All clients with neurological deficits affecting movement including:
A stroke is the rapidly developing loss of brain functions due to a disturbance in the blood vessels supplying blood to the brain. This can be due to ischemia (lack of blood supply) caused by thrombosis or embolism or due to a haemorrhagic. As a result, the affected area of the brain is unable to function, leading to inability to move one or more limbs on one side of the body, inability to understand or formulate speech or inability to see one side of the visual field.[1] In the past, stroke was referred to as cerebrovascular accident or CVA, but the term "stroke" is now preferred.
A stroke is a medical emergency and can cause permanent neurological damage, complications and death. It is the leading cause of adult disability in the United States and Europe. It is the number two cause of death world-wide and may soon become the leading cause of death worldwide.[2] Risk factors for stroke include advanced age, hypertension (high blood pressure), previous stroke or transient ischemic attack (TIA), diabetes, high cholesterol, cigarette smoking and atrial fibrillation. High blood pressure is the most important modifiable risk factor of stroke.[1]
The traditional definition of stroke, devised by the World Health Organisation in the 1970s,[3] 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.[1] 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.[4]
A stroke is occasionally treated with thrombolysis ("clot buster"), but usually with supportive care (physiotherapy and occupational therapy) in a "stroke unit" and secondary prevention with antiplatelet drugs (aspirin and often dipyridamole), blood pressure control, statins, and in selected patients with carotid endarterectomy and anticoagulation. back to the top
Strokes can be classified into two major categories: ischemic and haemorrhagic. Ischemia is due to interruption of the blood supply, while haemorrhagic is due to rupture of a blood vessel or an abnormal vascular structure. 80% of strokes are due to ischemia; the remainder are due to haemorrhagic. Some haemorrhagics develop inside areas of ischemia ("haemorrhagic transformation"). It is unknown how many haemorrhagics actually start off as ischemic stroke.
In an ischemic stroke, blood supply to part of the brain is decreased, leading to dysfunction and necrosis 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 (idem due to an embolus from elsewhere in the body, see below), systemic hypoperfusion (general decrease in blood supply, e.g. in shock) and 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.[8][9] 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). back to the top
Main articles: Intracranial haemorrhagic and intracerebral haemorrhagic
Intracranial haemorrhagic is the accumulation of blood anywhere within the skull vault. A distinction is made between intra-axial haemorrhagic (blood inside the brain) and extra-axial haemorrhagic (blood inside the skull but outside the brain). Intra-axial haemorrhagic is due to intraparenchymal haemorrhagic or intraventricular haemorrhagic (blood in the ventricular system). The main types of extra-axial haemorrhagic are epidural hematoma (bleeding between the dura mater and the skull), subdural hematoma (in the subdural space) and subarachnoid haemorrhagic (between the arachnoid mater and pia mater). Most of the haemorrhagic stroke syndromes have specific symptoms (e.g. headache, previous head injury). Intracerebral haemorrhagic (ICH) is bleeding directly into the brain tissue, forming a gradually enlarging hematoma (pooling of blood).[citation needed]
Signs and symptoms
Stroke symptoms typically start suddenly, over seconds to minutes, and in most cases don't progress further afterwards. 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: in intracranial haemorrhagic, the affected area may compress other structures. Most forms of stroke are not associated with headache, apart from subarachnoid haemorrhagic and cerebral venous thrombosis and occasionally intracerebral haemorrhagic.
Early recognition
Various systems have been proposed to increase recognition of stroke by patients, relatives and emergency first responders. Sudden-onset face weakness, arm drift, and abnormal speech are the findings most likely to lead to the correct identification of a case of stroke.[11] Proposed systems include FAST (face, arm and speech test),[12] the Los Angeles Prehospital Stroke Screen (LAPSS)[13] and the Cincinnati Prehospital Stroke Scale (CPSS).[14] Use of these scales is recommended by professional guidelines.[15]
For people referred to the emergency department, early recognition of stroke is deemed important as this can expediate diagnostic tests and treatments. A scoring system called ROSIER (recognition of stroke in the emergency department) is recommended for this purpose; it is based on features from the medical history and physical examination.[16][15]
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
In most cases, the symptoms affect only one side of the body (unilateral). The defect in the brain is usually on the opposite side of the body (depending on which part of the brain is affected). However, the presence of any one of these symptoms does not necessarily suggest a stroke, since these pathways also travel in the spinal cord and any lesion there can also produce these symptoms.
In addition to the above CNS pathways, the brainstem also consists of the 12 cranial nerves. A stroke affecting the brainstem 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 (inability to speak or understand language from involvement of Broca's or Wernicke's area)
* 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)
* anosognosia (persistent denial of the existence of a, usually stroke-related, deficit)
If the cerebellum is involved, the patient may have the following:
* trouble walking
* altered movement coordination
* vertigo and or disequilibrium
Associated symptoms
Loss of consciousness, headache, and vomiting usually occurs more often in haemorrhagic stroke than in thrombosis because of the increased intracranial pressure from the leaking blood compressing on the brain.
If symptoms are maximal at onset, the cause is more likely to be a subarachnoid haemorrhagic or an embolic stroke.
Causes
This section needs additional citations for verification.
Please help improve this article by adding reliable references. Unsourced material may be challenged and removed. (September 2008) back to the top
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". Thrombotic stroke can be divided into two types depending on the type of vessel the thrombus is formed on:
* Large vessel disease involves the common and internal carotids, vertebral, and the Circle of Willis. Diseases that may form thrombi in the large vessels include (in descending incidence): 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. back to the top
An embolic stroke refers to the blockage of an artery by an 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).
Because an embolus arises from elsewhere, local therapy only solves the problem 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.
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 vertricle, 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. back to the top
Systemic hypoperfusion
Systemic hypoperfusion is the reduction of blood flow to all parts of the body. It is most commonly due to cardiac pump failure from cardiac arrest or arrhythmias, or from reduced cardiac output as a result of myocardial infarction, pulmonary embolism, pericardial effusion, or bleeding. 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. Blood flow to these areas does not necessarily stop, but instead it may lessen to the point where brain damage can occur. This phenomenon is also referred to as "last meadow" to point to the fact that in irrigation the last meadow receives the least amount of water.
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 haemorrhagic transformation (leaking of blood into the damaged area) than other types of ischemic stroke. back to the top
It generally occurs in small arteries or arterioles and is commonly due to hypertension, trauma, bleeding disorders, amyloid angiopathy, illicit drug use (e.g. amphetamines or cocaine), and vascular malformations. 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 even the very deadly subarachnoid haemorrhage. back to the top
Pathophysiology
Ischemic stroke occurs due to 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 a few hours will suffer irreversible injury possibly leading to death of the tissue, i.e., infarction. Atherosclerosis may disrupt the blood supply by narrowing the lumen of blood vessels leading to a reduction of blood flow, by causing the formation of blood clots within the vessel, or by releasing showers of small emboli through the disintegration of atherosclerotic plaques. Embolic infarction occurs when emboli formed elsewhere in the circulatory system, typically in the heart as a consequence of atria fibriliation, or in the carotid arteries. These break off, enter the cerebral circulation, then lodge in and occlude brain blood vessels.
Due to collateral circulation, within the region of brain tissue affected by ischemia there is a spectrum of severity. Thus, part of the tissue may immediately die while other parts may only be injured and could potentially recover. The ischemia area where tissue might recover is referred to as the ischemic penumbra.
As oxygen or glucose becomes depleted in ischemic brain tissue, the production of high energy phosphate compounds such as adenosine triphosphate (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.
Ischaemia 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 .[17]
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.
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 excitotoxic neurotransmitters, for example, have been shown experimentally to reduce tissue injury due to 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 spintrap phenylbutylnitrone, is reported 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.[17]
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.
As is the case with any type of brain injury, the immune system is activated by cerebral infarction and may under some circumstances exacerbate the injury caused by the infarction. Inhibition of the inflammatory response has been shown experimentally to reduce tissue injury due to cerebral infarction, but this has not proved out in clinical studies. back to the top
haemorrhagic 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 haemorrhagic appears to have direct toxic effects on brain tissue and vasculature. back to the top
Diagnosis
Stroke is diagnosed through several techniques: a neurological examination, 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.[19]
Imaging
For diagnosing ischemic stroke in the emergency setting:[20]
* CT scans (without contrast enhancements)
sensitivity= 16%
specificity= 96%
* MRI scan
sensitivity= 83%
specificity= 98%
For diagnosing haemorrhagic stroke in the emergency setting:
* CT scans (without contrast enhancements)
sensitivity= 89%
specificity= 100%
* MRI scan
sensitivity= 81%
specificity= 100%
For detecting chronic haemorrhagics, MRI scan is more sensitive.[21]
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 etiology
When a stroke has been diagnosed, various other studies may be performed to determine the underlying etiology. 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 stroke, prevention is an important public health concern.[22] Primary prevention is less effective than secondary prevention (as judged by the number needed to treat to prevent one stroke per year).[22] Recent guidelines detail the evidence for primary prevention in stroke.[23] 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 prevents against first stroke in patients who have suffered a myocardial infarction.[24]
Risk factors
The most important modifiable risk factors for stroke are high blood pressure and atrial fibrillation. Other modifiable risk factors include high blood cholesterol levels, diabetes, cigarette smoking[25][26] (active and passive), heavy alcohol consumption[27] and drug use,[28] lack of physical activity, obesity and unhealthy diet.[29] Alcohol use could predispose to ischemic stroke, and intracerebral and subarachnoid haemorrhagic via multiple mechanisms (for example via hypertension, atrial fibrillation, rebound thrombocytosis and platelet aggregation and clotting disturbances).[30] The drugs most commonly associated with stroke are cocaine, amphetamines causing haemorrhagic stroke, but also over-the-counter cough and cold drugs containing sympathomimetics.[31][32]
No high quality studies have shown the effectiveness of interventions aimed at weight reduction, promotion of regular exercise, reducing alcohol consumption or smoking cessation.[33] Nonetheless, given the large body of circumstantial evidence, best medical management for stroke includes advice on diet, exercise, smoking and alcohol use.[34] 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 accounts for 35-50% of stroke risk.[35] Epidemiological studies suggest that even a small blood pressure reduction (5 to 6 mmHg systolic, 2 to 3 mmHg diastolic) would result in 40% fewer strokes.[36] Lowering blood pressure has been conclusively shown to prevent both ischemic and haemorrhagic strokes.[37][38] It is equally important in secondary prevention.[39] Even patients older than 80 years and those with isolated systolic hypertension benefit from antihypertensive therapy.[40][41][42] Studies show that intensive antihypertensive therapy results in a greater risk reduction.[43] 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.[43][44]
Atrial fibrillation
Patients with atrial fibrillation have a risk of 5% each year to develop stroke, and this risk is even higher in those with valvular atrial fibrillation.[45] Depending on the stroke risk, anticoagulation with medications such as coumarins or aspirin is warranted for stroke prevention.[46]
Blood lipids
High cholesterol levels have been inconsistently associated with (ischemic) stroke.[47][38] Statins have been shown to reduce the risk of stroke by about 15%.[48] Since earlier meta-analyses of other lipid-lowering drugs did not show a decreased risk,[49] statins might exert there effect through mechanisms other than their lipid-lowering effects.[48]
Diabetes mellitus
Patients with diabetes mellitus are 2 to 3 times more likely to develop stroke, and they commonly have hypertension and hyperlipidemia. Intensive disease control has been shown to reduce microvascular complications such as nephropathy and retinopathy but not macrovascular complications such as stroke.[50][51]
Anticoagulation drugs
Aspirin or other antiplatelet drugs are highly effective in secondary prevention after a stroke or transient ischemic attack. Low doses of aspirin (for example 75
