however, improve chances of survival.^[117] Benefit is greater the earlier it is used.^[119] Between three and four and a half hours the effects are less clear.^[120]^[121]^[122] A 2014 review found a 5% increase in the number of people living without disability at three to six months; however, there was a 2% increased risk of death in the short term.^[118] After four and a half hours thrombolysis worsens outcomes.^[120] These benefits or lack of benefits occurred regardless of the age of the person treated.^[123] There is no reliable way to determine who will have an intracranial hemorrhage post treatment versus who will not.^[124]

Its use is endorsed by the American Heart Association and the American Academy of Neurology as the recommended treatment for acute stroke within three hours of onset of symptoms as long as there are not other contraindications (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^[125] 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.^[126]^{[needs update]} 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.^[127] Additionally, the American Academy of Emergency Medicine states that objective evidence regarding the efficacy, safety, and applicability of tPA for acute ischemic stroke is insufficient to warrant its classification as standard of care.^[128] 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.^[129]

Surgery

Thrombectomy may improve outcomes if done early in those with an anterior circulation large artery clot.^[130]

Large territory strokes can cause significant brain swelling 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 infarction" because it carries a dismal prognosis. Relief of the pressure may be attempted with medication, but some require hemicraniectomy, the temporary surgical removal of the skull on one side of the head. This decreases the risk of death, although some more people survive with disability who would otherwise have died.^[131]

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.^[2]^[132]

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 patient. These include physicians trained in rehabilitation medicine, clinical pharmacists, nursing staff, physiotherapists, occupational therapists, speech and language therapists, and orthotists. Some teams may also include psychologists and social workers, since at least 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.^[133] 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.^[134] 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^[135] and apraxia of speech,^[136] aphasia,^[137]^{[needs update]} 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 mobilizations, commonly performed by a physiotherapist, combined with elongation of spastic muscles and sustained stretching through various positionings.^[26] Gaining initial improvement in range of motion is often achieved through rhythmic rotational patterns associated with the affected limb.^[26] 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.^[26] Cold in the form of ice wraps or ice packs have been proven to briefly reduce spasticity by temporarily dampening neural firing rates.^[26] Electrical stimulation to the antagonist muscles or vibrations has also been used with some success.^[26]

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.^[138] 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.^[138]

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)^[139] and robotic therapies.^[140]

A stroke can also reduce people's general fitness.^[141]^{[needs update]} Reduced fitness can reduce capacity for rehabilitation as well as general health.^[142] A systematic review found that there are inadequate long-term data about the effects of exercise and training on death, dependence and disability after a stroke.^[141] However, cardiorespiratory training added to walking programs in rehabilitation can improve speed, tolerance and independence during walking.^[141]

Prognosis

Disability affects 75% of stroke survivors enough to decrease their employability.^[143] Stroke can affect people physically, mentally, emotionally, or a combination of the three. The results of stroke vary widely depending on size and location of the lesion.^[144] 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 following a stroke can be due to 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. Other difficulties may include a decreased ability to communicate emotions through facial expression, body language and voice.^[145]

Disruption in self-identity, relationships with others, and emotional well-being can lead to social consequences after stroke due to the lack of ability to communicate. Many people who experience communication impairments after a stroke find it more difficult to cope with the social issues rather than physical impairments. Broader aspects of care must address the emotional impact speech impairment has on those who experience difficulties with speech after a stroke.^[146] Those who experience a stroke are at risk for paralysis which could result in a self disturbed body image which may also lead to other social issues.^[147]

30 to 50% of stroke survivors suffer post-stroke depression, which is characterized by lethargy, irritability, sleep disturbances, lowered self-esteem and withdrawal.^[148] Depression can reduce motivation and worsen outcome, but can be treated with antidepressants.

Emotional lability, another consequence of stroke, causes the person to switch quickly between emotional highs and lows and to express emotions inappropriately, for instance with an excess of laughing or crying with little or no provocation. While these expressions of emotion usually correspond to the person's actual emotions, a more severe form of emotional lability causes the affected person to laugh and cry pathologically, without regard to context or emotion.^[143] Some people show the opposite of what they feel, for example crying when they are happy.^[149] Emotional lability occurs in about 20% of those who have had a stroke.

Cognitive deficits resulting from stroke include perceptual disorders, aphasia,^[150] dementia,^[151] and problems with attention^[152] and memory.^[153] A stroke sufferer may be unaware of his or her own disabilities, a condition called anosognosia. In a condition called hemispatial neglect, the affected person is unable to attend to anything on the side of space opposite to the damaged hemisphere.

Cognitive and psychological outcome after a stroke can be affected by the age at which the stroke happened, pre-stroke baseline intellectual functioning, psychiatric history and whether there is pre-existing brain pathology.^[154]

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.^[155]^[156]

Epidemiology

Disability-adjusted life year for cerebral vascular disease per 100,000 inhabitants in 2004.^[157]

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 frequent cause of death worldwide in 2011, accounting for 6.2 million deaths (~11% of the total).^[158] Approximately 17 million people had a stroke in 2010 and 33 million people have previously had a stroke and were still alive.^[8] Between 1990 and 2010 the number of strokes decrease by approximately 10% in the developed world and increased by 10% in the developing world.^[8] Overall, two thirds of strokes occurred in those over 65 years old.^[8] South Asians are at particularly high risk for stroke, accounting for 40% of global stroke deaths.^[159]

It is ranked after heart disease and before cancer.^[2] In the United States stroke is a leading cause of disability, and recently declined from the third leading to the fourth leading cause of death.^[160] 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.^[161] 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.^[31]^[148] 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.^[162] 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,^[31] yet 60% of deaths from stroke occur in women.^[149] Since women live longer, they are older on average when they have their strokes and thus more often killed.^[31] 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.^[163] 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.^[164]^[165] The word stroke was used as a synonym for apoplectic seizure as early as 1599,^[166] 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.^[31]^[164] Wepfer also identified the main arteries supplying the brain, the vertebral and carotid arteries, and identified the cause of a type of ischemic stroke known as a cerebral infarction when he suggested that apoplexy might be caused by a blockage to those vessels.^[31] Rudolf Virchow first described the mechanism of thromboembolism as a major factor.^[167]

The term cerebrovascular accident was introduced in 1927, reflecting a "growing awareness and acceptance of vascular theories and (...) recognition of the consequences of a sudden disruption in the vascular supply of the brain".^[168] Its use is now discouraged by a number of neurology textbooks, reasoning that the connotation of fortuitousness carried by the word accident insufficiently highlights the modifiability of the underlying risk factors.^[169]^[170]^[171] Cerebrovascular insult may be used interchangeably.^[172]

The term brain attack was introduced for use to underline the acute nature of stroke according to the American Stroke Association,^[172] who since 1990 have used the term,^[173] and is used colloquially to refer to both ischemic as well as hemorrhagic stroke.^[174]

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.^[175]

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.^[176] Significant complications occur in about 7%.^[177]

Neuroprotection

Drugs that scavenge reactive oxygen species, inhibit programmed cell death, or inhibit excitatory neurotransmitters 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-scavenging phenylbutylnitrone, is reported to be neuroprotective in stroke.^[178] 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.^[31] Benefit of NXY-059 is questionable.^[179]

Hyperbaric oxygen therapy has been studied as a possible protective measure, but is currently not thought to be beneficial.^[180]

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^ Dubinsky R, Lai SM (2006). "Mortality of stroke patients treated with thrombolysis: analysis of nationwide inpatient sample". Neurology 66 (11): 1742–1744. doi:10.1212/01.wnl.0000218306.35681.38. PMID 16769953.
^ "Position Statement on the Use of Intravenous Thrombolytic Therapy in the Treatment of Stroke". American Academy of Emergency Medicine. Retrieved 2008-01-25.
^ Lee M, Hong KS, Saver JL (May 2010). "Efficacy of intra-arterial fibrinolysis for acute ischemic stroke: meta-analysis of randomized controlled trials". Stroke 41 (5): 932–7. doi:10.1161/STROKEAHA.109.574335. PMID 20360549.
^ Sardar, P; Chatterjee, S; Giri, J; Kundu, A; Tandar, A; Sen, P; Nairooz, R; Huston, J; Ryan, JJ; Bashir, R; Parikh, SA; White, CJ; Meyers, PM; Mukherjee, D; Majersik, JJ; Gray, WA (12 June 2015). "Endovascular therapy for acute ischaemic stroke: a systematic review and meta-analysis of randomized trials.". European heart journal. PMID 26071599.
^ Simard JM, Sahuquillo J, Sheth KN, Kahle KT, Walcott BP (April 2011). "Managing malignant cerebral infarction". Curr Treat Options Neurol 13 (2): 217–29. doi:10.1007/s11940-010-0110-9. PMC 3243953. PMID 21190097.
^ "Organised inpatient (stroke unit) care for stroke". Cochrane Database of Systematic Reviews. Sep 11, 2013. doi:10.1002/14651858.CD000197.pub3.
^ http://www.stroke.scot.nhs.uk/docs/UseOfAnkle-FootOrthosesFollowingStroke.pdf
^ O'Sullivan 2007, pp. 471, 484, 737, 740
^ Mackenzie C (April 2011). "Dysarthria in stroke: a narrative review of its description and the outcome of intervention". Int J Speech Lang Pathol 13 (2): 125–36. doi:10.3109/17549507.2011.524940. PMID 21480809.
^ West C, Hesketh A, Vail A, Bowen A (2005). West, Carolyn, ed. "Interventions for apraxia of speech following stroke". Cochrane Database Syst Rev (4): CD004298. doi:10.1002/14651858.CD004298.pub2. PMID 16235357.
^ Kelly H, Brady MC, Enderby P (2010). Brady, Marian C, ed. "Speech and language therapy for aphasia following stroke". Cochrane Database Syst Rev (5): CD000425. doi:10.1002/14651858.CD000425.pub2. PMID 20464716.
^ ^a ^b B. Lange, S. Flynn & A. Rizzo, B.; Flynn, S.; Rizzo, A. (2009). "Initial usability assessment of off-the-shelf video game consoles for clinical game-based motor rehabilitation". Physical Therapy Reviews 14 (5): 355–362. doi:10.1179/108331909X12488667117258.
^ Fregni F, Pascual-Leone A (2007). "Technology Insight: noninvasive brain stimulation in neurology—perspectives on the therapeutic potential of rTMS and tDCS". Nature Clinical Practice Neurology 3 (7): 383–393. doi:10.1038/ncpneuro0530. PMID 17611487.
^ Balasubramanian S, Klein J, Burdet E (2010). "Robot-assisted rehabilitation of hand function". Current Opinion in Neurology 23 (6): 661–70. doi:10.1097/WCO.0b013e32833e99a4. PMID 20852421.
^ ^a ^b ^c Brazzelli M, Saunders DH, Greig CA, Mead GE (2011). "Physical fitness training for stroke patients". The Cochrane Database of Systematic Reviews (11): CD003316. doi:10.1002/14651858.CD003316.pub4. PMID 22071806.
^ Institute for Quality and Efficiency in Health Care (IQWiG). "After a stroke: Does fitness training improve overall health and mobility?". Informed Health Online. Institute for Quality and Efficiency in Health Care (IQWiG). Retrieved 20 June 2013.
^ ^a ^b Coffey C. Edward, Cummings Jeffrey L, Starkstein Sergio, Robinson Robert (2000). Stroke - the American Psychiatric Press Textbook of Geriatric Neuropsychiatry (Second ed.). Washington DC: American Psychiatric Press. pp. 601–617.
^ Stanford Hospital & Clinics. "Cardiovascular Diseases: Effects of Stroke". Retrieved 2005.
^ editors, Tom A. Schweizer, R. Loch Macdonald, (2014). The behavioral consequences of stroke. New York, NY [u.a.]: Springer. pp. 119–133. ISBN 978-1-4614-7671-9.
^ Mackenzie, Catherine (2011). "Dysarthria in stroke: A narrative review of its description and the outcome of intervention". International Journal of Speech-Language Pathology: 125–136.
^ Ackley, Betty; Ladwig, Gail B.; Kelley, Helen (2010). Nursing diagnosis handbook: an evidence-based guide to planning care (9th ed.). Maryland Heights, MO.: Mosby.
^ ^a ^b Senelick Richard C., Rossi, Peter W., Dougherty, Karla (1994). Living with Stroke: A Guide for Families. Contemporary Books, Chicago. ISBN 0-8092-2607-3. OCLC 40856888 42835161.
^ ^a ^b Villarosa, Linda; Singleton, Lafayette; Johnson, Kirk A. (1993). The Black health library guide to stroke. New York: Henry Holt and Co. ISBN 0-8050-2289-9. OCLC 26929500.
^ Hamilton RH, Chrysikou EG, Coslett B (July 2011). "Mechanisms of aphasia recovery after stroke and the role of noninvasive brain stimulation". Brain Lang 118 (1–2): 40–50. doi:10.1016/j.bandl.2011.02.005. PMC 3109088. PMID 21459427.
^ Leys D, Hénon H, Mackowiak-Cordoliani MA, Pasquier F (November 2005). "Poststroke dementia". Lancet Neurol 4 (11): 752–9. doi:10.1016/S1474-4422(05)70221-0. PMID 16239182.
^ Coulthard E, Singh-Curry V, Husain M (December 2006). "Treatment of attention deficits in neurological disorders". Current Opinion in Neurology 19 (6): 613–8. doi:10.1097/01.wco.0000247605.57567.9a. PMID 17102702.
^ Lim C, Alexander MP (December 2009). "Stroke and episodic memory disorders". Neuropsychologia 47 (14): 3045–58. doi:10.1016/j.neuropsychologia.2009.08.002. PMID 19666037.
^ Murray ED, Buttner N, Price BH (2012). "Depression and Psychosis in Neurological Practice". In Bradley WG, Daroff RB, Fenichel GM, Jankovic J. Bradley's neurology in clinical practice. 1 (6th ed.). Philadelphia, PA: Elsevier/Saunders. pp. 100–1. ISBN 1-4377-0434-4.
^ Reith J, Jørgensen HS, Nakayama H, Raaschou HO, Olsen TS (August 1997). "Seizures in acute stroke: predictors and prognostic significance. The Copenhagen Stroke Study". Stroke 28 (8): 1585–9. doi:10.1161/01.STR.28.8.1585. PMID 9259753.
^ Burn J, Dennis M, Bamford J, Sandercock P, Wade D, Warlow C (December 1997). "Epileptic seizures after a first stroke: the Oxfordshire Community Stroke Project". BMJ 315 (7122): 1582–7. doi:10.1136/bmj.315.7122.1582. PMC 2127973. PMID 9437276.
^ "WHO Disease and injury country estimates". World Health Organization. 2009. Archived from the original on 11 November 2009. Retrieved November 11, 2009.
^ "The top 10 causes of death". WHO.
^ Indian Heart Association Why South Asians Facts Web. May 8, 2015. http://indianheartassociation.org/why-indians-why-south-asians/overview/
^ Towfighi A, Saver JL (August 2011). "Stroke declines from third to fourth leading cause of death in the United States: historical perspective and challenges ahead". Stroke 42 (8): 2351–5. doi:10.1161/STROKEAHA.111.621904. PMID 21778445.
^ Ellekjaer H, Holmen J, Indredavik B, Terent A (November 1, 1997). "Epidemiology of Stroke in Innherred, Norway, 1994 to 1996 : Incidence and 30-Day Case-Fatality Rate". Stroke 28 (11): 2180–2184. doi:10.1161/01.STR.28.11.2180. PMID 9368561. Retrieved 2008-01-22.
^ Bongers TN, de Maat MP, van Goor ML, Bhagwanbali V, van Vliet HH, Gómez García EB, Dippel DW, Leebeek FW (2006). "High von Willebrand factor levels increase the risk of first ischemic stroke: influence of ADAMTS13, inflammation, and genetic variability". Stroke 37 (11): 2672–7. doi:10.1161/01.STR.0000244767.39962.f7. PMID 16990571.
^ Ashrafian H (2010). "Familial stroke 2700 years ago". Stroke 41 (4): e187. doi:10.1161/STROKEAHA.109.573170. PMID 20185778.
^ ^a ^b Thompson JE (August 1, 1996). "The evolution of surgery for the treatment and prevention of stroke. The Willis Lecture". Stroke 27 (8): 1427–34. doi:10.1161/01.STR.27.8.1427. PMID 8711815.
^ Kopito, Jeff (September 2001). "A Stroke in Time". MERGINET.com 6 (9). ^{[dead link]}
^ R. Barnhart, ed. The Barnhart Concise Dictionary of Etymology (1995)
^ Schiller F (April 1970). "Concepts of stroke before and after Virchow". Med Hist 14 (2): 115–31. doi:10.1017/S0025727300015325. PMC 1034034. PMID 4914683.
^ Stanley Finger; François Boller; Kenneth L. Tyler (2010). Handbook of Clinical Neurology. North-Holland Publishing Company. p. 401. ISBN 978-0-444-52009-8. Retrieved 1 October 2013.
^ John W. Scadding (December 2011). Clinical Neurology. CRC Press. p. 488. ISBN 978-0-340-99070-4. Retrieved 1 October 2013.
^ Joseph I. Sirven; Barbara L. Malamut (2008). Clinical Neurology of the Older Adult. Lippincott Williams & Wilkins. p. 243. ISBN 978-0-7817-6947-1. Retrieved 1 October 2013.
^ David Myland Kaufman; Mark J Milstein (5 December 2012). Kaufman's Clinical Neurology for Psychiatrists. Elsevier Health Sciences. p. 892. ISBN 978-1-4557-4004-8. Retrieved 1 October 2013.
^ ^a ^b Mosby's Medical Dictionary, 8th edition. Elsevier. 2009.
^ "What is a Stroke/Brain Attack?" (PDF). National Stroke Association. Retrieved 27 February 2014.
^ Segen's Medical Dictionary. Farlex, Inc. 2010.
^ Derdeyn CP, Chimowitz MI; Chimowitz (August 2007). "Angioplasty and Stenting for Atherosclerotic Intracranial Stenosis: Rationale for a Randomized Clinical Trial". Neuroimaging Clin. N. Am. 17 (3): 355–63, viii–ix. doi:10.1016/j.nic.2007.05.001. PMC 2040119. PMID 17826637.
^ Tenser MS, Amar AP, Mack WJ; Amar; Mack (December 2011). "Mechanical thrombectomy for acute ischemic stroke using the MERCI retriever and penumbra aspiration systems". World neurosurgery 76 (6 Suppl): S16–23. doi:10.1016/j.wneu.2011.07.003. PMID 22182267.
^ Ortega-Lopez Y, Llanos-Mendez A (2010). "[Mechanical thrombectomy with MERCI device. Ischaemic stroke]". Andalusian Agency for Health Technology Assessment.
^ Lees KR, Zivin JA, Ashwood T, Davalos A, Davis SM, Diener HC, Grotta J, Lyden P, Shuaib A, Hårdemark HG, Wasiewski WW; Zivin; Ashwood; Davalos; Davis; Diener; Grotta; Lyden; Shuaib; Hårdemark; Wasiewski; Stroke-Acute Ischemic NXY Treatment (SAINT I) Trial Investigators (February 2006). "NXY-059 for acute ischemic stroke". The New England Journal of Medicine 354 (6): 588–600. doi:10.1056/NEJMoa052980. PMID 16467546.
^ Koziol JA, Feng AC; Feng (October 2006). "On the analysis and interpretation of outcome measures in stroke clinical trials: lessons from the SAINT I study of NXY-059 for acute ischemic stroke". Stroke; a journal of cerebral circulation 37 (10): 2644–7. doi:10.1161/01.STR.0000241106.81293.2b. PMID 16946150.
^ Bennett, MH; Weibel, S; Wasiak, J; Schnabel, A; French, C; Kranke, P (12 November 2014). "Hyperbaric oxygen therapy for acute ischaemic stroke.". The Cochrane database of systematic reviews 11: CD004954. doi:10.1002/14651858.CD004954.pub3. PMID 25387992.

External links

Stroke at DMOZ
DRAGON Score for Post-Thrombolysis
THRIVE score for stroke outcome

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. 脳卒中評価の概要 overview of the evaluation of stroke
3. 脳卒中の二次予防のための抗血小板療法 antiplatelet therapy for secondary prevention of stroke
4. 急性虚血性脳卒中および一過性脳虚血発作に対する抗血栓治療 antithrombotic treatment of acute ischemic stroke and transient ischemic attack
5. 脳卒中の病因、分類、および疫学 etiology classification and epidemiology of stroke

English Journal

Eicosapentaenoic Acid as long-term secondary prevention after ischemic stroke.

Nakase T1, Sasaki M, Suzuki A.
Clinical and translational medicine.Clin Transl Med.2015 Dec;4(1):62. doi: 10.1186/s40169-015-0062-5. Epub 2015 Jun 11.
BACKGROUND: It is sometimes difficult to choose anti-thrombotic agents for secondary prevention in stroke patients at high bleeding risk. Recently, Eicosapentaenoic Acid (EPA) was reported to reduce the recurrence of stroke in hypercholesterolemic patients without increasing hemorrhagic risk. In thi
PMID 26084813

Respiratory variation in carotid peak systolic velocity predicts volume responsiveness in mechanically ventilated patients with septic shock: a prospective cohort study.

Ibarra-Estrada MÁ1, López-Pulgarín JA, Mijangos-Méndez JC, Díaz-Gómez JL, Aguirre-Avalos G.
Critical ultrasound journal.Crit Ultrasound J.2015 Dec;7(1):29. doi: 10.1186/s13089-015-0029-1. Epub 2015 Jun 26.
BACKGROUND: The evaluation of fluid responsiveness in patients with hemodynamic instability remains to be challenging. This investigation aimed to determine whether respiratory variation in carotid Doppler peak velocity (ΔCDPV) predicts fluid responsiveness in patients with septic shock and lung pr
PMID 26123610

Oral Levosimendan Increases Cerebral Blood Flow Velocities in Patients with a History of Stroke or Transient Ischemic Attack: A Pilot Safety Study.

Kivikko M1, Kuoppamäki M2, Soinne L3, Sundberg S4, Pohjanjousi P2, Ellmen J2, Roine RO5.
Current therapeutic research, clinical and experimental.Curr Ther Res Clin Exp.2015 Jan 29;77:46-51. doi: 10.1016/j.curtheres.2015.01.001. eCollection 2015.
BACKGROUND: Intravenous levosimendan is indicated for acute heart failure. The compound has shown promising beneficial effects in ischemic stroke models.OBJECTIVE: We evaluated the efficacy and safety of oral levosimendan in patients with a history of cerebral ischemia.METHODS: In a randomized, doub
PMID 26082815

Imaging of reactive oxygen species in focal ischemic mouse brain using a radical trapping tracer [(3)H]hydromethidine.

Abe K1, Tonomura M, Ito M, Takai N, Imamoto N, Rokugawa T, Momosaki S, Fukumoto K, Morimoto K, Inoue O.
EJNMMI research.EJNMMI Res.2015 Dec;5(1):115. doi: 10.1186/s13550-015-0115-1. Epub 2015 Jun 26.
BACKGROUND: Reactive oxygen species (ROS) have been implicated in the pathophysiology of the brain after ischemic stroke. In this study, we investigate the generation of brain ROS after transient focal ischemia in mice using a radical trapping radiotracer, [(3)H]-labeled N-methyl-2,3-diamino-6-pheny
PMID 26160496

Japanese Journal

Transradial Approach for Mechanical Thrombectomy of Posterior Circulation Stroke

JNET : journal of neuroendovascular therapy : official journal of the Japanese Society for Neuroendovascular Therapy 12(6), 314-319, 2018-06
NAID 40021567234

Case Report : A Subtype of Bow Hunter's Syndrome Requiring Specific Method for Detection : A Case of Recurrent Posterior Circulation Embolism due to "Hidden Bow Hunter's Syndrome"

JNET : journal of neuroendovascular therapy : official journal of the Japanese Society for Neuroendovascular Therapy 12(6), 295-302, 2018-06
NAID 40021567215

脳卒中領域との協働 (特集医療・医学の課題としての身体合併症)

精神医学 = Clinical psychiatry 60(6), 619-627, 2018-06
NAID 40021561083

High Cardiac Troponin I Is Associated With Transesophageal Echocardiographic Risk of Thromboembolism and Ischemic Stroke Events in Non-Valvular Atrial Fibrillation Patients

Circulation journal : official journal of the Japanese Circulation Society 82(6), 1699-1704, 2018-06
NAID 40021555296

Related Pictures

★リンクテーブル★

国試過去問	「105F015」
リンク元	「意識障害」「脳卒中」「ascertain」「attack」「apoplexy」
拡張検索	「ischaemic stroke」「stroke in evolution」

「105F015」

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

『Stroke』
Scars Borough のスタジオ・アルバム
リリース	2010年4月7日
ジャンル	ロック
レーベル	Dynamord Label
プロデュース	Scars Borough
Scars Borough 年表
	テンプレートを表示

　　[★]

疾患と診療分野の組合せで適切でないのはどれか。

[正答]

※国試ナビ4※　［105F014］←［国試_105］→［105F016］

「意識障害」

　　[★]

英: consciousness disturbance, disturbance of consciousness
関: 意識

分類

時間による分類

急性/慢性, 持続性/一過性

急性＋一過性：失神、てんかん
慢性＋持続性：植物状態、認知症

PSY.38

単純な意識障害

明識困難状態 < 昏蒙 < 傾眠 < 昏眠 < 昏睡

複雑な意識障害

せん妄　　　　　意識混濁　＋　(高度)精神運動興奮

振戦せん妄

作業せん妄

夜間せん妄

もうろう状態　　意識狭窄　＋　(軽度)精神運動興奮
アメンチア

意識障害に関連した特殊な病態

意識レベルの分類覚醒度

Mayo Clinicの分類

救急意識障害をみたら

AIUEOTIPS (also see DIF.96)

	症候学プリント		DIF.95
A	alcohol	アルコール関連	accidents, arterial occlusions, arteriosclerosis, aneurysms, autoimmune disorders
I	insulin	インスリン関連(低血糖、糖尿病性ケトアシドーシス、非ケトン性高浸透圧性昏睡)	inflammatory, intoxication (encephalitis, cerebral abcess, meningitis, alcoholism, opiates, barbiturates)
U	uremia	尿毒症、電解質異常、内分泌異常、肝性脳症	undefined disorders (narcolepsy, conversion hysteria)
E	encephalopathy, endocrinopathy, electrolyte	脳症(脳炎、脳血管障害)、てんかん後	endocrine disorders(myxedema coma, hyperparathyroidism, diabetic coma, insulin shock), epileptic coma
O	opiate, other overdose of O2 & CO2	薬物中毒	organ failure(hepatic coma, respiratory failure, uremia)
T	trauma, tumor, temparature	頭部外傷、脳挫傷、硬膜外血腫、硬膜下血腫
I	infection	感染症、髄膜炎
P	psychogenic	精神疾患
S	syncope, seizure, stroke, shock, senile	失神、クモ膜下出血

意識障害を来した患者が来た場合：どのような疾患を鑑別に挙げるべきか(IMD.237)

1. 脳原発の疾患(一次性)

a. テント上病変(脳幹の圧迫性病変ないし脳ヘルニアをきたす疾患)

1) 脳血管障害:脳出血、脳梗塞
2) 硬膜下血腫
3) 脳腫瘍:原発性、転移性
4) 脳膿瘍

b. テント下病変(脳幹網様体の障害)

1) 脳幹出血、脳幹梗塞、小脳出血、小脳梗塞、脳腫痛、多発性硬化症など

c. びまん性病変

1) くも膜下出血、中枢神経感染症:髄膜炎、脳炎、播種性血管内凝固症候群など

2. 全身疾患に伴う病態(二次性)

a. 代謝性またはびまん性病変

1) ショック:心筋梗塞、大出血など
2) 薬物、毒物
3) 無酸素ないし低酸素血症
4) DIC、全身性感染症:敗血症など
5) 肝不全、腎不全、糖尿病性高血糖、重症肝炎、内分泌疾患など
6) 低血糖、ビタミンB1欠乏: Wernicke脳症
7) 脳振盪、てんかん大発作後
8) 酸塩基平衡および電解質異常
9) 栄養障害

b. 心因性無反応

1) ヒステリー、統合失調症

意識障害をきたす電解質異常

QB.D-345

カリウムは静止膜電位にかかわるが、ニューロンの活動にはそれほど関わらないから、意識障害はきたしにくいのかもしれない。

pHの異常も局所的に干渉されるため意識障害をきたしにくいのかもしれない。

高カルシウム血症　：ニューロンの活動に関わる？
高ナトリウム血症、低ナトリウム血症　：APの発生に関わる
低リン血症　　　：ATP産生↓
低酸素血症　　　：ATP産生↓
高炭酸ガス血症　：CO2麻酔

意識障害の評価法

英: evaluation of consciousness disturbance

Glasgow coma scale GCS
Japan coma scale JCS

「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

「ascertain」

　　[★]

vt.

(調査・観察などで)～を確かめる。(～であることを/～かどうかを)確かめる[that節/wh節]。(SCO tobe C)(人が)O(人・物)が～であることを確かめる。

We were unable to completely ascertain the prevalence of TNA prior to stroke because patients do not always recognize TNA.

vi.

確かめる。

関: affirm、ascertainment、confirm、confirmation、identify、validate、validation、verify

「attack」

　　[★]

n.

発作、攻撃

v.

攻撃する、襲う、非難する、襲撃する

関: aggressive、assault、blame、bout、challenge、crises、crisis、criticise、criticism、criticize、insult、offense、offensive、paroxysm、seizure、strike、stroke、thrust

「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

「ischaemic stroke」

　　[★]

虚血性脳卒中

関: ischemic stroke

「stroke in evolution」

　　[★]

進行性脳卒中、進行性卒中

[HLB2014W-1] "What Is a Stroke?". http://www.nhlbi.nih.gov/. March 26, 2014. Retrieved 26 February 2015.

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Contents

Classification

Definition

Ischemic

Hemorrhagic

Signs and symptoms

Early recognition

Subtypes

Associated symptoms

Causes

Thrombotic stroke

Embolic stroke

Cerebral hypoperfusion

Venous thrombosis

Intracerebral hemorrhage

Silent stroke

Pathophysiology

Ischemic

Hemorrhagic

Diagnosis

Physical examination

Imaging

Underlying cause

Prevention

Risk factors

Blood pressure

Blood lipids

Diabetes mellitus

Anticoagulation drugs

Surgery

Diet

Women

Previous stroke or TIA

Management

Ischemic stroke

Thrombolysis

Surgery

Hemorrhagic stroke

Stroke unit

Rehabilitation

Prognosis

Epidemiology

History

Research

Angioplasty and stenting

Mechanical thrombectomy

Neuroprotection

See also

References

Further reading

External links

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