Stroke
From Wikipedia, the free encyclopedia.
- For other uses, see Stroke (disambiguation).
Cerebrovascular accident | ||
---|---|---|
ICD-10 code: | I61-I64 | |
ICD-9 code: | 435-436 |
A stroke or cerebrovascular accident (CVA) occurs when the blood supply to a part of the brain is suddenly interrupted. In brain tissue, ischemia, a reduction of blood flow, leads to an ischemic cascade that can damage or kill brain cells. Death of brain tissue can lead to loss of the function controlled by that tissue. Thus stroke is the third leading cause of death and leading cause of adult disability in the US and industrialized European nations (Jauch, 2005), and is a medical emergency. To underscore the seriousness of stroke, in recent years the term brain attack has become increasingly popular, in relation to the established term heart attack used for myocardial infarctions.
Contents |
Types of stroke
Ischemic stroke
Stroke is classified by its cause into two main types: ischemic and hemorrhagic. In ischemic stroke, which occurs in approximately 90% of strokes, a blood vessel becomes occluded and the blood supply to part of the brain is totally or partially blocked.
Ischemic stroke is further divided into thrombotic and embolic (Stroke Center, 2005). In embolic stroke, an embolus, or a travelling particle in a blood vessel, flows with the bloodstream into progressively smaller arteries until it becomes lodged, prohibiting passage of blood. An embolus is most frequently a blood clot, but it can also be a plaque broken off from an atherosclerotic blood vessel or a number of other things including fat, air, and even cancerous cells (Perry and Miller 1961). An embolism may also be formed when the heart pumps ineffectively, allowing the blood to pool and coagulate, as occurs in a condition called atrial fibrillation (NINDS 1999).
In thrombotic stroke, the clot does not travel; it builds up and finally occludes the artery where it forms. When there is a tear in an artery wall, platelets and clotting factors in the blood are drawn to the area and aggregate there, forming a clot. They send out chemicals that can trigger a clotting cascade. Arterial clots usually form around atherosclerotic plaques (NINDS 1999). Since occlusion takes longer, onset of thrombotic strokes is slower.
Blood flow can also be restricted in a condition called arterial stenosis, in which plaques build up on the artery wall, causing the vessel to become narrow and stiff (NINDS 1999).
Hemorrhagic stroke
Hemorrhagic stroke, or intracranial hemorrhage, occurs in about 10% of strokes, when a blood vessel in the brain bursts, spilling blood into the spaces surrounding the brain cells. The Hemorrhagic strokes generally carry greater risk of death and permanent disability than ischemic strokes do.
Watershed stroke
A small proportion of strokes are watershed strokes caused by hypoperfusion (usually due to hypotension) or other vascular problems including vasculitis.
Causes
Ischemic stroke
Ischemic stroke is usually caused by atherosclerosis (fatty lumps in the artery wall), embolism (obstruction of blood vessels by blood clots from elsewhere in the body), or microangiopathy (small artery disease, the occlusion of small cerebral vessels).
Atrial fibrillation and other arrhythmias can lead to clot formation in the heart, which can become emboli and lodge in the brain. Some forms of thrombophilia (increased coagulation tendency) have a predilection for arterial thrombosis and stroke; these include polycythemia vera and the rare paroxysmal nocturnal hemoglobinuria.
Risk factors (for atherosclerosis and small vessel disease) are advanced age, hypertension (high blood pressure), diabetes mellitus, high cholesterol, and cigarette smoking. High blood pressure is the most important modifiable risk factor of stroke.
Hemorrhagic stroke
Causes of hemorrhagic stroke include hypertension, cerebral AVM, cerebral aneurysms, cerebral arteriosclerosis, head injury, congophilic angiopathy, congenital artery defects and prematurity.
Watershed stroke
As opposed to hemorrhagic stroke or embolic (or other atherogenic) stroke, watershed strokes occur in parts of the brain that lie at the boundary between zones of arterial distribution from different arteries. When there is hypotension from any cause, these watershed areas are more susceptible to damage than other areas of the brain.
Signs and symptoms
The symptoms of stroke include the following:
- sudden numbness or weakness, especially on one side of the body hemiplegia;
- reflexes can initially be decreased on the affected side, but are often more exaggerated than on the unaffected side;
- the face is normally spared (as this is served by both hemispheres), but the corner of the mouth can be affected on the same side as the limb symptoms;
- sudden confusion or aphasia (trouble speaking) or understanding speech;
- sudden trouble seeing in one eye (or rarely both);
- pupils of unequal size;
- impaired swallowing reflex;
- sudden trouble walking, dizziness, or loss of balance or coordination.
Some patients lose consciousness as part of the initial presentation. This occurs more often in hemorrhagic stroke than in thrombosis.
A sudden-onset severe headache can denote subarachnoid hemorrhage, which is a stroke-like clinical entity. Some other forms of stroke can feature headaches.
If the symptoms resolve within an hour, or maximum 24 hours, the diagnosis is transient ischemic attack (TIA), and not a stroke. This syndrome may be a warning sign, and a proportion of patients develop strokes in the future. The chances of suffering a stroke can be reduced by using aspirin, which inhibits platelets from aggregating and forming obstructive clots.
Diagnosis
Stroke is diagnosed through several techniques: a neurological examination, blood tests, CT scans (without contrast enhancements) or MRI scans, Doppler ultrasound, and arteriography.
If a stroke is confirmed on imaging, various other studies may be performed to determine whether there is a peripheral source of emboli:
- an ultrasound/doppler study of the carotid arteries (to detect carotid stenosis)
- an electrocardiogram (ECG) and echocardiogram (to identify arrhythmias and resultant clots in the heart which may spread to the brain vessels through the bloodstream)
- a Holter monitor study to identify intermittent arrhythmias
- an angiogram of the cerebral vasculature (if a bleed is thought to have originated from an aneurysm or arteriovenous malformation)
Pathophysiology
When neurons and glia receive insufficient oxygen and nutrients due to inadequate blood supply, a biochemical cascade called the ischemic cascade is unleashed. The ischemic cascade, as well as sudden bleeding from ruptured blood vessels into or around the brain, can injure and kill cells. These damaged cells can linger in a compromised state for several hours. With timely treatment, these cells can be saved. Intriguingly, when the brain cells suffer the ischemia, they begin to fill up with free zinc ions which are released from some of their proteins, especially metallothionein, which can release 7 zinc ions per molecule. This released zinc is a major player in the ensuing death of the brain cells. Drugs that buffer the zinc and reduce the level of free zinc are already being tested to reduce brain cell death after stroke.
Prevention
Prevention is an important public health concern. Identification of patients with treatable risk factors for stroke is paramount. Treatment of risk factors in patients who have already had strokes (secondary prevention) is also very important as they are at high risk of subsequent events compared with those who have never had a stroke. Medication or drug therapy is the most common method of stroke prevention. Surgery such as Carotid endarterectomy can be used to remove significant narrowing of the neck (internal) carotid artery which supplies blood to the brain and this operation has been shown to be an effective way to prevent stroke in particular groups of patients.
Some brain damage that results from stroke may be secondary to the initial death of brain cells caused by the lack of blood flow to the brain tissue. This brain damage is a result of a toxic reaction to the primary damage. Researchers are studying the mechanisms of this toxic reaction and ways to prevent this secondary injury to the brain. Scientists hope to develop neuroprotective agents to prevent this damage. Another area of research involves experiments with vasodilators, medications that expand or dilate blood vessels and thus increase the blood flow to the brain. Basic research has also focused on the genetics of stroke and stroke risk factors. One area of research involving genetics is gene therapy. A promising area of stroke animal research involves hibernation. The dramatic decrease of blood flow to the brain in hibernating animals is extensive enough that it would kill a non-hibernating animal. If scientists can discover how animals hibernate without experiencing brain damage, then maybe they can discover ways to stop the brain damage associated with decreased blood flow in stroke patients. Other studies are looking at the role of hypothermia, or decreased body temperature, on metabolism and neuroprotection. Scientists are working to develop new and better ways to help the brain repair itself and restore important functions to stroke patients. Some evidence suggests that transcranial magnetic stimulation (TMS), in which a small magnetic current is delivered to an area of the brain, may possibly increase brain plasticity and speed up recovery of function after stroke.
Treatment
Early assessment
It is important to identify a stroke as early as possible because patients who are treated earlier are more likely to survive and have better recoveries.
If a patient is suspected of having a stroke, emergency services should be contacted immediately. The patient should be transported to the nearest hospital that can provide a rapid evaluation and treatment with the latest available therapies targeted to the type of stroke. The faster these therapies are started for hemorrhagic and ischemic stroke, the chances for recovery from each type improves greatly. Quick decisions about medication and the need for surgery have been shown to improve outcome.
Only detailed physical examination and medical imaging provide information on the presence, type, and extent of stroke.
Studies show that patients treated in hospitals with a dedicated Stroke Team or Stroke Unit and a specialized care program for stroke patients have improved odds of recovery.
Ischemic stroke
As ischemic stroke is due to a thrombus (blood clot) occluding a cerebral artery, a patient is given anticoagulant medication (aspirin, clopidogrel, or warfarin, dependant on the cause) when this type of stroke has been found. As such treatment would be dangerous in hemorrhagic stroke, it is essential that this form of stroke is ruled out with medical imaging.
In increasing numbers of specialist centers, thrombolysis ("clot busting") is used to dissolve the clot and unblock the artery. However, this treatment is new, expensive, potentially dangerous and often contraindicated. There is also a time constraint: studies indicate that after three hours of symptom onset the damage to the brain is irreversible, and that after this time thrombolysis provides no benefit. These requirements prevent routine thrombolysis of ischemic stroke in most hospitals, especially when no stroke expert is available.
Whether thrombolysis is performed or not, the following investigations are required:
- Stroke symptoms are documented, often using scoring systems such as the National Institutes of Health Stroke Scale, the Cincinnati Stroke Scale, and the Los Angeles Prehospital Stroke Scale. The latter is used by emergency medical technicians (EMTs) to determine whether a patient needs transport to a stroke center.
- A CT scan is performed to rule out hemorrhagic stroke
- Blood tests, such as a full blood count, coagulation studies (PT/INR and APTT), and tests of electrolytes, renal function, liver function tests and glucose levels are carried out.
Other immediate strategies to protect the brain during stroke include ensuring that blood sugar is as normal as possible (such as commencement of an insulin sliding scale in known diabetics), and that the stroke patient is receiving adequate oxygen and intravenous fluids. The patient may be positioned so that his or her head is flat on the stretcher, rather than sitting up, since studies have shown that this increases blood flow to the brain. Additional therapies for ischemic stroke include aspirin (50 to 325 mg daily), clopidogrel (75 mg daily), and combined aspirin and dipyridamole extended release (25/200 mg twice daily).
It is common for the blood pressure to be elevated immediately following a stroke. Studies indicated that while high blood pressure causes stroke, it is actually beneficial in the emergency period to allow better blood flow to the brain.
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 the stroke has been the result of cardiac arrhythmia (such as atrial fibrillation) with cardiogenic emboli, treatment of the arrhythmia and anticoagulation with warfarin or high-dose aspirin may decrease the risk of recurrence.
Hemorrhagic stroke
Patients with bleeding into (intracerebral hemorrhage) or around the brain (subarachnoid hemorrhage), require neurosurgical evaluation to detect and treat the cause of the bleeding. Anticoagulants and antithrombotics, key in treating ischemic stroke, can make bleeding worse and cannot be used in intracerebral hemorrhage. Patients are monitored and their blood pressure, blood sugar, and oxygenation are kept at optimum levels.
Care and rehabilitation
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 is multidisciplinary in the fact that it involves a team 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 rehabiliation medicine. Some teams may also include psychologists and social workers and pharmacists.
Good nursing care is fundamental in maintaining skin care, feeding, hydration, and positioning as well as the monitoring of vital signs such as temperature, pulse, and blood pressure. Stroke rehabilitation begins almost immediately.
For most stroke patients, physical therapy is the cornerstone of the rehabilitation process. Another type of therapy involving relearning daily activities is occupational therapy (OT). OT involves exercise and training to help the stroke patient relearn everyday activities sometimes called the Activities of daily living (ADLs) such as eating, drinking and swallowing, dressing, bathing, cooking, reading and writing, and toileting. Speech and language therapy is appropriate for patients with problems understanding speech or written words, or problems forming speech.
Patients may have particular problems such as complete or partial inability to swallow, 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 after a week the swallow is still not safe then a percutaneous endoscopic gastrostomy (PEG) tube is passed and this can remain indefinitely.
Stroke rehabilitation can last anywhere from a few days to several months. Most return of function is seen in the first few days and weeks, and then improvement falls off. Complete recovery is unusual but not impossible. Most patients will improve to some extent.
Prognosis
Disability affects 75% of stroke survivors enough to decrease their employability (Coffey et al., 2000 p.601). 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 (Stanford, 2005). Dysfunctions correspond to areas in the brain that have been damaged.
Some of the physical disabilities that can result from stroke include paralysis, numbness, pressure sores, pneumonia, incontinence, apraxia (inability to perform learned movements), difficulties carrying out daily activities, appetite loss, vision loss, and pain. If the stroke is severe enough, 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 (Senelick et al., 1994). 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 (Coffey et al., 2000 p.613). Some patients show the opposite of what they feel, for example crying when they are happy (Villarosa et al., 1993). Emotional lability occurs in about 20% of stroke patients.
Cognitive deficits resulting from stroke include perceptual disorders, speech problems, dementia, and problems with attention and memory. A stroke sufferer may be perpetually unaware of his or her own disabilities or even the fact that he or she has suffered a stroke. In a condition called agnosia, or neglect, a patient is unable to see anything on the left or right side and is unaware of and unable to conceive of anything on the neglected side.
Risk factors
The most important risk factors for stroke are hypertension, heart disease, diabetes, and cigarette smoking. Other risks include heavy alcohol consumption, high blood cholesterol levels, illicit drug use, and genetic or congenital conditions. Family members may have a genetic tendency for stroke or share a lifestyle that contributes to stroke. Having had a stroke in the past greatly increases one's risk of future strokes.
One of the most significant stroke risk factors is advanced age. 95% of strokes occur in people age 45 and older (Senelick, Rossi, Dougherty 1994), and two-thirds of strokes occur in those over the age of 65 (NINDS 1999, Senelick et al., 1994). 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 fetuses.
Sickle cell anemia, which can cause blood cells to clump up and block blood vessels, also increases stroke risk. Stroke is the second leading killer of people under 20 who suffer from sickle-cell anemia (NINDS 1999).
Men are 1.25 times more likely to suffer CVA's than women (NINDS 1999), yet 60% of deaths from stroke occur in women (Villarosa et al., 1993). Since women live longer, they are older on average when they have their strokes and thus more often killed (NINDS 1999, NIMH 2002). Some risk factors for stroke apply only to women. Primary among these are pregnancy, childbirth, menopause and the treatment thereof (HRT). Stroke seems to run in some families.
History
Over 2,400 years ago, Hippocrates (460 to 370 BC) was first to describe the phenomenon of sudden paralysis, which we now know is caused by stroke. Apoplexy, from the Greek word meaning "struck down with violence,” first appeared in Hippocratic writings to describe stroke symptoms (Kopito 2001; Thompson 1996).
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 (NINDS 1999; Thompson 1996). Wepfer also identified the main arteries supplying the brain, the vertebral and carotid arteries, and identified the cause of ischemic stroke when he suggested that apoplexy might be caused by a blockage to those vessels (NINDS 1999).
See also
External links
- The original text for this article was taken from the National Institute of Neurological Disorders and Stroke public domain resource at this page
- Cerebrovascular disease and risk of stroke
- Stroke Center of the Washington University School of Medicine
- Stroke Engine. Heart and Stroke Foundation of Canada. Edited by a consorsium of researchers of McGill University, Canada. Information on stroke rehabilitation.
References
- Coffey C. Edward, Cummings Jeffrey L, Starkstein Sergio, Robinson Robert. "Stroke". The American Psychiatric Press Textbook of Geriatric Neuropsychiatry, Second Edition. Washington DC: American Psychiatric Press, Inc, 2000. pp.601-617.
- Jauch, Edward C. 2005. “Acute Stroke Management.” eMedicine.com, Inc.
- Kopito, Jeff. 1996. "A Stroke in Time". MERGINET.com, September 2001, Volume 6 Number 9. Available.
- National Institute of Neurological Disorders and Stroke (NINDS). 1999. National Institutes of Health., Stroke: Hope Through Research.
- Perry, Thomas and Miller Frank. Pathology: A Dynamic Introduction to Medicine and Surgery. Boston: Little, Brown and Company, 1961.
- Senelick Richard C., Rossi, Peter W., Dougherty, Karla. Living with Stroke: A Guide For Families. Contemporary Books, Inc., Chicago IL, 1994.
- Stanford Hospital & Clinics. 2005. Cardiovascular Diseases: Effects of Stroke.
- Stroke Center of the Washington University School of Medicine.
- Thompson, Jesse E. " The Evolution of Surgery for the Treatment and Prevention of Stroke: The Willis Lecture". Stroke. 27:1427-1434.
- Villarosa, Linda, Ed., Singleton, LaFayette, MD, Johnson, Kirk A., Black Health Library Guide to Stroke. Henry Holt and Company, New York, 1993.