
[Middle English, probably from Old English *strāc.]

[Middle English stroken, from Old English strācian, from *strāc, stroke. See stroke1.]
stroker strok'er n.For more information on stroke, visit Britannica.com.
(1) In printing, the weight, or thickness, of a character. For example, in the LaserJet, one of the specifications of the font description is the stroke weight from lightest to boldest. See stroke weight.
(2) In computer graphics, a pen or brush stroke. The stroke function lets you set the width of the line being drawn.
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Also known as cerebrovascular accident (CVA); damage to brain tissue by hypoxia due to blockage of a blood vessel as a result of thrombosis, atherosclerosis, or haemorrhage. The severity and nature of the effects of the stroke depend on the region of the brain affected and the extent of damage. Hypertension and hypercholesterolaemia are major risk factors.
An interruption of the blood supply to the brain. A blood clot, a head injury, or a burst blood vessel in the brain (an aneurysm) can cause strokes. The main risk factors associated with strokes are high blood pressure, heart diseases, diabetes, smoking, obesity, and physical inactivity.
A stroke results in a portion of the brain being deprived of oxygen often leading to some type of paralysis, but small strokes may occur without symptoms. Large strokes can result in severe paralysis or death. Regular exercise and a healthy, balanced diet lower blood pressure and cholesterol levels, and so can reduce the risk of a stroke.
Apoplexy or stroke has been recognized at least since the beginning of Western medicine, in ancient Greece. Stroke arises from injury to the brain caused by interruption of the blood supply, rather like a heart attack: in fact stroke is now sometimes called a ‘brain attack’. Over 250 000 people suffer some type of stroke in the UK each year. Stroke now is the third leading cause of death and the most common cause of adult disability.
The most typical manifestations include sudden weakness of the face, arm, or leg, and altered sensation or numbness, on the side of the body opposite the stroke. Language expression and comprehension can be impaired, usually for strokes in the left cerebral hemisphere. A stroke in the occipital lobe, at the back of the hemisphere, can cause blindness in the opposite half of the visual field. Sometimes a stroke in the parietal lobe of the right hemisphere renders the patient unable to attend to the left hand side of objects or even without awareness of the left side of their own body (the so-called neglect syndrome). Most bizarre of all, damage to the right hemisphere can produce anosagnosia — denial by the patient of any deficit at all, despite virtual paralysis of the left arm and leg.
The brain — especially the cerebral cortex, a frequent target of strokes — is divided into distinct regions, functionally specialized for one sense or another, for the control of movement, for aspects of language, etc. The sensory, motor, linguistic, and cognitive deficits caused by small strokes can therefore be extraordinarily specific, and their interpretation by neuropsychologists has been a major source of evidence about the organization of the human brain. But major strokes can have devastating effects, sometimes eliminating consciousness completely, or, perhaps even worse, leaving a conscious mind in a useless body. The French writer Jean-Dominique Bauby gives a unique view of this state in his autobiography — paralysed except for the capacity to blink an eye, he described himself as a ‘butterfly’ trapped inside a ‘diving bell’.
In 1761, Battista Morgagni, Professor of Anatomy in Padua, first clearly attributed strokes to limitation of blood flow to the brain. In 85% of cases this comes from blockage of a blood vessel giving a so-called ischaemic stroke. Most of the remaining 15% are due to sudden bleeding into the substance of the brain to create a haemorrhagic stroke. A small percentage are due to rupture of an artery in the surface of the brain — a subarachnoid haemorrhage.
The brain is metabolically highly active. Although it accounts for only about 2% of the body weight, it uses 20% of the total oxygen intake and has a high demand for the blood sugar, glucose. At least 15% of the blood output from the heart is needed to supply this amount of oxygen and glucose. If this blood flow is interrupted, even for minutes, then brain cells die. The pattern of clinical deficits after strokes (other than subarachnoid haemorrhage) is determined by the particular blood vessel that is primarily affected. Interruption of flow in the left middle cerebral artery, for example, typically leads to specific impairments of language or calculation, while occlusion of the right middle cerebral artery may disturb visual-spatial skills. Subarachnoid haemorrhages lead to changes in pressure on the brain and chemical effects that cause more general deficits.
The most common cause of ischaemic strokes is blocking of a vessel by a so-called embolus, which forms on a pathologically abnormal wall of a larger vessel and then detaches and circulates in the blood. The wall of the larger vessel, particularly in areas of high-flow turbulence and around major bifurcations (e.g. the point at which the internal carotid artery branches off from the aorta), may become thickened and irregular, and calcified atherosclerotic plaques may form. Rupture of these plaques can form a blood clot, fragments of which can be carried along the course of flowing blood to block smaller vessels. Alternatively, platelets that aggregate on the abnormal surface of a plaque, or fragments of the plaque, can themselves act as emboli. Emboli also can be formed in the heart, or, more rarely, can come from elsewhere in the body.

— Paul M. Matthews
Bibliography
See also apoplexy; brain; language and the brain; paralysis.
Definition
A stroke, also called a cerebral infarction, is a life-threatening condition marked by a sudden disruption in the blood supply to the brain.
Description
A disruption in the blood supply to the brain starves the brain of oxygen-rich blood and causes the nerve cells in that area to become damaged and die within minutes. The body parts controlled by those damaged brain cells lose their ability to function.
Depending on the area of the brain that is affected, a stroke can alter many aspects of a child's functioning such as speech, movement, behavior and learning. A stroke also may cause weakness or paralysis on one side of the body. The loss of function may be mild or severe, temporary or permanent.
If medical treatment begins within hours after symptoms are recognized, brain damage can be limited and the risk of permanent medical effects can be decreased.
Types of Stroke
An ischemic stroke—the most common form of stroke in children under age 15—is caused by a blocked or narrowed artery. In children, blockages may be caused by a blood clot, injury to the artery, or rarely in children, atherosclerosis (build-up of fatty deposits on the blood vessel walls). A cerebral thrombosis is a blood clot that develops at the clogged part of the blood vessel. A cerebral embolism is a blood clot that travels to the clogged blood vessel from another location in the circulatory system.
A hemorrhagic stroke—the more common form of stroke in infants and children under age two—occurs when a weakened blood vessel leaks or bursts, causing bleeding in the brain tissue or near the surface of the brain.
Two types of weakened blood vessels usually cause hemorrhagic stroke, including:
A transient ischemic attack (TIA), also called a "mini stroke," is characterized by a short-term blood vessel obstruction or clot that tends to resolve itself quickly, usually within 10–20 minutes, or up to 24 hours. A TIA usually does not require intervention. However, a TIA is a strong indicator of an ischemic stroke and should be evaluated in the same way as a stroke to prevent a more serious attack.
In children, strokes can be categorized as:
Demographics
Childhood stroke is relatively rare, occurring in about two to three of every 100,000 children aged one to 14 per year. In comparison, stroke occurs in about 100 of every 100,000 adults per year. The rate of ischemic stroke and hemorrhagic stroke is similar among children aged one to 14.
Stroke occurs more frequently in children under age two, and peaks in the perinatal period. In the National Hospital Discharge Survey from 1980-1998, the rate of stroke for infants less than 30 days old (per 100,000 live births per year) was 26.4, with rates of 6.7 for hemorrhagic stroke and 17.8 for ischemic stroke.
More fatal strokes occur in African-American children than white children, mirroring the racial differences of stroke in adults. Compared to the stroke risk of white children, African-American children have an increased relative risk of 2.12, Hispanics a decreased relative risk of 0.76 and Asians have a similar risk. Boys have a 1.28-fold higher risk of stroke than girls and have a higher case-fatality rate for ischemic stroke than girls. The increased risk among African Americans is not explained by the presence of sickle cell disease, nor is the excess risk among boys explained by trauma.
Research conducted by the National Institute of Neurological Diseases and Stroke (NINDS) indicates a "stroke belt," or geographical area where fatal strokes are more predominant. This stroke belt includes Alabama, Arkansas, Georgia, Indiana, Kentucky, Louisiana, Mississippi, North Carolina, South Carolina, Tennessee, and Virginia. Researchers examined death certificates over a 19-year period and found a 21 percent higher risk of death from stroke in people under age 20 in the stroke belt states had compared with the same age group in other states. During the same period, people over age 25 in the stroke belt region had a 20 percent higher risk of death from stroke. Because the overall rate of stroke in children is low, researchers warn parents in these states not to be too alarmed. However, the findings indicate further investigation is needed.
Causes and Symptoms
Causes
The cause of childhood stroke is unknown in one-third of cases, and an underlying medical condition or multiple conditions appear to contribute to over half of the cases. The most common causes of stroke are congenital (present at birth) and acquired heart diseases, and sickle cell anemia.
About 10–15 percent of children with sickle cell disease suffer a stroke, usually ischemic stroke. Sickle cell disease is a blood disorder in which the blood cells cannot carry oxygen to the brain because the blood vessels to the brain are either narrowed or closed.
One rare cause of stroke is an extreme case of the chickenpox virus, which causes a narrowing of blood vessels in the head for some children.
RISK FACTORS. Although obesity, high cholesterol, high blood pressure, atherosclerosis, and smoking are common stroke risk factors in adults, they rarely contribute to stroke risk in children. Risk factors for childhood stroke include a family history of stroke, cardiovascular disease or diabetes, as well as the presence of the conditions listed below.
Some of the more common congenital heart diseases that increase the risk of childhood stroke include:
Some of the acquired heart conditions that increase the risk of childhood stroke include:
Possible traumas that increase the risk of childhood stroke include birth injury or trauma, child abuse, or other injury or trauma.
Because of the wide range of secondary conditions that contribute to stroke, it is difficult for researchers to assess the relative contribution of each risk factor to the problem of cerebrovascular disease as a whole, according to the Child Neurology Society Ad Hoc Committee on Stroke in Children. In addition, this variability also hinders clinical research.
Symptoms
In infants and very young children, stroke symptoms are sudden and include:
In older children, stroke symptoms are sudden and include:
Other stroke signs and symptoms include:
If the child seems to recover quickly from these stroke symptoms, a TIA may have occurred. All neurological symptoms should serve as a stroke "warning sign" and could indicate a pending, more serious attack. The child should receive prompt evaluation so necessary preventive therapies can be initiated.
WHEN TO CALL THE DOCTOR. If a child has any of the symptoms listed above, the parent or caregiver should immediately dial 9-1-1 to seek emergency care. It is important not to wait to see if symptoms subside; a stroke is a medical emergency. Until the paramedics arrive, the parent or caregiver should follow these first aid guidelines:
Diagnosis
In most children, the diagnosis of stroke is delayed by more than 24 hours from the onset of symptoms. This delay is thought to occur because there is a lack of general awareness by physicians and families of cerebrovascular disorders in children. However, early recognition and treatment of a stroke could improve management, reduce the risk of brain damage and permanent disability, help prevent a recurrence, and initiate a proper treatment and rehabilitation program to maximize functional recovery.
The diagnosis of pediatric stroke generally occurs in the emergency room and includes:
The medical history helps the physician evaluate the presence of other conditions or disorders that might have caused the stroke. The child's family medical history is evaluated to determine if there is a history of cardiovascular or neurological diseases that might increase the risk of blood clots.
The brief neurological exam includes a review of the patient's mental status, motor and sensory system, deep tendon reflexes, coordination, and walking pattern (gait). The cranial nerve function also will be evaluated and includes a review of the patient's visual function and eye movement, strength of facial muscles, the gag reflex, tongue and lip movements, ability to smell and taste, hearing, and sensation and movement of the face, head, and neck.
Questions about the child's condition may include:
During the physical exam, the child's pulse, blood pressure, and height and weight are checked and recorded.
Diagnostic tests include:
MRI is more sensitive than CT scanning for the diagnosis of an ischemic stroke within 24 hours. However, the two tests are comparable when used to evaluate the effects of a hemorrhagic stroke.
In rare cases or when carotid artery disease is suspected, additional tests may include a carotid ultrasound or cerebral or carotid angiogram. Other tests to diagnose stroke may include a transcranial Doppler ultrasound and neurosonogram. In a transcranial Doppler ultrasound, sound waves are used to measure blood flow in the vessels of the brain. In a neurosonogram, ultra high frequency sound waves are used to analyze blood flow and possible blockages in the blood vessels in or leading to the brain.
If a pediatric stroke is diagnosed, additional tests may be performed to assess the overall function
Treatment
Initial treatment depends on the type of stroke. For an ischemic stroke, initial emergent treatment focuses on restoring blood flow to the brain. For a hemorrhagic stroke, the goal of initial treatment is to control the bleeding. Children with a hemorrhagic stroke may be transferred to a center with neurosurgical facilities so the proper treatment, such as decompression or hydrocephalus drainage, can be provided by skilled specialists.
Emergency-room treatment may include: oxygen to ensure the brain is getting the maximum amount, control of body temperature, assessment and treatment of breathing difficulties, intravenous fluids to prevent or treat dehydration, and medications to control blood pressure and prevent blood clotting. Blood transfusions may be used to treat children with sickle cell disease.
Treatment Team
Treatment should be provided by a pediatric neurologist and a multi-disciplinary team of specialists that may include a physical therapist, occupational therapist, speech therapist, social worker, and other specialists as needed to meet the child's individual needs.
Medications
Adult stroke patients who receive treatment within three hours after the onset of stroke symptoms may receive a "clot-busting" medication called t-PA. However, the diagnosis of stroke is rarely made within three hours, so the use of this drug in children is uncommon.
Anticoagulant medications, including heparin or warfarin and low-dose aspirin, may be used to reduce the risk of blood clot formation. Although experience with these medications in children suggests they are safe, their use in children remains controversial because of the risk of Reye's syndrome. Sometimes the potential benefits of these medications outweigh the small risk of side effects. Researchers agree that further studies are needed to determine the proper dosage and effectiveness of aspirin and other anticoagulant medications for treating stroke in children.
The most important medication guidelines are: 1) Ensure your child takes all medications exactly as prescribed; 2) Never discontinue any medication without first talking to the child's doctor, even if the medication does not seem to be working or is causing unwanted side effects; and 3) Follow-up with the child's health care provider as recommended to monitor the effects of the medication. Frequent blood tests are required for people taking anticoagulants to evaluate the dosage and effects of the medication.
Other stroke medications that are still being tested in clinical trials include:
Rehabilitation
After the child's condition has stabilized, rehabilitation is initiated. Rehabilitation includes physical, occupational, and speech therapy. Therapy is usually initiated as soon as possible after a stroke and is often the most intense in the early stages of recovery. Clinicians should work with the child and the parents or caregivers to develop an individual treatment plan. Specific treatment goals will vary from one child to the next but will focus on restoring maximum function and independence, helping the child return to normal activities, and improving the child's quality of life. The child's progress after rehabilitation will depend upon which area of the brain was affected, the cause of stroke, the extent of injury, and the presence of other medical conditions.
Physical therapy includes stretching exercises, muscle group strengthening exercises, and range of motion exercises to preserve flexibility and range of motion. Exercises should be practiced daily, as recommended by the physical therapist. A physical therapist can instruct the patient on proper posture guidelines to maintain proper alignment of the hips and back. Balancing rest and exercise is also important.
Occupational therapy may include splints, casts, or braces on the affected arm or leg to enable proper limb positioning, prevent joint stiffness, and maintain flexibility and range of motion. An occupational therapist can recommend assistive equipment and devices to help the child with activities of daily living, such as bathing, dressing, and eating. If a walker or wheelchair are needed, an occupational therapist can provide specific instructions.
Physical and occupational therapists can provide guidelines on how to adapt the child's home and school environments to ensure safety and comfort.
Speech therapy will focus on the child's specific needs which may include any or all aspects of language use, such as speaking, reading, writing, and understanding the spoken word. Speech and language problems (aphasia) usually occur when a stroke affects the right side of the body.
Behavioral problems and learning disabilities, such as difficulties with attention or concentration, may become apparent when the child goes to school, so specific treatments and educational assistance may be needed to address these problems. A formal assessment can help parents identify potential behavioral and learning problems.
Surgery
The need for surgical treatment for pediatric stroke will depend on a number of factors, including the type of stroke, extent of damage from stroke, the child's age, and potential benefits and risks. Sometimes urgent surgery is necessary soon after the child is admitted to the emergency room to remove a blood clot and restore oxygen flow to the brain tissue.
Treatment options for hemorrhagic stroke may include surgery, sterotactic radiotherapy, or interventional neuroradiology to treat the underlying aneurysm or arteriovenous malformation.
There are several surgical procedures to repair an aneurysm that may have caused a hemorrhagic stroke. A clip may be placed across the neck of the aneurysm (like a clip at the end of a balloon) to stop the bleeding. A newer approach is to thread a long, thin tube through the artery that leads to the aneurysm. Then a tiny coil is fed through the tube into the aneurysm "balloon" to fill the space and seal off the bleeding.
An interventional procedure called carotid angioplasty may be performed to treat a blockage or blockages in the carotid arteries. During the procedure, a tiny balloon at the end of a long, thin tube (called a catheter) is pushed through the artery to the blockage. When the balloon is inflated, it opens the artery. In addition, a mesh tube (called a stent) may be placed inside the artery to help hold it open.
Carotid endarterectomy is a surgical procedure performed to remove a blockage from the carotid artery. During the operation, the surgeon scrapes away plaque from the wall of the artery so blood can flow freely through the artery to the brain.
Intracranial bypass surgery is a surgical procedure performed to restore blood flow around a blocked blood vessel in the brain. During the surgery, a healthy blood vessel, on the outside of the scalp, is re-routed to the part of the brain that is not getting enough blood flow. This new blood vessel bypasses the blocked vessel and provides an additional blood supply to areas of the brain that were deprived of blood. When blood flow is restored, the brain works normally, and the symptoms disappear. This procedure is not as common as the other surgical treatments listed above to treat pediatric stroke but it may be used to treat recurrent TIAs.
Alternative Treatment
Alternative and complementary therapies include approaches that are considered to be outside the mainstream of traditional health care.
Techniques that induce relaxation and reduce stress, such as yoga, Tai Chi, meditation, guided imagery, and relaxation training, may be helpful in controlling blood pressure. Acupuncture and biofeedback training also may help induce relaxation. Before learning or practicing any particular technique, it is important for the parent/caregiver and child to learn about the therapy, its safety and effectiveness, potential side effects, and the expertise and qualifications of the practitioner. Although some practices are beneficial, others may be harmful to certain patients.
Alternative treatments should not be used as a substitute for medical therapies prescribed by a doctor. Parents should discuss these techniques and treatments with the child's doctor to determine the remedies that may be beneficial for the child.
Nutritional Concerns
Dietary guidelines are individualized, based on the child's age, diagnosis, overall health, and level of functioning. Specific nutritional problems, such as swallowing or feeding difficulties, may be a concern in some patients and should be managed by a team of specialists including a speech therapist. Early identification, treatment, and correction of specific feeding problems will improve the health and nutritional status of the child.
A child's self-feeding skills can impact his or her health outcome. One study indicated that 90 percent of children with good to fair motor and feeding skills reached adulthood. In contrast, a lack of self-feeding skills was associated with a six-fold increase in mortality (rate of death).
Maintaining a healthy weight is important to prevent the development of chronic diseases such as diabetes, high blood pressure (hypertension), and heart disease.
Tube feedings may be required in some patients with failure to thrive, aspiration pneumonia, difficulty swallowing, or an inability to ingest adequate calories orally to maintain nutritional status or promote growth.
A well-balanced and carefully planned diet will help maintain general good health for children who have suffered a stroke. In general, children should follow the same low-fat, high fiber diet that is recommended for the general population.
In children older than age two, the following low-fat dietary guidelines are recommended:
If the child has high blood pressure, the DASH diet is recommended. The "Dietary Approaches to Stop Hypertension (DASH)" study, sponsored by the National Institutes of Health (NIH), showed that elevated blood pressures were reduced by an eating plan that emphasized fruits, vegetables, and low-fat dairy foods and was low in saturated fat, total fat, and cholesterol. The DASH diet includes whole grains, poultry, fish, and nuts. Fats, red meats, sodium, sweets, and sugar-sweetened beverages are limited. Sodium should also be reduced to no more than 1,500 milligrams per day.
Prognosis
Cerebrovascular disorders are among the top 10 causes of death in children, with rates highest in the first year of life. From 1979 to 1998 in the United States, childhood mortality from stroke declined sharply, by 58 percent, with reductions in all major subtypes: ischemic stroke decreased by 19 percent, subarachnoid hemorrhage by 79 percent, and intracerebral hemorrhage by 54 percent.
Some children survive a pediatric stroke with no life-long consequences. In other children, long-term complications of stroke may develop right away or within months to years after a stroke. According to a 2000 study published in the Journal of Child Neurology, the outcome of childhood stroke was a moderate or severe deficit in 42 percent of cases. Adverse outcomes after childhood stroke—including death in 10 percent, recurrence in 20 percent, and neurological deficits in two-thirds of survivors—can be reduced with available stroke treatments.
When a stroke affects a child whose brain is still developing, it is thought that the developing brain may be able to compensate for the functions that were lost as a result of a stroke.
Recovery from stroke is different with each child. Overall, the degree of permanent disability after a stroke is less in children than in adults. Speech and language problems usually improve rapidly in the first year after a stroke. Children may only have minor delays in the development of coordinated movement or in cognitive functioning. Almost all children recover the ability to walk independently after a stroke, unless there is another condition that causes disability. Recovery of function in the affected arm and hand is usually the most significant movement problem after a stroke. Most children who suffer from a stroke can expect to lead independent lives as adults.
Prevention
Despite current treatment, one out of 10 children with ischemic stroke will have a recurrence within five years. Although there is a high risk of repeat strokes in patients with sickle cell anemia, the risk can be reduced with regular blood transfusions. If no cause of the stroke was identified, the risk of a recurrence is low. If a cause was identified, the underlying condition should be treated, and anticoagulant or low-dose aspirin therapy may be initiated, depending on the child's diagnosis.
There is no screening for stroke, but screening exists for many of its risk factors. To prevent stroke, risk factors should be treated and managed by the child's primary care doctor or specialist. The doctor can advise if specific preventive treatment is needed.
Management of high cholesterol—especially high LDL (low-density lipoprotein) levels—high blood pressure and diabetes can help reduce the risk of a stroke.
Nutritional Concerns
An adequate intake of folic acid (vitamin B9) has been linked to the prevention of stroke and heart disease by lowering homocysteine, an amino acid related to the early development of cardiovascular disease when high levels are present in the blood. Dietary sources of folic acid include: vegetables, especially green vegetables; potatoes; cereal and cereal products; fruits; and organ meats (liver or kidney). It is best to eat fresh fruits and vegetables whenever possible to get the most vitamins. Recommended daily intake in micrograms (mcg) for folic acid supplements (oral tablets) include: 25–100 mcg in newborns to age three; 75–400 mcg in children aged four to six; 100-400 mcg in children aged seven to 10; and 150–400 mcg in children aged 11 and above.
Vitamin K is an important nutrient needed to regulate normal blood clotting. A diet deficient in vitamin K can cause prolonged blood-clotting time and easy bleeding and bruising. Vitamin K is found in: alfalfa, asparagus, broccoli, Brussels sprouts, cabbage cheddar cheese, green tea, green leafy lettuce, liver, seaweed, spinach, and turnip greens. Recommended daily intake for vitamin K supplements (for patients not on anticoagulant therapy) include: 10 mcg in newborns to age three; 20 mcg in children aged four to six; 30 mcg in children aged seven to 14; 65 mcg in boys and 55 mcg in girls aged 15–18; 70–80 mcg for males over age 18 and 60–65 mcg for females over age 18. If the patient is taking anticoagulant medications, vitamin K supplements are not recommended, and foods high in vitamin K are limited, since they counteract the action of the medication.
Vitamin E and beta carotene supplements were once thought to help decrease the risk of stroke and prevent the development of heart disease, but newer studies disprove their effectiveness. Researchers at The Cleveland Clinic Heart Center performed a meta-analysis of seven large randomized trials of vitamin E (given alone or in combination with other antioxidants) and eight of beta carotene. All trials included 1,000 or more patients and follow-up ranged from 1.4 to 12 years. The doses of vitamin E given in these trials ranged from 50–800 international units (IU) and 15–50 milligrams (mg) for beta carotene. The meta-analysis reviewed the effect of these antioxidants on death from cardiovascular disease or from any other cause ("all-cause mortality").
Their findings, published in the June, 2003 issue of The Lancet journal, do not support the continued use of vitamin E supplementation nor the inclusion of vitamin E in further studies. Regardless of the dosage given or the patient population, Vitamin E did not provide any benefit in lowering mortality compared to control treatments, and it did not significantly decrease the risk of cardiovascular death or stroke (cerebrovascular accident). In addition, they recommend that vitamin supplements containing beta carotene be "actively discouraged" because of the small but statistically significant increased risk of death. Researchers discourage further study of beta carotene because of the mortality risk.
Even though studies have demonstrated that vitamin E and beta carotene supplements do not reduce stroke risk, foods rich in antioxidants are still encouraged because they also contain beneficial nutrients such as flavonoids and lycopenes that are not usually included in standard oral vitamin supplements. A diet rich in antioxidant-containing foods, such as fruits, vegetables and whole grains, is linked to a reduced risk of cardiovascular disease.
Dietary supplements should not be used as a substitute for medical therapies prescribed by a doctor. Parents should discuss these nutrition supplements with the child's doctor to determine the remedies that may be beneficial for the child.
Parental Concerns
It is common for a child to feel sad or depressed after a stroke. These emotions may be the result of not knowing what to expect or not being able to do simple tasks without becoming overly tired. Temporary feelings of sadness are normal, and should gradually go away within a few weeks, as the child starts a rehabilitation program and returns to some of his or her normal routines and activities.
When a depressed mood is severe and accompanied by other symptoms that persist every day for two or more weeks, the parent should ask for a referral to a mental health professional who can help the child cope and recover. There are many treatments for depression. A healthy lifestyle including regular exercise, proper sleep, a well-balanced diet, as well as relaxation and stress management techniques can help manage depression. Major depressive disorder may be treated with antidepressants, psychotherapy (supportive counseling or "talk therapy"), or a combination of both.
Regular follow-up visits with the child's health care provider will help identify and manage risk factors and other medical conditions. If the child has a known medical condition that increases the risk of stroke, it is important for parents and caregivers to learn the warning signs and symptoms of stroke in children and infants. If the child experiences any unexpected neurological problem, the parent should have the child evaluated by a physician. Lastly, it is important for parents to carefully follow the child's treatment plan, including following the medication schedule exactly as prescribed.
Resources
Books
Burkman, Kip. The Stroke Recovery Book: A Guide for Patients and Families. Nebraska: Addicus Books, Inc., May, 1998.
Senelick, Richard C., Peter W. Rossi, and Karla Dougherty. Living with Stroke: A Guide For Families: Help and New Hope for All Those Touched by Stroke. New York: McGraw-Hill/Contemporary Books, June, 1999.
Zimmer, Judith and John P. Cooke. The Cardiovascular Cure: How to Strengthen Your Self-Defense Against Heart Attack and Stroke. New York: Broadway Books, August, 2002.
Periodicals
Abram, Harry S., MD. "Childhood Strokes: Evaluation and Treatment." Duval County Medical Society. www.dchmsonline.org/jax-medicine/1998journals/november1998/childhoodstrokes.htm.
deVeber, G., ES Roach, AR Riela, and M. Wiznitzer. "Stroke in Children: Recognition, Treatment, and Future Directions." Seminars in Pediatric Neurology. 7:4 (December, 2000): 309-317.
deVeber, G., ES Roach, AR Riela, and M. Wiznitzer. "Recognition and Treatment of Stroke in Children." Child Neurology Society Ad Hoc Committee on Stroke in Children. July, 2001.
Kirkham, FJ. "Stroke in Childhood." Archives of Disease in Childhood. 81 (July, 1999): 85-89.
Nicolaides, P. and R.E. Appleton. "Stroke in Children." Developmental Medicine and Child Neurology. 38:2 (February, 1996): 172-180.
Organizations
American Stroke Foundation. 11902 Lowell, Overland Park, KS 66213. (913) 649-1776. www.americanstroke.org.
American Stroke Association, A Division of American Heart Association, 7272 Greenville Ave., Dallas, TX 75231. (888) 4-STROKE (787653). E-mail: strokeassociation@heart.org. www.strokeassociation.org.
Children's Hemiplegia and Stroke Association. 4101 W. Green Oaks, Ste. 305, PMB 149, Arlington, TX 76016. (817) 492-4325. E-mail: info@chasa.org. www.chasa.org.
National Heart, Lung and Blood Institute. National Institutes of Health, Building 1, 1 Center Dr., Bethesda, MD 20892. E-mail: NHLBIinfo@rover.nhlbi. www.nhlbi.nih.gov.
National Institute on Disability and Rehabilitation Research, Office of Special Education and Rehabilitative Services, U.S. Department of Education, 400 Maryland Ave. S.W., Washington, DC 20202-7100. (202) 245-7640. www.ed.gov/about/offices/list/osers/nidrr/.
National Institute of Neurological Disorders and Stroke (NINDS), National Institutes of Health. P.O. Box 5801, Bethesda, MD 20824. (800) 352-9424 or (301) 496-5751. www.ninds.nih.gov/about_ninds.
National Rehabilitation Information Center (NARIC).4200 Forbes Blvd., Ste. 202, Lanham, MD 20700. (800) 346-2742 or (301) 459-5900. www.naric.com.
National Stroke Association. 9707 E. Easter Ln., Englewood, CO 80112-3747. (800) STROKES (787-6537) or (303) 649-9299. www.stroke.org.
Stroke Clubs International. 805 12th St. Galveston, TX 77550. (409) 762-1022 attn. Ellis Williamson. E-mail: strokeclub@aol.com.
Web Sites
The Brain Attack Coalition. www.stroke-site.org
The Brain Matters, American Academy of Neurology Foundation. www.thebrainmatters.org
Different Strokes—A Charity for Younger Stroke Survivors. www.differentstrokes.co.uk/
HeartCenterOnline. www.heartcenteronline.com
HemiHelp—Information and Support for Children and Young People with Hemiplegia. www.hemihelp.org.uk
Pediatric Stroke Network. www.pediatricstrokenetwork.com
[Article by: Angela M. Costello]
Stroke, or cerebrovascular accident (CVA), is the third leading cause of death (after heart disease and cancer) in the United States and the industrialized countries of the world. The term "stroke," which comes from subjects being suddenly "struck down" with neurological deficits, is commonly used by both professional and lay groups. Efforts are being made to replace the term with "brain attack" to dramatize its analogous effects to a "heart attack," the term used for myocardial infarction. The term "cerebrovascular accident" is used interchangeably with stroke ("accident" indicates the catastrophic nature of strokes, not a traumatic origin as the term implies). More than 600,000 strokes occur annually in the United States, according to the American Heart Association, and stroke prevalence (number of living stroke victims) is approximately 4.5 million with an annual cost in 1997, both direct and indirect, of over $40 billion.
Stroke refers to the usually sudden onset of a neurological deficit, such as hemiparesis (weakness on one side of the body), or aphasia (impairment of language comprehension and production), which can be attributed to either the occlusion or rupture of a cerebral vessel. Resulting specific neurological symptoms and signs are determined by the area of the brain that is affected, and since the complex functions of the brain are either localized in specialized areas or diffusely distributed, stroke symptoms may similarly be localized or generalized in nature. For example, the long pathway of motor fibers can be interrupted, with resulting hemiparesis involving various cerebral arteries or their branches, such as the anterior, middle, or vertebrobasilar arteries. Occlusion of smaller arterioles which feed smaller areas of brain may result in more isolated effects, such as pure sensory or motor hemiparesis. On the other hand, occlusion or rupture of vessels in "silent" areas of the brain, as in the frontal or parietal cortex, can lead to subtle nonfocal symptoms reflected in impaired cognition, executive function, or memory. Other symptoms of impaired specialized brain functions from strokes include apraxia (impairment in the execution of motor actions), and agnosia (loss of ability to recognize familiar objects). Leukoaraiosis, or increased T2-signal intensity, on magnetic resonance imaging (MRI) of brain white matter results predominantly from small-vessel disease, and this syndrome is associated with increased risks for strokes and dementia.
Ischemic Strokes
The causes of arterial occlusion, or ischemic strokes, are multiple. The most frequent is atherosclerotic disease of extracranial and/or intracranial arteries; the former is more common in Caucasians, while the latter is more frequent among African Americans and Asians. A thrombus (stationary blood clot) formed on atherosclerotic plaques in these locations, as well as on the aorta, can dislodge and embolize to occlude a distal artery. Strokes due to atherosclerosis account for approximately two-thirds of all strokes. If seen within three hours of stroke onset, treatment with tissue plasminogen activator (tPA), a thrombolytic agent, may substantially improve a patient's neurological outcome. Otherwise, therapeutic efforts are aimed at optimizing cerebral blood flow to ischemically impaired brain tissue, providing neural protection to avert brain damage, and maximizing neurorehabilitation. Research on stem cell and neural progenitor cell implantation into an ischemically damaged brain to promote recovery is a recently promising area of stroke research.
Transient Ischemic Attacks (TIAs). Strokes may be heralded by transient neurological deficits, called transient ischemic attacks (TIAs), such as temporary blindness of one eye (amaurosis fugax), hemiparesis, or aphasia. Most frequently, TIAs occur with significant atherosclerotic disease of the extracranial carotid arteries. Control of risk factors for atherosclerosis, such as hypertension, smoking, diabetes mellitus, elevated cholesterol, stress, and, perhaps, sedentary lifestyle, will hopefully minimize strokes from this cause to an irreducible minimum. For significant extracranial disease (>70% diameter stenosis [constriction] at the carotid bifurcation), carotid endarterectomy in competent surgical hands has been shown to reduce stroke recurrence significantly. Aspirin and other antiplatelet drugs in nonsurgical candidates can prevent subsequent strokes.
Cardiogenic strokes. Ischemic strokes can be caused by emboli from the heart as a result of more than a dozen cardiac disorders, the most common being arrhythmias, particularly atrial fibrillation (AF). Suspected cardiogenic strokes require workup, including transthoracic and transesophageal echocardiography (TTE and TEE), which can detect valvular pathologies, wall-motion abnormalities, thrombi, and patent foramen ovale (PFO). This group, in aggregate, may account for up to a quarter or more of all ischemic strokes. For AF, the treatment of choice to prevent embolic strokes is long-term anticoagulation. Patients who are not anticoagulation candidates should be treated with antiplatelet drugs. Conditions such as PFO can be treated medically with anticoagulation; surgical and percutaneous options are also available for PFO closure.
Lacunar Strokes. These strokes refer to small branch occlusions (noted previously), and include discrete syndromes such as pure sensory and motor hemiparesis. Lacunar strokes result primarily from chronic sustained hypertension, and the pathological change is "lipohyalinosis" of arterioles. This syndrome may account for 10 to 15 percent of all strokes. Adequate control of hypertension should prevent this condition.
Two final categories of diseases-causing ischemic strokes are more frequently considered in younger persons, especially those under fifty-five years of age, and involve arteries and blood elements. For the former, vessel diseases other than atherosclerosis include inflammatory processes, such as the arteritides; migraine; dissection—either spontaneous or traumatic; moyamoya syndrome; fibromuscular disorders; MELAS syndrome (mitochondrial encephalopathy, lactic acidosis, and stroke-like symptoms) and a few others. For the latter, blood-element disorders include clotting, and platelets and erythrocyte abnormalities. The most common clotting disorders are resistance to protein C activation—most frequently due to Factor V Leiden mutation (506Q); antiphospholipid syndrome, which includes the lupus anticoagulant and anticardiolipin antibodies; reduced antithrombin III; protein C & S deficiencies; plus a few others. Treatment of vascular disorders is tailored to the individual condition; for example, migraine is treated with prophylactic agents, which prevent vasospasm; arteritides with steroids and immunosuppressive agents; and moyamoya syndrome with a variety of bypass surgical procedures. Many of the hypercoagulable or prothrombotic conditions are treated with long-term anticoagulation.
Intracerebral and Subarachnoid Hemorrhages
Rupture of vessels include two large categories. The more common is intracerebral hemorrhage (ICH), which results from chronic sustained hypertension and accounts for approximately 10 percent of all strokes. An infrequent cause of ICH is amyloid angiopathy; its cause (and cure) is unknown. A second category of vessel rupture is subarachnoid hemorrhage (SAH), most frequently due to aneurysmal rupture, but occasionally from arteriovenous malformations. SAH accounts for about 5 percent of all strokes. Gene and molecular pathological markers to identify persons at risk will hopefully provide interventional tools to both prevent and treat subjects at risk before aneurysmal rupture.
ICH occurs in five brain sites, most commonly in the putamen. With substantial cerebellar ICH in a noncomatose patient, surgical evacuation can be life-saving. The only other site that may benefit from surgery is polar or white matter ICH. In neurologically viable patients, SAH can be treated successfully with surgical extirpation of the aneurysm, or with a variety of endovascular procedures, such as aneurysmal obliteration.
Public Health Importance of Strokes
As the third leading cause of death and disability, there are important public health implications for strokes, especially since many of the stroke syndromes are preventable. This is particularly true for those due to atherosclerosis, which is the most common cause of strokes. Except for increasing age, all of the risk factors for atherosclerosis can be either controlled or eliminated. To accomplish this goal, better strategies to educate and motivate the general public are vital.
In addition to controlling risk factors, a better understanding of the nature of stroke symptoms by the public is required for expeditious corrective and therapeutic measures, much as has happened with the public's general awareness of chest pain as a symptom of a potential heart attack. Investigations on proteomic and gene expression profiles for strokes to identify individuals at increased risk for strokes will hopefully provide public health planners with an even more powerful tool to intervene effectively for stroke prevention, the ultimate best treatment of strokes.
(SEE ALSO: American Heart Association; Atherosclerosis; Cardiovascular Diseases; Transient Ischemic Attacks)
Bibliography
Barnett, H. J. M.; Mohr, J. P.; Stein, B.; and Yatsu, F. M., eds. (1998). Stroke: Pathophysiology, Diagnosis & Management. Philadelphia, PA: Churchill-Livingstone.
— FRANK YATSU
An interruption in the blood supply to the brain. Causes include a blood clot, a head injury, or an aneurysm, but the primary cause is usually disease of the heart or blood vessels, with the effects on the head being secondary. A stroke results in a part of the brain being deprived of oxygen. Small strokes may occur without symptoms and go unnoticed by the victim, but the most common manifestation is some degree of paralysis; large strokes may be fatal. Regular aerobic exercise produces a number of benefits (e.g. reduction of blood pressure in those with moderate hypertension) that can reduce the risk of a stroke.
Symptoms of stroke develop suddenly. In cases of severe brain damage there may be deep coma, paralysis of one side of the body, and loss of speech, followed by death or permanent neurological disturbances after recovery. If the brain damage sustained has been slight, there is usually complete recovery, but most survivors of stroke require extensive rehabilitation. Hypertension, which is a major cause of intracranial hemorrhage and stroke, can be treated by preventive measures using diet (e.g., increasing nutrients such as antioxidants and folate), drug therapy, and stress reduction techniques. Other preventive measures for people at high risk include daily aspirin to retard clot formation and surgical correction of the narrowed carotid artery. Sometimes surgical removal of the clot is possible on larger vessels, but it is usually pointless after the stroke or when blockage is widespread. The thrombolytic drug tissue plasminogen activator, widely used to treat heart attacks, has been approved for use within three hours of the onset of strokes caused by clots.
A sudden loss of brain function caused by an interruption in the supply of blood to the brain. A ruptured blood vessel or cerebral thrombosis may cause the stroke, which can occur in varying degrees of severity from temporary paralysis and slurred speech to permanent brain damage and death.
1. Can strokes be avoided?
Much attention has been given in recent years to identifying 'risk factors', with a view to setting up programmes of stroke prevention. The major treatable factor is hypertension (high blood pressure). There is now clear evidence that the effective treatment of hypertension can reduce (although not eliminate) the risk of an acute stroke. This places considerable logistical demands on general practitioners and others who have the responsibility of both detecting and treating the condition.2. Assessment of neurological deficits
The patient usually becomes 'medically stable' within the first ten days. At the end of this time, he or she is likely to be fit enough to start the process of 'rehabilitation'. Most patients will have weakness or paralysis of the arm and leg on one side of the body (a hemiplegia). In many instances, this 'motor' loss is accompanied by impairment of sensation in the limbs. The paralysed limbs require careful positioning, and it is essential to avoid excessive pulling and stretching of the affected joints. A variety of other deficits may occur.Hemianopia. A homonymous hemianopia occurs if the visual pathways in the affected hemisphere have been damaged (see visual system: organization). If the disturbance is severe, the patient will not see objects on one side. Thus, a patient with a right homonymous hemianopia may not react to his wife and family, if they are sitting at his bedside on his right side. If mobile, he may walk into door frames and other objects on the right side.Aphasia (in this context, the terms 'aphasia' and 'dysphasia' are used synonymously) involves a disturbance of language function, and usually results from damage to the left cerebral hemisphere. In its mildest form, it may simply involve the inability to name objects such as a table, clock, or pen. In most instances, however, there is a disturbance of comprehension, and reading is impaired. In the worst cases, the patient has almost complete loss of the ability to comprehend language, and cannot speak, though, happily, the problem is rarely so severe.Visuospatial disorders. Damage to the right cerebral hemisphere often produces disorders of spatial orientation (see spatial coordination) and perception. These can be complicated and difficult to understand, but are of enormous importance to those who are caring for the stroke patient. Some patients neglect one side of the body (usually the left), and may even deny the existence of the left arm. Occasionally, the patient's perception of the arm is distorted so that it appears much longer or shorter than normal, or appears to be covered in hair. Patients with a severe disturbance of spatial function may be, for instance, unable to draw symmetrical objects, such as a house, or a clock-face, the left side of the object being usually less well drawn than the right. Such people are frequently unable to dress because they cannot organize their clothes, and may, for instance, try to don a jacket which is inside out and back to front.3. How much recovery will occur?
There is now considerable literature on the subject of recovery after stroke (for example, Skilbeck et al. 1983, Barnett, Stein, and Mohr 1986). The three adverse factors occurring in the first few days are unconsciousness, urinary incontinence, and deviation of the eyes to one side. Only 5–10 per cent of patients who are unconscious in the first week will survive, and those who do survive will usually be left very severely disabled.— Richard Langton-Hewer
Remember that not getting what you want is sometimes a wonderful stroke of luck.
— The Dalai Lama
LearnThatWord.com is a free vocabulary and spelling program where you only pay for results!

1. a sudden and severe attack.
2. in humans, rupture or blockage of a blood vessel in the brain, depriving parts of the brain of blood supply, resulting in loss of consciousness, paralysis or other symptoms depending on the site and extent of brain damage; see also cerebral vascular accident. A very uncommon occurrence in animals.
1. a single, unbroken movement made by an instrument or the mandible. 2. common term for accident, cerebrovascular.

| Stroke | |
|---|---|
| Classification and external resources | |
CT scan slice of the brain showing a right-hemispheric ischemic stroke (left side of image). |
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| ICD-10 | I61-I64ner |
| ICD-9 | 434.91 |
| OMIM | 601367 |
| DiseasesDB | 2247 |
| MedlinePlus | 000726 |
| eMedicine | neuro/9 emerg/558 emerg/557 pmr/187 |
| MeSH | D020521 |
A stroke, or cerebrovascular accident (CVA), is the rapid loss of brain function(s) due to disturbance in the blood supply to the brain. This can be due to ischemia (lack of blood flow) caused by blockage (thrombosis, arterial embolism), or a hemorrhage (leakage of blood).[1] As a result, the affected area of the brain cannot function, which might result in an inability to move one or more limbs on one side of the body, inability to understand or formulate speech, or an inability to see one side of the visual field.[2]
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 and the second leading cause of death worldwide.[citation needed] Risk factors for stroke include old age, hypertension (high blood pressure), previous stroke or transient ischemic attack (TIA), diabetes, high cholesterol, cigarette smoking and atrial fibrillation.[2] High blood pressure is the most important modifiable risk factor of stroke.[2]
An ischemic stroke is occasionally treated in a hospital with thrombolysis (also known as a "clot buster"), and some hemorrhagic strokes benefit from neurosurgery. Treatment to recover any lost function is termed stroke rehabilitation, ideally in a stroke unit and involving health professions such as speech and language therapy, physical therapy and occupational therapy. Prevention of recurrence may involve the administration of antiplatelet drugs such as aspirin and dipyridamole, control and reduction of hypertension, and the use of statins. Selected patients may benefit from carotid endarterectomy and the use of anticoagulants.[2]
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Strokes can be classified into two major categories: ischemic and hemorrhagic.[3] Ischemic strokes are those that are caused by interruption of the blood supply, while hemorrhagic strokes are the ones which result from rupture of a blood vessel or an abnormal vascular structure. About 87% of strokes are caused by ischemia, and the remainder by hemorrhage. Some hemorrhages develop inside areas of ischemia ("hemorrhagic transformation"). It is unknown how many hemorrhages actually start as ischemic stroke.[2]
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:
Stroke without an obvious explanation is termed "cryptogenic" (of unknown origin); this constitutes 30-40% of all ischemic strokes.[2][6]
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.[7][8] 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).[2][9]
Intracranial hemorrhage is the accumulation of blood anywhere within the skull vault. A distinction is made between intra-axial hemorrhage (blood inside the brain) and extra-axial hemorrhage (blood inside the skull but outside the brain). Intra-axial hemorrhage is due to intraparenchymal hemorrhage or intraventricular hemorrhage (blood in the ventricular system). The main types of extra-axial hemorrhage are epidural hematoma (bleeding between the dura mater and the skull), subdural hematoma (in the subdural space) and subarachnoid hemorrhage (between the arachnoid mater and pia mater). Most of the hemorrhagic stroke syndromes have specific symptoms (e.g., headache, previous head injury).
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.
Various systems have been proposed to increase recognition of stroke by patients, relatives and emergency first responders. A systematic review, updating a previous systematic review from 1994, looked at a number of trials to evaluate how well different physical examination findings are able to predict the presence or absence of stroke. It was found that 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 (+ likelihood ratio of 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).[10] 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 (stroke) (face, arm, speech, and time),[11] as advocated by the Department of Health (United Kingdom) and The Stroke Association, the American Stroke Association (www.strokeassociation.org), National Stroke Association (US www.stroke.org), the Los Angeles Prehospital Stroke Screen (LAPSS)[12] and the Cincinnati Prehospital Stroke Scale (CPSS).[13] Use of these scales is recommended by professional guidelines.[14]
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.[14][15]
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:
In most cases, the symptoms affect only one side of the body (unilateral). Depending on the part of the brain affected, the defect in the brain is usually on the opposite side of the body. However, since these pathways also travel in the spinal cord and any lesion there can also produce these symptoms, the presence of any one of these symptoms does not necessarily indicate a stroke.
In addition to the above CNS pathways, the brainstem gives rise to most of the twelve cranial nerves. A stroke affecting the brain stem and brain therefore can produce symptoms relating to deficits in these cranial nerves:
If the cerebral cortex is involved, the CNS pathways can again be affected, but also can produce the following symptoms:
If the cerebellum is involved, the patient may have the following:
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.
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In thrombotic stroke a thrombus[17] (blood clot) usually forms around atherosclerotic plaques. Since blockage of the artery is gradual, onset of symptomatic thrombotic strokes is slower. A thrombus itself (even if non-occluding) can lead to an embolic stroke (see below) if the thrombus breaks off, at which point it is called an "embolus." Two types of thrombosis can cause stroke:
Sickle-cell anemia,[22] 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.[23]
An embolic stroke refers to the blockage of an artery by an arterial embolus, a travelling particle or debris in the arterial bloodstream originating from elsewhere. An embolus is most frequently a thrombus, but it can also be a number of other substances including fat (e.g., from bone marrow in a broken bone), air, cancer cells or clumps of bacteria (usually from infectious endocarditis).
Because an embolus arises from elsewhere, local therapy solves the problem only temporarily. Thus, the source of the embolus must be identified. Because the embolic blockage is sudden in onset, symptoms usually are maximal at start. Also, symptoms may be transient as the embolus is partially resorbed and moves to a different location or dissipates altogether.
Emboli most commonly arise from the heart (especially in atrial fibrillation) but may originate from elsewhere in the arterial tree. In paradoxical embolism, a deep vein thrombosis embolises through an atrial or ventricular septal defect in the heart into the brain.
Cardiac causes can be distinguished between high and low-risk:[24]
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. 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. 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 hemorrhagic transformation (leaking of blood into the damaged area) than other types of ischemic stroke.[5]
It generally occurs in small arteries or arterioles and is commonly due to hypertension,[25] intracranial vascular malformations (including cavernous angiomas or arteriovenous malformations), cerebral amyloid angiopathy, or infarcts into which secondary haemorrhage 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]).
A silent stroke is a stroke that does not have any outward symptoms, and the patients are typically unaware they have suffered a stroke. Despite not causing identifiable symptoms, a silent stroke still causes damage to the brain, and places the patient at increased risk for both transient ischemic attack and major stroke in the future. Conversely, those who have suffered a major stroke are at risk of having silent strokes.[26] 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.[27][28] The risk of silent stroke increases with age, but may also affect younger adults and children, especially those with acute anemia.[27][29]
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Ischemic stroke occurs because of a loss of blood supply to part of the brain, initiating the ischemic cascade.[30] 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.[31] Embolic infarction occurs when emboli formed elsewhere in the circulatory system, typically in the heart as a consequence of atrial fibrillation, or in the carotid arteries, break off, enter the cerebral circulation, then lodge in and occlude brain blood vessels. Since blood vessels in the brain are now occluded, the brain becomes low in energy, and thus it resorts into using anaerobic respiration within the region of brain tissue affected by ischemia. Unfortunately, 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 is an acid and disrupts the normal acid-base balance in the brain. The ischemia area is referred to as the "ischemic penumbra".[32]
Then, as oxygen or glucose becomes depleted in ischemic brain tissue, the production of high energy phosphate compounds such as adenosine triphosphate (ATP) fails, leading to failure of energy-dependent processes (such as ion pumping) necessary for tissue cell survival. This sets off a series of interrelated events that result in cellular injury and death. A major cause of neuronal injury is release of the excitatory neurotransmitter glutamate. The concentration of glutamate outside the cells of the nervous system is normally kept low by so-called uptake carriers, which are powered by the concentration gradients of ions (mainly Na+) across the cell membrane. However, stroke cuts off the supply of oxygen and glucose which powers the ion pumps maintaining these gradients. As a result the transmembrane ion gradients run down, and glutamate transporters reverse their direction, releasing glutamate into the extracellular space. Glutamate acts on receptors in nerve cells (especially NMDA receptors), producing an influx of calcium which activates enzymes that digest the cells' proteins, lipids and nuclear material. Calcium influx can also lead to the failure of mitochondria, which can lead further toward energy depletion and may trigger cell death due to apoptosis.
Ischemia also induces production of oxygen free radicals and other reactive oxygen species. These react with and damage a number of cellular and extracellular elements. Damage to the blood vessel lining or endothelium is particularly important. In fact, many antioxidant neuroprotectants such as uric acid and NXY-059 work at the level of the endothelium and not in the brain per se. Free radicals also directly initiate elements of the apoptosis cascade by means of redox signaling.[23]
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 excitatory neurotransmitters, for example, have been shown experimentally to reduce tissue injury caused by ischemia. Agents that work in this way are referred to as being neuroprotective. Until recently, human clinical trials with neuroprotective agents have failed, with the probable exception of deep barbiturate coma. However, more recently NXY-059, the disulfonyl derivative of the radical-scavenging spintrap phenylbutylnitrone, is reported to be neuroprotective in stroke.[33] 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.[23]
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.
Hemorrhagic strokes result in tissue injury by causing compression of tissue from an expanding hematoma or hematomas. This can distort and injure tissue. In addition, the pressure may lead to a loss of blood supply to affected tissue with resulting infarction, and the blood released by brain hemorrhage appears to have direct toxic effects on brain tissue and vasculature.[23][34] Inflammation contributes to the secondary brain injury after hemorrhage.[34]
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.[35]
The traditional definition of stroke, devised by the World Health Organization in the 1970s,[36] 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.[2] 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.[37]
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.
For diagnosing ischemic stroke in the emergency setting:[38]
For diagnosing hemorrhagic stroke in the emergency setting:
For detecting chronic hemorrhages, MRI scan is more sensitive.[39]
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.
When a stroke has been diagnosed, various other studies may be performed to determine the underlying cause. With the current treatment and diagnosis options available, it is of particular importance to determine whether there is a peripheral source of emboli. Test selection may vary, since the cause of stroke varies with age, comorbidity and the clinical presentation. Commonly used techniques include:
Given the disease burden of strokes, prevention is an important public health concern.[40] Primary prevention is less effective than secondary prevention (as judged by the number needed to treat to prevent one stroke per year).[40] Recent guidelines detail the evidence for primary prevention in stroke.[41] Because stroke may indicate underlying atherosclerosis, it is important to determine the patient's risk for other cardiovascular diseases such as coronary heart disease. Conversely, aspirin confers some protection against first stroke in patients who have suffered a myocardial infarction or patients with a high cardiovascular risk.[42][43]
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[44][45]). Other modifiable risk factors include high blood cholesterol levels, diabetes, cigarette smoking[46][47] (active and passive), heavy alcohol consumption[48] and drug use,[49] lack of physical activity, obesity, processed red meat consumption[50] and unhealthy diet.[51] 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).[52] The drugs most commonly associated with stroke are cocaine, amphetamines causing hemorrhagic stroke, but also over-the-counter cough and cold drugs containing sympathomimetics.[53][54]
No high quality studies have shown the effectiveness of interventions aimed at weight reduction, promotion of regular exercise, reducing alcohol consumption or smoking cessation.[55] Nonetheless, given the large body of circumstantial evidence, best medical management for stroke includes advice on diet, exercise, smoking and alcohol use.[56] Medication or drug therapy is the most common method of stroke prevention; carotid endarterectomy can be a useful surgical method of preventing stroke.
Hypertension accounts for 35-50% of stroke risk.[57] 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.[58] Lowering blood pressure has been conclusively shown to prevent both ischemic and hemorrhagic strokes.[59][60] It is equally important in secondary prevention.[61] Even patients older than 80 years and those with isolated systolic hypertension benefit from antihypertensive therapy.[62][63][64] Studies show that intensive antihypertensive therapy results in a greater risk reduction.[65] 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.[65][66]
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.[67] Depending on the stroke risk, anticoagulation with medications such as coumarins or aspirin is warranted for stroke prevention.[68]
High cholesterol levels have been inconsistently associated with (ischemic) stroke.[60][69] Statins have been shown to reduce the risk of stroke by about 15%.[70] Since earlier meta-analyses of other lipid-lowering drugs did not show a decreased risk,[71] statins might exert their effect through mechanisms other than their lipid-lowering effects.[70]
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.[72][73]
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.[42] 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.[74] Thienopyridines (clopidogrel, ticlopidine) "might be slightly more effective" than aspirin and have a decreased risk of gastrointestinal bleeding, but they are more expensive.[75] Their exact role remains controversial. Ticlopidine has more skin rash, diarrhea, neutropenia and thrombotic thrombocytopenic purpura.[75] Dipyridamole can be added to aspirin therapy to provide a small additional benefit, even though headache is a common side effect.[76] Low-dose aspirin is also effective for stroke prevention after sustaining a myocardial infarction.[43] Except for in atrial fibrillation, oral anticoagulants are not advised for stroke prevention —any benefit is offset by bleeding risk.[77]
In primary prevention however, antiplatelet drugs did not reduce the risk of ischemic stroke while increasing the risk of major bleeding.[78][79] Further studies are needed to investigate a possible protective effect of aspirin against ischemic stroke in women.[80][81]
Surgical procedures such as carotid endarterectomy or carotid angioplasty can be used to remove significant atherosclerotic narrowing (stenosis) of the carotid artery, which supplies blood to the brain. There is a large body of evidence supporting this procedure in selected cases.[56] Endarterectomy for a significant stenosis has been shown to be useful in the secondary prevention after a previous symptomatic stroke.[82] Carotid artery stenting has not been shown to be equally useful.[83][84] Patients are selected for surgery based on age, gender, degree of stenosis, time since symptoms and patients' preferences.[56] 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.[85][86]
Screening for carotid artery narrowing has not been shown to be a useful screening test in the general population.[87] Studies of surgical intervention for carotid artery stenosis without symptoms have shown only a small decrease in the risk of stroke.[88][89] 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.[56]
Nutrition, specifically the Mediterranean-style diet, has the potential for decreasing the risk of having a stroke by more than half.[90]
With regard to lowering homocysteine, a meta-analysis of previous trials has concluded that lowering homocysteine with folic acid and other supplements may reduce stroke risk.[91] However, the two largest randomized controlled trials included in the meta-analysis had conflicting results. One reported positive results;[92] whereas the other was negative.[93]
The European Society of Cardiology and the European Association for Cardiovascular Prevention and Rehabilitation have developed an interactive tool for prediction and managing the risk of heart attack and stroke in Europe. HeartScore is aimed at supporting clinicians in optimising individual cardiovascular risk reduction. The Heartscore Programme is available in 12 languages and offers web based or PC version.[94]
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]
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. 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.
An ischemic stroke is caused by a thrombus (blood clot) occluding blood flow to an artery supplying the brain. Definitive therapy is aimed at removing the blockage by breaking the clot down (thrombolysis), or by removing it mechanically (thrombectomy). The more rapidly blood flow is restored to the brain, the fewer brain cells die.[95]
Other medical therapies are aimed at minimizing clot enlargement or preventing new clots from forming. To this end, treatment with medications such as aspirin, clopidogrel and dipyridamole may be given to prevent platelets from aggregating.[42]
Tight control of blood sugars in the first few hours does not improve outcomes and may cause harm.[96] High blood pressure is also not typically lowered as this has not been found to be helpful.
In an increasing number of primary stroke centers, pharmacologic thrombolysis ("clot busting") with the drug tissue plasminogen activator (tPA), is used to dissolve the clot and unblock the artery. However, the use of tPA in acute stroke is controversial. On one hand, it is endorsed by the American Heart Association and the American Academy of Neurology as the recommended treatment for acute stroke within three hours of onset of symptoms as long as there are not other contraindications (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[97] 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.[98] A recent study using alteplase for thrombolysis in ischemic stroke suggests clinical benefit with administration 3 to 4.5 hours after stroke onset.[99] However, in the NINDS trial 6.4% of patients with large strokes developed substantial brain hemorrhage as a complication from being given tPA. A recent study found the mortality to be higher among patients receiving tPA versus those who did not.[100] Additionally, it is the position of the American Academy of Emergency Medicine that objective evidence regarding the efficacy, safety, and applicability of tPA for acute ischemic stroke is insufficient to warrant its classification as standard of care.[101] 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.[102]
Another intervention for acute ischemic stroke is removal of the offending thrombus directly. This is accomplished by inserting a catheter into the femoral artery, directing it into the cerebral circulation, and deploying a corkscrew-like device to ensnare the clot, which is then withdrawn from the body. Mechanical embolectomy devices have been demonstrated effective at restoring blood flow in patients who were unable to receive thrombolytic drugs or for whom the drugs were ineffective,[103][104][105][106] though no differences have been found between newer and older versions of the devices.[107] The devices have only been tested on patients treated with mechanical clot embolectomy within eight hours of the onset of symptoms.
Angioplasty and stenting have begun to be looked at as possible viable options in treatment of acute ischemic stroke. In a systematic review of six uncontrolled, single-center trials, involving a total of 300 patients, of 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.[108] This data suggests that a large, randomized controlled trial is needed to more completely evaluate the possible therapeutic advantage of this treatment.
Large territory strokes can cause significant edema of the brain with secondary brain injury in surrounding tissue. This phenomenon is mainly encountered in strokes of the middle cerebral artery territory, and is also called "malignant cerebral infaction" because it carries a dismal prognosis. Relief of the pressure may be attempted with medication, but some require hemicraniectomy, the temporary surgical removal of the skull on one side of the head. This confers a marked improvement in the risk of death, although some more people survive with disability who would otherwise have died.[109]
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%.[110] However, a recent meta-analysis suggests harm from anti-coagulation started early after an embolic stroke.[111] Stroke prevention treatment for atrial fibrillation is determined according to the CHADS/CHADS2 system. The most widely used anticoagulant to prevent thromboembolic stroke in patients with nonvalvular atrial fibrillation is the oral agent Warfarin while dabigatran is a new alternative which does not require prothrombin time monitoring.
If studies show carotid stenosis, and the patient has residual function in the affected side, carotid endarterectomy (surgical removal of the stenosis) may decrease the risk of recurrence if performed rapidly after stroke.
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 and cannot be used in intracerebral hemorrhage. Patients are monitored for changes in the level of consciousness, and their blood pressure, blood sugar, and oxygenation are kept at optimum levels.
Stroke rehabilitation is the process by which patients with disabling strokes undergo treatment to help them return to normal life as much as possible by regaining and relearning the skills of everyday living. 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 nursing staff, physiotherapy, occupational therapy, speech and language therapy, and usually a physician trained in rehabilitation medicine. Some teams may also include psychologists, social workers, and pharmacists since at least one third of the patients 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 stroke patients, physical therapy (PT), occupational therapy (OT) and speech-language pathology (SLP) are the cornerstones of the rehabilitation process. Often, assistive technology such as a wheelchair, walkers, canes, and orthosis may be beneficial. 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.[112] OT is involved in training to help relearn everyday activities known as the Activities of daily living (ADLs) such as eating, drinking, dressing, bathing, cooking, reading and writing, and toileting. Speech and language therapy is appropriate for patients with the speech production disorders: dysarthria and apraxia of speech, aphasia, cognitive-communication impairments and/or dysphagia (problems with swallowing).
Patients may have particular problems, such as dysphagia, which can cause swallowed material to pass into the lungs and cause aspiration pneumonia. The condition may improve with time, but in the interim, a nasogastric tube may be inserted, enabling liquid food to be given directly into the stomach. If swallowing is still deemed unsafe, then a percutaneous endoscopic gastrostomy (PEG) tube is passed and this can remain indefinitely.
Treatment of spasticity related to stroke often involves early mobilisations, commonly performed by a physiotherapist, combined with elongation of spastic muscles and sustained stretching through various positioning.[16] Gaining initial improvements in range of motion is often achieved through rhythmic rotational patterns associated with the affected limb.[16] 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.[16] Cold in the form of ice wraps or ice packs have been proven to briefly reduce spasticity by temporarily dampening neural firing rates.[16] Electrical stimulation to the antagonist muscles or vibrations has also been used with some success.[16]
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.[113] 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.[113].
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)[114] and robotic therapies.[115]
Disability affects 75% of stroke survivors enough to decrease their employability.[116] Stroke can affect patients physically, mentally, emotionally, or a combination of the three. The results of stroke vary widely depending on size and location of the lesion.[117] Dysfunctions correspond to areas in the brain that have been damaged.
Some of the physical disabilities that can result from stroke include muscle weakness, numbness, pressure sores, pneumonia, incontinence, apraxia (inability to perform learned movements), difficulties carrying out daily activities, appetite loss, speech loss, vision loss, and pain. If the stroke is severe enough, or in a certain location such as parts of the brainstem, coma or death can result.
Emotional problems resulting from stroke can result from direct damage to emotional centers in the brain or from frustration and difficulty adapting to new limitations. Post-stroke emotional difficulties include anxiety, panic attacks, flat affect (failure to express emotions), mania, apathy, and psychosis.
30 to 50% of stroke survivors suffer post stroke depression, which is characterized by lethargy, irritability, sleep disturbances, lowered self esteem, and withdrawal.[118] Depression can reduce motivation and worsen outcome, but can be treated with antidepressants.
Emotional lability, another consequence of stroke, causes the patient to switch quickly between emotional highs and lows and to express emotions inappropriately, for instance with an excess of laughing or crying with little or no provocation. While these expressions of emotion usually correspond to the patient's actual emotions, a more severe form of emotional lability causes patients to laugh and cry pathologically, without regard to context or emotion.[116] Some patients show the opposite of what they feel, for example crying when they are happy.[119] Emotional lability occurs in about 20% of stroke patients.
Cognitive deficits resulting from stroke include perceptual disorders, Aphasia, dementia, and problems with attention and memory. A stroke sufferer may be unaware of his or her own disabilities, a condition called anosognosia. In a condition called hemispatial neglect, a patient is unable to attend to anything on the side of space opposite to the damaged hemisphere.
Up to 10% of all stroke patients develop seizures, most commonly in the week subsequent to the event; the severity of the stroke increases the likelihood of a seizure.[120][121]
Stroke could soon be the most common cause of death worldwide.[122] Stroke is currently the second leading cause of death in the Western world, ranking after heart disease and before cancer,[2] and causes 10% of deaths worldwide.[123] 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.[124] 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.[118][23] 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.[125] 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,[23] yet 60% of deaths from stroke occur in women.[119] Since women live longer, they are older on average when they have their strokes and thus more often killed (NIMH 2002).[23] Some risk factors for stroke apply only to women. Primary among these are pregnancy, childbirth, menopause and the treatment thereof (HRT).
Episodes of stroke and familial stroke have been reported from the 2nd millennium BC onward in ancient Mesopotamia and Persia.[126] 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.[127][128]
The word stroke was used as a synonym for apoplectic seizure as early as 1599,[129] 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.[127][23] Wepfer also identified the main arteries supplying the brain, the vertebral and carotid arteries, and identified the cause of ischemic stroke [also known as cerebral infarction] when he suggested that apoplexy might be caused by a blockage to those vessels.[23]
Rudolf Virchow first described the mechanism of thromboembolism as a major factor.[130]
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Dansk (Danish)
n. - hug, slag, stød, tag, strøg, skrifttræk, slagtilfælde
v. tr. - stryge, glatte, klappe
idioms:
Nederlands (Dutch)
aaien, slag, zwemslag, beroerte, streek, inslag, klap
Français (French)
n. - (gén) coup, (fig) coup, (Sport) mouvement des bras, nage, (Sport) coup d'aviron, chef de nage, (Art) trait, touche, coup de pinceau/crayon, barre oblique, coup, (Méd) congestion cérébrale, attaque, (Tech) course, caresse
v. tr. - caresser, (Sport) être le chef de nage (aviron)
idioms:
Deutsch (German)
n. - Strich, Schlag, Hieb, Stoß, Zug, Hub, Schachzug, Schlagmann, Schlaganfall
v. - streicheln, als Schlagmann rudern
idioms:
Ελληνική (Greek)
n. - χτύπημα, πλήγμα, χτύπος, χάδι, κίνηση κολυμβητή, απλωτή, παλμός ρίψης, κονδυλιά, πινελιά, κίνηση κωπηλασίας, "κουπιά", αναπάντεχο περιστατικό, πετυχημένη προσπάθεια, (αθλοπ.) κτύπημα της μπάλας, μπαλιά, (μηχαν.) διαδρομή εμβόλου, (παθολ.) αποπληξία, (τυπογρ.) κάθετος, μπάρα
v. - χαϊδεύω, εξομαλύνω, στρώνω, κωπηλατώ
idioms:
Italiano (Italian)
accarezzare, tratto, botta, carezza, bracciata, colpo apoplettico, tocco, colpo di fulmine
idioms:
Português (Portuguese)
n. - curso (m) (Mec.), impacto (m), apoplexia (f) (Med.)
v. - acariciar
idioms:
Русский (Russian)
удар, припадок, взмах, прием, неожиданный случай, штрих, мазок, черта, бой часов, биение (сердца), стиль (плавания), ход (поршня), поглаживание рукой, похвала, задавать темп, испещрять полосами, перечеркивать, гладить, хвалить, уговаривать
idioms:
Español (Spanish)
n. - línea, golpe, cachetazo, caricia, brazada, tacada, apoplejía, ataque, brochazo, pincelada, rayo
v. tr. - acariciar, frotar suavemente, pasar suavemente la mano, alisar, irritar a uno, ordeñar, poner tilde o trazo
idioms:
Svenska (Swedish)
n. - slag, hugg, stöt, slaglängd, simsätt, rodd, roddsätt, drag, grep, strykning
v. - stryka, smeka, blidka, släta till, glätta
中文(简体)(Chinese (Simplified))
1. 打, 敲, 击, 一抽, 打法, 一击, 一划, 划法, 敲声, 鸣声, 画短线于, 抽, 勾销, 删掉
idioms:
2. 抚, 捋, 摸
中文(繁體)(Chinese (Traditional))
1.
v. tr. - 撫, 捋, 摸
n. - 撫, 捋, 摸
2.
n. - 打, 敲, 擊, 一抽, 打法, 一擊, 一劃, 劃法, 敲聲, 鳴聲
v. tr. - 畫短線於, 擊, 抽, 勾銷, 刪掉
v. intr. - 勾銷, 刪掉
idioms:
한국어 (Korean)
n. - 타격, (벼락의) 일격
v. tr. - ~에 선을 긋다, (공을) 치다
idioms:
日本語 (Japanese)
n. - 打つこと, ひと打ち, ストローク, ひと動作, ひとかき, 脈拍, ひと彫り, ひと筆, 打つ音, なでること, 一撃, 筆づかい
v. - なでる, 線を引く, ボールを打つ
idioms:
العربيه (Arabic)
(الاسم) ضربه, جلطه, حركه مباغته, دقه (فعل) داعب, لاطف, ملمس, مسد
עברית (Hebrew)
n. - מכה, שבץ, חבטה, תנועה, הצלפה, משוטאי אחורי, לטיפה, משיכת-קולמוס, תנועת-מכחול, צלצול-שעון, סיסוב, שיטת חבטה במחבט, שחייה בסגנון חתירה, תנועת בוכנה, מאמץ מיומן
v. tr. - ליטף, חתר במשוט אחורי, היכה, חבט
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