Stroke Preventive Health Tips:
According to the Wikipedia Encyclopedia:
previously known medically as cerebrovascular accident (CVA), is rapidly developing loss of brain function(s) due to disturbance in blood supply to brain. This can be due to ischemia (lack of blood flow) caused by blockage (thrombosis, arterial embolism), or haemorrhage (leakage of blood). Resulting in affected area of brain is unable to function, & might result in an inability to move one or more limbs on one side of body, inability to understand, formulate speech, or an inability to see one side of visual field.
is a medical emergency & can cause permanent neurological damage, complications, & death. It’s leading cause of adult disability in US & Europe & second leading cause of death worldwide. Risk factors for stroke include: old age, hypertension (high blood pressure(hbp), previous stroke or transient ischemic attack (TIA), diabetes, high cholesterol(hc), cigarette smoking & atrial fibrillation. High blood pressure is most important modifiable risk factor of stroke.
is a stroke doesn’t have any identifiable outward symptoms, & patient is typically unaware they have suffered a stroke. A silent stroke still causes damage to brain, & places patient at increased risk for both transient ischemic attack & major stroke in future. Conversely, those who have suffered a major stroke are at risk of having silent stroke(s). In a broad study in ’98, more than 11 million people were estimated to have experienced a stroke in US. Approximately 770,000 of these strokes were symptomatic &11 million were first-ever silent MRI infarcts or hemorrhages. Silent strokes typically cause lesions which are detected via use of neuroimaging or MRI. Silent stroke are estimated to occur at five times rate of symptomatic stroke. Risk of silent stroke increases with age but may affect younger adults & children, especially those with acute anemia.
is occasionally treated in hospital with thrombolysis (“clot buster”), & some hemorrhagic strokes benefit from neurosurgery. Treatment to recover any lost function is termed stroke rehabilitation, ideally in a stroke unit & involving health professions: speech & language therapy, physical therapy & occupational therapy. Prevention of recurrence may involve administration of antiplatelet drugs: aspirin & dipyridamole, control & reduction of hypertension, & use of statins. Selected patients may benefit from carotid endarterectomy & use of anticoagulants.
Traditional definition of stroke, devised by World Health Organization in ’70s, 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 reversibility of tissue damage & was devised for purpose, with time frame of 24 hours being chosen arbitrarily. The 24-hour limit divides stroke from transient ischemic attack, which is a related syndrome of stroke symptoms that resolve completely within 24 hours. With availability of treatments , when given early, can reduce stroke severity, many now prefer alternative concepts, brain attack & acute ischemic cerebrovascular syndrome (modeled after heart attack & acute coronary syndrome respectively), reflect urgency of stroke symptoms & need to act swiftly.
Strokes classified into 2 major categories: ischemic & hemorrhagic.
Ischemic strokes: are those that are caused by interruption of the blood supply.
Hemorrhagic strokes: are those resulting from rupture of a blood vessel or an abnormal vascular structure. About 87% of strokes are caused by ischemia, & remainder by hemorrhage. Some hemorrhages develop inside areas of ischemia (“hemorrhagic transformation”). It’s unknown how many hemorrhages actually start as ischemic stroke.
Main articles: Cerebral infarction & Brain ischemia
Ischemic stroke:blood supply to part of brain is decreased, leads to dysfunction of brain tissue in area.
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),
Systemic hypoperfusion (general decrease in blood supply, e.g., in shock)
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: Oxford Community Stroke Project classification (OCSP(Bamford or Oxford classification) relies primarily on initial symptoms; based on extent of symptoms, 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 extent of stroke, area of brain affected, underlying cause, & prognosis. The TOAST (Trial of Org 10172 in Acute Stroke Treatment) classification is based on clinical symptoms as well as results of further investigations; on this basis, a stroke is classified as being due to (1) thrombosis or embolism due to atherosclerosis of a large artery, (2) embolism of cardiac origin, (3) occlusion of a small blood vessel, (4) other determined cause, (5) undetermined cause (two possible causes, no cause identified, or incomplete investigation).
Intracranial hemorrhage & intracerebral hemorrhage
Intracranial hemorrhage is the accumulation of blood anywhere within the skull vault. A distinction is made between intra-axial hemorrhage (blood inside the brain) and extra-axial hemorrhage (blood inside the skull but outside the brain). Intra-axial hemorrhage is due to intraparenchymal hemorrhage or intraventricular hemorrhage (blood in the ventricular system). Main types of extra-axial hemorrhage are epidural hematoma (bleeding between dura mater & skull), subdural hematoma (in the subdural space) and subarachnoid hemorrhage (between the arachnoid mater and pia mater). Most of the hemorrhagic stroke syndromes have specific symptoms (e.g., headache, previous head injury).
Signs & symptoms: Stroke symptoms typically start suddenly, over seconds to minutes, & in most cases don’t progress further. Symptoms depend on area of brain affected. More extensive area of brain affected, more functions that’re likely to be lost. Some forms of stroke can cause additional symptoms. Example, in intracranial hemorrhage, affected area may compress other structures. Most forms of stroke aren’t associated with headache, apart from subarachnoid hemorrhage & cerebral venous thrombosis & occasionally intracerebral hemorrhage.
Various systems have been proposed to increase recognition of stroke by patients, relatives & emergency first responders. A systematic review, updating a previous systematic review from ’94, looked at a number of trials to evaluate how well different physical examination findings are able to predict presence or absence of stroke. It was found sudden-onset face weakness, arm drift (person, when asked to raise both arms, involuntarily lets one arm drift downward) & abnormal speech are findings most likely to lead to correct identification of a case of stroke (+ likelihood ratio of 5.5 when at least one of these is present). Similarly, when all three of these are absent, likelihood of stroke is significantly decreased (- likelihood ratio of 0.39). While these findings aren’t perfect for diagnosing stroke, fact that they can be evaluated relatively rapidly & easily make them very valuable in acute setting.
Proposed systems include FAST (stroke) (face, arm, speech, & time), as advocated by Department of Health (United Kingdom) & Stroke Association, American Stroke Association (www.strokeassociation.org) , National Stroke Association (US www.stroke.org), Los Angeles Prehospital Stroke Screen (LAPSS) & Cincinnati Prehospital Stroke Scale (CPSS). Use of these scales is recommended by professional guidelines.
For people referred to emergency room, early recognition of stroke is deemed important as this can expedite diagnostic tests & treatments. A scoring system called ROSIER (recognition of stroke in emergency room) is recommended for this purpose; it’s based on features from medical history & physical examination.
Sub type seIf-area of brain affected contains one of 3 prominent central nervous system pathways- spinothalamic tract, corticospinal tract, & dorsal column (medial lemniscus)
Symptoms may include:
hemiplegia & muscle weakness of the face
reduction in sensory or vibratory sensation
initial flaccidity (hypotonicity), replaced by spasticity (hypertonicity), hyperreflexia, & obligatory synergies.
In most cases, symptoms affect only one side of body (unilateral). Depending on part of brain affected, defect in brain is usually on opposite side of the body. Since these pathways travel in spinal cord & any lesion there can produce these symptoms, presence of any one of these symptoms doesn’t necessarily indicate a stroke.
In addition to above CNS pathways, brain stem give rise to most of the twelve cranial nerves. A stroke affecting brain stem & brain can produce symptoms relating to:
Deficits in cranial nerves:
altered smell, taste, hearing, or vision (total or partial)
drooping of eyelid (ptosis) & weakness of ocular muscles
decreased reflexes: gag, swallow, pupil reactivity to light
decreased sensation & muscle weakness of face
balance problems & nystagmus
altered breathing & heart rate
weakness in sternocleidomastoid muscle with inability to turn head to one side
weakness in tongue (inability to protrude &/or move from side to side)
If cerebral cortex is involved, CNS pathways can again be affected, & can produce following symptoms:
aphasia (difficulty with verbal expression, auditory comprehension, reading &/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)
anosognosia (persistent denial existence of a, usually stroke-related, deficit)
If cerebellum is involved, patient may have following:
altered movement coordination
vertigo &/or disequilibrium
Loss of consciousness, headache, & vomiting occurs more often in hemorrhagic stroke than in thrombosis because of increased intracranial pressure from leaking blood compressing brain.
If symptoms are maximal at onset, cause is more likely to be a subarachnoid hemorrhage or an embolic stroke.
In thrombotic stroke a thrombus (blood clot) usually forms around atherosclerotic plaques. Since blockage of as artery is gradual, onset of symptomatic thrombotic strokes is slower. A thrombus itself (even if non-occluding) can lead to an embolic stroke if thrombus breaks off, at which point it’s called an “embolus.”
2 types of thrombosis can cause stroke:
Large vessel disease: involves common & internal carotids, vertebral, & Circle of Willis. Diseases may form thrombi in large vessels include (in descending incidence): atherosclerosis, vasoconstriction (tightening of artery), aortic, carotid or vertebral artery dissection, various inflammatory diseases of blood vessel wall (Takayasu arteritis, giant cell arteritis, vasculitis), noninflammatory vasculopathy, Moyamoya disease & fibromuscular dysplasia.
Small vessel disease: involves smaller arteries inside brain: branches of circle of Willis, middle cerebral artery, stem, & arteries arising from distal vertebral & basilar artery. Diseases that may form thrombi in small vessels include (in descending incidence): lipohyalinosis (build-up of fatty hyaline matter in blood vessel as a result of high blood pressure & aging) & fibrinoid degeneration (stroke involving these vessels are known as lacunar infarcts) & microatheroma (small atherosclerotic plaques).
Sickle cell anemia, can cause blood cells to clump up & block blood vessels, can lead to stroke. A stroke is second leading killer of people under 20 who suffer from sickle-cell anemia.
An embolic stroke refers to blockage of an artery by an arterial embolus, a travelling particle or debris in the arterial bloodstream originating from elsewhere. An embolus is most frequently a thrombus,(obstruction of a blood vessel by a blood clot forming locally) but it can also be a number of other substances including fat (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 solves problem only temporarily. Source of embolus must be identified. Because embolic blockage is sudden in onset, symptoms usually are maximal at start. Symptoms may be transient as embolus is partially resorbed & 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 arterial tree. In paradoxical embolism, a deep vein thrombosis embolises through an atrial or ventricular septal defect in heart into brain.
Cardiac causes can be distinguished between high & low-risk:
High risk: atrial fibrillation & paroxysmal atrial fibrillation, rheumatic disease of mitral or aortic valve disease, artificial heart valves, known cardiac thrombus of atrium or ventricle, sick sinus syndrome, sustained atrial flutter, recent myocardial infarction, chronic myocardial infarction together with ejection fraction
Low risk/potential: calcification of annulus (ring) of 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 ascending aorta or proximal arch
Systemic hypoperfusion is reduction of blood flow to all parts of body. It’s 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 hypoperfusion. Because reduction in blood flow is global, all parts of brain may be affected: “watershed” areas – border zone regions supplied by major cerebral arteries. A watershed stroke refers to condition when blood supply to these areas is compromised. Blood flow to these areas doesn’t necessarily stop, but instead it may lessen to point where brain damage can occur. This phenomenon is referred to as “last meadow”. In irrigation, the last meadow receives least amount of water.
Cerebral venous sinus thrombosis leads to stroke due to locally increased venous pressure, & exceeds pressure generated by arteries. Infarcts are more likely to undergo hemorrhagic transformation (leaking of blood into damaged area) than other types of ischemic stroke.
It generally occurs in small arteries or arterioles & is commonly due to hypertension, intracranial vascular malformations (including cavernous angiomas or arteriovenous malformations), cerebral amyloid angiopathy, or infarcts into which secondary haemorrhage has occurred. Other potential causes are trauma, bleeding disorders, amyloid angiopathy, illicit drug use (amphetamines or cocaine). Hematoma enlarges until pressure from surrounding tissue limits its growth, or until it decompresses by emptying into the ventricular system, CSF or pial surface. A third of intracerebral bleed is into brain’s ventricles. ICH has a mortality rate of 44 percent after 30 days, higher than ischemic stroke or even very deadly subarachnoid hemorrhage (classified as type of stroke).
occurs because of a loss of blood supply to part of brain, initiating ischemic cascade. Brain tissue ceases to function if deprived of oxygen for more than 60 to 90 seconds & after approximately 3 hours, will suffer irreversible injury possibly leading to death of tissue, i.e., infarction. (This is why TPAs (Streptokinase, Alteplase) are given only until 3 hours since onset of a stroke.) Atherosclerosis may disrupt the blood supply by narrowing lumen of blood vessels leading to reduction of blood flow, by causing formation of blood clots within vessel, or by releasing showers of small emboli through disintegration of atherosclerotic plaques. Embolic infarction occurs when emboli formed elsewhere in circulatory system, typically in heart as a consequence of atrial fibrillation, or in carotid arteries, break off, enter cerebral circulation, then lodge in & occlude(block,shut in or out, fitting closely) brain blood vessels. Since blood vessels in brain are now occluded, brain becomes low in energy, & thus it resorts into using anaerobic respiration within region of brain tissue affected by ischemia. But, this kind of respiration 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’s an acid & disrupts normal acid-base balance in brain. The ischemia area is referred to as “ischemic penumbra”.
As oxygen or glucose becomes depleted in ischemic brain tissue, production of high energy phosphate compounds: adenosine triphosphate (ATP) fails, leading to failure of energy-dependent processes ( ion pumping) necessary for tissue cell survival. This sets off a series of interrelated events resulting in cellular injury & death. A major cause of neuronal injury is release of excitatory neurotransmitter glutamate. Concentration of glutamate outside cells of nervous system is normally kept low by so-called uptake carriers, which are powered by concentration gradients of ions (mainly Na+) across cell membrane. Stroke cuts off supply of oxygen & glucose which powers ion pumps maintaining these gradients. As a result transmembrane ion gradients run down, & glutamate transporters reverse their direction, releasing glutamate into extracellular space. Glutamate acts on receptors in nerve cells (especially NMDA receptors), producing an influx of calcium which activates enzymes that digest cells’ proteins, lipids & nuclear material. Calcium influx can lead to failure of mitochondria, & can lead further toward energy depletion & may trigger cell death due to apoptosis.
induces production of oxygen free radicals & other reactive oxygen species. These react with & damage number of cellular & extracellular elements. Damage to blood vessel lining or endothelium is particularly important. Many antioxidant neuroprotectants: uric acid & NXY-059 work at level of endothelium & not in brain per se. Free radicals directly initiate elements of apoptosis cascade by means of redox signaling.
These processes are same for any type of ischemic tissue & are referred to collectively as ischemic cascade. Brain tissue is vulnerable to ischemia since it has little respiratory reserve & 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 excitatory neurotransmitters, for example, have been shown experimentally to reduce tissue injury caused by ischemia. Agents that work in this way are referred to as being neuroprotective. Until recently, human clinical trials with neuroprotective agents have failed, with probable exception of deep barbiturate coma. Recently NXY-059, disulfonyl derivative of radical-scavenging spin trap phenylbutylnitrone, is reported to be neuroprotective in stroke. The agent appears to work at level of blood vessel lining or endothelium. After producing favorable results in one large-scale clinical trial, second trial failed to show favorable results.
In addition to injurious effects on brain cells, ischemia & infarction can result in loss of structural integrity of brain tissue & blood vessels, partly through release of matrix metalloproteases, & are zinc- & calcium-dependent enzymes that break down collagen, hyaluronic acid, & elements of connective tissue. Proteases contribute to this process. Loss of vascular structural integrity results in a breakdown of protective blood brain barrier that contributes to cerebral edema, which can cause secondary progression of brain injury.
In case with of any type of brain injury, immune system is activated by cerebral infarction & may under some circumstances exacerbate injury caused by infarction. Inhibition of inflammatory response has been shown experimentally to reduce tissue injury due to cerebral infarction, but this hasn’t proved out in clinical studies.
result in tissue injury by causing compression of tissue from an expanding hematoma or hematomas. This can distort & injure tissue. Pressure may lead to loss of blood supply to affected tissue with resulting infarction, & blood released by brain hemorrhage appears to have direct toxic effects on brain tissue & vasculature.
Stroke is diagnosed through several techniques: neurological examination (Nihss), CT scans (most often without contrast enhancements) or MRI scans, Doppler ultrasound, & arteriography. Ddiagnosis of stroke itself is clinical, with assistance from imaging techniques. Imaging techniques also assist in determining subtypes & cause of stroke. There’s yet no commonly used blood test for stroke diagnosis itself, though blood tests may be of help in finding out likely cause of stroke.
A physical examination, including taking a medical history of symptoms & a neurological status, helps giving an evaluation of location & severity of stroke. It can give standard score on e.g., NIH stroke scale.
Imaging: For diagnosing ischemic stroke in emergency setting:
CT scans (without contrast enhancements)
For diagnosing hemorrhagic stroke in emergency setting:
CT scans (without contrast enhancements)
For detecting chronic hemorrhages, MRI scan is more sensitive.
For the assessment of stable stroke, nuclear medicine scans SPECT & PET/CT may be helpful. SPECT documents cerebral blood flow & PET with FDG isotope metabolic activity of neurons.
When a stroke has been diagnosed, various other studies may be performed to determine underlying etiology. With current treatment & diagnosis options available, it’s of particular importance to determine whether there’s a peripheral source of emboli. Test selection may vary, since cause of stroke varies with age, comorbidity & clinical presentation.
Commonly used techniques include:
study of carotid arteries(detect carotid stenosis) or dissection of precerebral arteries
electrocardiogram (ECG) & echocardiogram: (identify arrhythmias & resultant clots in heart which may spread to brain vessels through bloodstream)
Holter monitor study: to identify intermittent arrhythmias
angiogram of cerebral vasculature: (if a bleed is thought to have originated from an aneurysm or arteriovenous malformation)
blood tests: to determine hypercholesterolemia, bleeding diathesis & some rarer cause: homocysteinuria
Given disease burden of strokes, prevention is an important public health concern. Primary prevention is less effective than secondary prevention (as judged by number needed to treat to prevent one stroke per year). Recent guidelines detail evidence for primary prevention in stroke. Because stroke may indicate underlying atherosclerosis, it’s important to determine patient’s risk for other cardiovascular diseases coronary heart disease. Conversely, aspirin confers some protection against first stroke in patients who’ve suffered myocardial infarction or patients with high cardiovascular risk.
Most important modifiable risk factors for stroke are high blood pressure(hbp) & atrial fibrillation (although magnitude of this effect is small: evidence from Medical Research Council trials is that 833 patients have to be treated for 1 year to prevent one stroke).
Other modifiable risk factors:
high blood cholesterol levels, diabetes, cigarette smoking (active & passive), heavy alcohol consumption & drug use, lack of physical activity, obesity, red meat consumption & unhealthy diet.
Alcohol use could predispose to ischemic stroke, & intracerebral & subarachnoid hemorrhage via multiple mechanisms (Example: via hypertension, atrial fibrillation, rebound thrombocytosis & platelet aggregation & clotting disturbances). Drugs most commonly associated with stroke are cocaine, amphetamines causing hemorrhagic stroke, but over-the-counter cough & cold drugs containing sympathomimetics.
No high quality studies have shown effectiveness of interventions aimed at weight reduction, promotion of regular exercise, reducing alcohol consumption or smoking cessation. Nonetheless, given large body of circumstantial evidence, best medical management for stroke includes advice on diet, exercise, smoking & alcohol use. Medication or drug therapy is 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. 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. Lowering blood pressure has been conclusively shown to prevent both ischemic & hemorrhagic strokes. It is equally important in secondary prevention. Even patients older than 80 years & those with isolated systolic hypertension benefit from antihypertensive therapy. Studies show that intensive antihypertensive therapy results in greater risk reduction. Available evidence doesn’t show large differences in stroke prevention between antihypertensive drugs. Other factors protection against other forms of cardiovascular disease should be considered & cost.
Patients with atrial fibrillation have a risk of 5% each year to develop stroke, & this risk is even higher in those with valvular atrial fibrillation. Depending on stroke risk, anticoagulation with medications coumarins or aspirin is warranted for stroke prevention.
High cholesterol levels have been inconsistently associated with (ischemic) stroke. Statins have been shown to reduce risk of stroke by about 15%. Since earlier meta-analyses of other lipid-lowering drugs didn’t show decreased risk, statins might exert their effect through mechanisms other than their lipid-lowering effects.
Patients with diabetes mellitus are 2 to 3 times more likely to develop stroke, & they commonly have hypertension & hyperlipidemia. Intensive disease control has been shown to reduce microvascular complications: nephropathy & retinopathy but not macrovascular complications like stroke.
Oral anticoagulants like warfarin have been mainstay of stroke prevention for over 50 years. However, several studies have shown that aspirin & antiplatelet drugs are highly effective in secondary prevention after a stroke or transient ischemic attack. Low doses of aspirin (E xample 75-150 mg) are as effective as high doses but have fewer side effects; lowest effective dose remains unknown. Thienopyridines (clopidogrel, ticlopidine) “might be slightly more effective” than aspirin & have a decreased risk of gastrointestinal bleeding, but they are more expensive. Their exact role remains controversial. Ticlopidine has more skin rash, diarrhea, neutropenia & thrombotic thrombocytopenic purpura. Dipyridamole can be added to aspirin therapy to provide a small additional benefit, even though headache is common side effect. Low-dose aspirin is also effective for stroke prevention after sustaining a myocardial infarction. Except for in atrial fibrillation, oral anticoagulants aren’t advised for stroke prevention; any benefit is offset by bleeding risk.
In primary prevention, antiplatelet drugs didn’t reduce risk of ischemic stroke while increasing risk of major bleeding. Further studies are needed to investigate possible protective effect of aspirin against ischemic stroke in women.
Surgical procedures, carotid endarterectomy or carotid angioplasty, can be used to remove significant atherosclerotic narrowing (stenosis) of carotid artery, which supplies blood to brain. There’s a large body of evidence supporting this procedure in selected cases. Endarterectomy for a significant stenosis has been shown to be useful in the secondary prevention after a previous symptomatic stroke. Carotid artery stenting hasn’t been shown to be equally useful. Patients are selected for surgery based on age, gender, degree of stenosis, time since symptoms & patients’ preferences. Surgery is most efficient when not delayed too long. Risk of recurrent stroke in patient who has 50% or greater stenosis is up to 20% after 5 years, but endarterectomy reduces this risk to around 5%. Number of procedures needed to cure one patient was 5 for early surgery (within two weeks after the initial stroke), but 125 if delayed longer than 12 weeks.
Screening for carotid artery narrowing hasn’t been shown to be useful screening test in general population. Studies of surgical intervention for carotid artery stenosis without symptoms have shown only a small decrease in risk of stroke. To be beneficial, complication rate of 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 surgery itself, & 89 will remain stroke-free but would also have done so without intervention.
Nutritional & metabolic interventions:
Nutrition, specifically Mediterranean-style diet, has potential of more than halving stroke risk.
With regard to lowering homocysteine, meta-analysis of previous trials has concluded lowering homocysteine with folic acid & other supplements may reduce stroke risk. However, 2 largest randomized controlled trials included in meta-analysis had conflicting results. One reported positive results; whereas other was negative.
European Society of Cardiology & European Association for Cardiovascular Prevention & Rehabilitation have developed an interactive tool for prediction & managing risk of heart attack & stroke in Europe. Heart Score is aimed at supporting clinicians in optimising individual cardiovascular risk reduction. Heartscore Programme is available in 12 languages & offers web based or PC version.
Tredit Stroke unitIdeally, people who have had a stroke are admitted to a “stroke unit”, a ward or dedicated area in hospital staffed by nurses & therapists with experience in stroke treatment. It has been shown people admitted to a stroke unit have a higher chance of surviving than those admitted elsewhere in hospital, even if they are being cared for by doctors without experience in stroke.
When an acute stroke is suspected by history & physical examination, goal of early assessment is to determine cause. Treatment varies according to underlying cause of stroke, thromboembolic (ischemic) or hemorrhagic. A non-contrast head CT scan can rapidly identify a hemorrhagic stroke by imaging bleeding in or around the brain. If no bleeding is seen, a presumptive diagnosis of ischemic stroke is made.
Treatment of ischemic stroke:
An ischemic stroke is caused by thrombus (blood clot) occluding blood flow to an artery supplying brain. Definitive therapy is aimed at removing blockage by breaking clot down (thrombolysis), or by removing it mechanically (thrombectomy). More rapidly blood flow is restored to brain, fewer brain cells die.
Other medical therapies are aimed at minimizing clot enlargement or preventing new clots from forming. Treatment with medications: aspirin, clopidogrel, & dipyridamole may be given to prevent platelets from aggregating.
In regards to definitive therapies, management of acute stroke includes control of blood sugars, ensuring patient has adequate oxygenation & adequate intravenous fluids. Patients may be positioned with their heads flat on stretcher, rather than sitting up, to increase blood flow tobrain. It’s common for blood pressure to be elevated immediately following stroke. Although high blood pressure may cause some strokes, hypertension during acute stroke is desirable to allow adequate blood flow to brain.
Increasing numbers of primary stroke centers, pharmacologic thrombolysis (“clot busting”) with drug tissue plasminogen activator (tPA), is used to dissolve clot & unblock artery. Use of tPA in acute stroke is controversial. It’s endorsed by American Heart Association & American Academy of Neurology recommended treatment for acute stroke within 3 hours of onset of symptoms as long as there’re not other contraindications (like abnormal lab values, high blood pressure, or recent surgery). This position for tPA is based upon findings of 2 studies by one group of investigators which showed tPA improves chances for good neurological outcome. When administered within first 3 hours thrombolysis improves functional outcome without affecting mortality.
A recent study using alteplase for thrombolysis in ischemic stroke suggests clinical benefit with administration 3 to 4.5 hours after stroke onset. However, in NINDS trial 6.4% of patients with large strokes developed substantial brain hemorrhage as a complication from being given tPA. A recent study found mortality to be higher among patients receiving tPA versus those who didn’t. It ‘s position of American Academy of Emergency Medicine objective evidence regarding efficacy, safety, & applicability of tPA for acute ischemic stroke is insufficient to warrant its classification as standard of care. Intra-arterial fibrinolysis, where a catheter is passed up an artery into brain & medication is injected at site of thrombosis, has been found to improve outcomes in people with acute ischemic stroke.
Another intervention for acute ischemic stroke is removal of offending thrombus directly. This is accomplished by inserting a catheter into emoral artery, directing it into cerebral circulation, & deploying a corkscrew-like device to ensnare clot, which is then withdrawn from body. Mechanical embolectomy devices have been demonstrated effective at restoring blood flow in patients who were unable to receive thrombolytic drugs or for whom drugs were ineffective, though no differences have been found between newer & older versions of devices. Devices have only been tested on patients treated with mechanical clot embolectomy within 8 hours of onset of symptoms.
Angioplasty & stenting:
Angioplasty & stenting have begun to be looked at as possible viable options in treatment of acute ischemic stroke. Systematic review of 6 uncontrolled, single-center trials, involving total of 300 patients, of intra-cranial stenting in symptomatic intracranial arterial stenosis, rate of technical success (reduction to stenosis of
Secondary prevention of ischemic stroke:
Anticoagulation can prevent recurrent stroke. Among patients with nonvalvular atrial fibrillation, anticoagulation can reduce stroke by 60% while antiplatelet agents can reduce stroke by 20%. Recent meta-analysis suggests harm from anti-coagulation started early after an embolic stroke. Stroke prevention treatment for atrial fibrillation is determined according to CHADS/CHADS2 system. Most widely used anticoagulant to prevent thromboembolic stroke in patients with nonvalvular atrial fibrillation is oral agent Warfarin while dabigatran is new alternative & doesn’t require prothrombin time monitoring.
If studies show carotid stenosis, & patient has residual function in affected side, carotid endarterectomy (surgical removal of stenosis) may decrease risk of recurrence if performed rapidly after stroke.
Treatment of hemorrhagic stroke:
Patients with intracerebral hemorrhage require neurosurgical evaluation to detect & treat cause of bleeding, many may not need surgery. Anticoagulants & antithrombotics, key in treating ischemic stroke, can make bleeding worse & cann’t be used in intracerebral hemorrhage. Patients are monitored for changes in level of consciousness, & blood pressure, blood sugar, & oxygenation are kept at optimum levels.
Care and rehabilitation:
Stroke rehabilitation is process by which patients with disabling strokes undergo treatment to help them return to normal life by regaining & relearning skills of everyday living. It aims to help survivor understand & adapt to difficulties, prevent secondary complications & educate family members to play supporting role.
Rehabilitation team is usually multidisciplinary as it involves staff with different skills working together to help patient. These include nursing staff, physiotherapy, occupational therapy, speech & language therapy, & usually a physician trained in rehabilitation medicine. Some teams may include psychologists, social workers, & pharmacists since at least one third of patients manifest post stroke depression. Validated instruments: Barthel scale may be used to assess 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 & monitoring vital signs: temperature, pulse, & blood pressure. Stroke rehabilitation begins almost immediately.
For most stroke patients, physical therapy (PT), occupational therapy (OT) & speech-language pathology (SLP) are cornerstones of rehabilitation process. Assistant technology: wheelchair, walkers, canes, & orthosis may be beneficial. PT & OT have overlapping areas of working but their main attention fields are; PT focuses on joint range of motion & strength by performing exercises & re-learning functional tasks: bed mobility, transferring, walking & other gross motor functions. Physiotherapists can work with patients to improve awareness & use of hemiplegic side. Rehabilitation involves working on ability to produce strong movements or ability to perform tasks using normal patterns. Emphasis is often concentrated on functional tasks & patient’s goals. Example: physiotherapists employ to promote motor learning involves constraint-induced movement therapy. Through continuous practice patient relearns to use & adapt hemiplegic limb during functional activities to create lasting permanent changes. OT is involved in training to help relearn everyday activities known as Activities of daily living (ADLs): eating, drinking, dressing, bathing, cooking, reading , writing, & toileting. Speech & language therapy is appropriate for patients with speech production disorders: dysarthria & apraxia of speech, aphasia, cognitive-communication impairments &/or dysphagia (problems with swallowing).
Patients may have particular problems, like dysphagia , which can cause swallowed material to pass into lungs & cause aspiration pneumonia. Condition may improve with time, but in interim, nasogastric tube may be inserted, enabling liquid food to be given directly into stomach. If swallowing is still deemed unsafe, a percutaneous endoscopic gastrostomy (PEG) tube is passed & can remain indefinitely.
Treatment of spasticity related to stroke nvolves early mobilisations, commonly performed by physiotherapist, combined with elongation of spastic muscles & sustained stretching through various positioning. Gaining initial improvements in range of motion is often achieved through rhythmic rotational patterns associated with affected limb. After full range has been achieved by therapist, limb should be positioned in lengthened positions to prevent against further contractures, skin breakdown, & disuse of limb with use of splints or other tools to stabilize joint. Cold in form of ice wraps or ice packs have been proven to briefly reduce spasticity by temporarily dampening neural firing rates. Electrical stimulation to antagonist muscles or vibrations has been used with some success.
Stroke rehabilitation should be started quickly as possible & can last anywhere from a few days to over a year. Most return of function is seen in first few months, & then improvement falls off with “window” considered officially by U.S. state rehabilitation units & others to be closed after 6 months, with little chance of further improvement. However, patients have been known to continue to improve for years, regaining & strengthening abilities like writing, walking, running, & talking. Daily rehabilitation exercises should continue to be part of stroke patient’s routine. Complete recovery is unusual but not impossible & most patients will improve to some extent: proper diet & exercise are known to help brain to recover.
Some current & future therapy methods include use of virtual reality & video games for rehabilitation. These forms of rehabilitation offer potential for motivating patients to perform specific therapy tasks that many other forms don’t. Many clinics & hospitals are adopting use of these off-the-shelf devices for exercise, social interaction & rehabilitation because they are affordable, accessible & can be used within clinic & home.
Disability affects 75% of stroke survivors enough to decrease their employability. Stroke can affect patients physically, mentally, emotionally, or a combination of the 3. Results of stroke vary widely depending on size & location of lesion. Dysfunctions correspond to areas in brain that have been damaged.
Some physical disabilities 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, & pain. If stroke is severe enough, or in certain location like parts of brainstem, coma, or death can result.
Emotional problems resulting from stroke can result from direct damage to emotional centers in brain or from frustration & difficulty adapting to new limitations. Post-stroke emotional difficulties include: anxiety, panic attacks, flat affect (failure to express emotions), mania, apathy, & psychosis.
30 to 50% of stroke survivors suffer post stroke depression, characterized by lethargy, irritability, sleep disturbances, lowered self esteem, & withdrawal. Depression can reduce motivation & worsen outcome, but can be treated with antidepressants.
Emotional liability, another consequence of stroke, causes patient to switch quickly between emotional highs & lows & to express emotions inappropriately. Example: excess of laughing or crying with little or no provocation. While these expressions of emotion usually correspond to patient’s actual emotions, a more severe form of emotional liability causes patients to laugh & cry pathologically, without regard to context or emotion. Some patients show opposite of what they feel. Example: crying when they are happy. Emotional lability occurs in about 20% of stroke patients.
Cognitive deficits resulting from stroke: perceptual disorders, speech problems, dementia, & problems with attention & memory. A stroke sufferer may be unaware of his or her own disabilities, a condition called anosognosia. In a condition called hemispatial neglect, patient is unable to attend to anything on side of space opposite to damaged hemisphere.
Up to 10% of all stroke patients develop seizures, most commonly in week subsequent to event; severity of stroke increases likelihood of a seizure.
Stroke could soon be most common cause of death worldwide. Stroke is currently second leading cause of death in Western world, ranking after heart disease & before cancer, & causes 10% of deaths worldwide. Geographic disparities in stroke incidence have been observed & existence of a “stroke belt” in southeastern US, but causes of disparities haven’t been explained.
Incidence of stroke increases exponentially from 30 years of age, & etiology varies by age. Advanced age is one of most significant stroke risk factors. 95% of strokes occur in people age 45 & older, & two-thirds of strokes occur in those over age of 65. Person’s risk of dying if he or she does have a stroke increases with age. Stroke can occur at any age, including in childhood.
Family members may have genetic tendency for stroke or share lifestyle that contributes to stroke. Higher levels of Von Willebrand factor are more common amongst people who have had ischemic stroke for first time. Results of this study found only significant genetic factor was person’s blood type. Having had a stroke in past greatly increases one’s risk of future strokes.
Men are 25% more likely to suffer strokes than women, yet 60% of deaths from stroke occur in women. Women live longer, are older on average when they have their strokes, & are more often killed. Some risk factors for stroke apply only to women. Primary among these are pregnancy, childbirth, menopause & treatment thereof (HRT).
Episodes of stroke & familial stroke have been reported from 2nd millennium BC onward in ancient Mesopotamia & Persia. Hippocrates (460 to 370 BC) was first to describe phenomenon of sudden paralysis that is often associated with ischemia. Apoplexy, from Greek word meaning “struck down with violence,” first appeared in Hippocratic writings to describe this phenomenon.
Word “stroke” was used as a synonym for apoplectic seizure as early as 1599, & is a fairly literal translation of Greek term.
In 1658, in his Apoplexia, Johann Jacob Wepfer (1620-1695) identified cause of hemorrhagic stroke when he suggested that people who had died of apoplexy had bleeding in their brains. Wepfer identified the main arteries supplying the brain, the vertebral & carotid arteries, and identified the cause of ischemic stroke (or cerebral infarction) when he suggested that apoplexy might be caused by blockage to those vessels.
Rudolf Virchow first described mechanism of thromboembolism as a major factor.
Second Stroke Risk NOT Tied to Aspirin:
Risk of suffering a second bleeding, or “hemorrhagic” stroke, after having suffered 1st isn’t increased by taking aspirin, new study finds. Past research had raised concerns whether aspirin & hemorrhagic stroke risk; aspirin is known blood thinner & may increase bleeding; new study published in Journal Neurology concludes: there’s no evidence of aspirin users experiencing higher repeat-strokes than those patients who don’t take aspirin. Doctors frequently prescribe aspirin to victims of ischemic stroke-type of stroke which is caused by blockage of blood vessels, resulting in insufficient oxygen to brain. Study’s authors hope to put to rest concerns about aspirin; don’t recommend that aspirin be prescribed as widely among hemorrhagic stroke sufferers as among ischemic stroke sufferers.
Symptoms: start suddenly, over seconds to minutes, & in most cases don’t progress further. Symptoms depend on area of brain affected. More extensive area of brain affected, more functions are likely to be lost. Some forms of stroke can cause additional symptoms. Most forms of stroke aren’t associated with headache, apart from sub arachnoid hemorrhage & cerebral venous thrombosis & occasionally in tracerebral hemorrhage.
Various systems have been proposed to increase recognition of stroke by patients, relatives & emergency first responders. A systematic review, updating a previous systematic review from ’94, looked at number of trials to evaluate how well different physical examination findings are able to predict presence or absence of stroke. It was found sudden-onset face weakness, arm drift (when person asked to raise both arms, involuntarily lets one arm drift downward) & abnormal speech are findings most likely to lead to correct identification of a case of stroke (+ likelihood ratio of 5.5 when at least one of these is present). Similarly, when all three of these are absent, likelihood of stroke is significantly decreased (likelihood ratio of 0.39). While these findings aren’t perfect for diagnosing stroke, fact that they can be evaluated relatively rapid & easily make them very valuable.
Proposed systems include FAST (stroke) (face, arm, speech, & time), as advocated by Dept. of Health (United Kingdom) & Stroke Association, American Stroke Association (http://www.strokeassociation.org/) , National Stroke Association (US http://www.stroke.org/), Los Angeles Prehospital Stroke Screen (LAPSS) & Cincinnati Prehospital Stroke Scale (CPSS). Use of scales is recommended by professional guidelines.
People referred to emergency room, early recognition of stroke is deemed important as this can expedite diagnostic tests & treatments. A scoring system called ROSIER (recognition of stroke in emergency room) is recommended for this purpose; it’s based on features from medical history & physical examination.