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Strokes
Strokes |
Strokes
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Strokes are the third leading cause of death in the United States. There are approximately 700,000 strokes in the United States each year, and about 160,000 deaths. An estimated 11 million Americans annually suffer small strokes every year that are silent; they do not produce symptoms that are recognized but indicate an increased risk of larger strokes in the future.
A stroke is a highly treatable disease like a heart attack, but one must immediately get to a stroke center or hospital for early treatments. Unfortunately,due to delays, many are left with major physical debilities that totally change their lives.
Strokes are the second most common cause of disability in high income countries and death worldwide. The incidence varies with age, and in Western societies about 80% of strokes are caused by focal cerebral ischemia due to arterial occlusion, and 20% is due to hemorrhage.1
It is a complex process of extracellular excitatory amino acids, free-radical formation, and inflammation. Initially, a central core of low perfusion is surrounded by dysfunction due to a loss of structural integrity from ischemia. In a few minutes to hours, there are clinical deficits, many of which can be reversible with immediate care (less than three hours), and much depends on the remaining blood flow to the ischemic area. The thirty-day mortality in Western society is between 10-17%, and this percentage increases with age and comorbidities, such as ischemic heart disease, diabetes, and, most importantly, the size of the infarct. After a few months, mortality is reported at 2.5% with lacunars infarcts to 70% with space occupying hemisphere infarction.
- Facts:
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- Stroke is characterized by a sudden onset of a focal neurological deficit with a stepwise gradual progression of symptoms, including vision loss, speech loss, weakness, unstable balance, sensory loss, usually unilateral, and, sometimes, loss of consciousness.
- Occasionally, onset is with seizures or unconsciousness, with the differential being migraine, postictal (seizure) paralysis, low blood sugar, and difficulty with conversation versus a subdural hematoma or brain tumor.
- A cardioembolism may cause brain ischemia, often in younger patients less than age 50 with no known cardiovascular risk factors. Rarely, carotid artery dissection, fever, a cardiac murmur, suggesting infective endocarditis, with headache and an increased sedimentation rate, and giant cell arteritis in patients over age 50 are seen. - Signs of a Stroke:
- Each year, 700,000 Americans suffer from strokes. About half do not realize that they are having a stroke. About 150,000 Americans die of stroke per year.
- Red flags:
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- Sudden weakness on one side of the body, slurred speech or inability to speak, numbness and tingling in an arm or leg, facial droop, decreased vision in one eye.
- Keep a record of your medications in your wallet, as well as your medical history.
- The sudden onset of dizziness, unsteadiness or a sudden fall, visual dimness especially in one eye, difficulty speaking or trouble understanding speech, and numbness, weakness in face, arms or legs, especially on one side of the body are significant signs of a stroke. - The Risk Factors for a Stroke
Risk evaluation is dependent on many factors, some of which cannot be changed. -
1. Age - as one ages, the risk doubles every ten years after age 55.
2. Sex - men have more strokes than women.
3. Race - African Americans, Hispanics, and Asian Americans have a higher rate of strokes than non-Hispanic whites.
4. Genetics - a family history of a stroke places family members at greater risk.
5. Previous strokes - one in six people with ischemic (atherosclerotic) strokes, who survive, are at greater risk of another stroke within two years.
6. People who have TIAs (transient ischemic attacks - a mini stroke) are at about a ten-times greater risk of having a major stroke.
7. Hypertension - increases the strain on the blood vessels in the brain.
8. Heart disease - cardiovascular coronary artery disease.
9. Poor nutrition - not eating fruits, vegetables, whole grains and fish with excess dietary sodium and a low potassium diet.
10. Lack of a daily exercise program.
11. Overweight and obesity.
12. Diabetes is a stroke risk and requires active treatment.
13. Cigarette smoking almost doubles the risk of stroke. -
Strokes can be prevented through controlling blood pressure (hypertension), cholesterol (HD/LD/triglycerides lipids), and other modifiable factors. Changes in lifestyle, such as not smoking, moderate to vigorous exercise thirty minutes a day, maintaining a healthy weight and eating a prudent heart-healthy diet are also very important.
It has been estimated that about 80% of the risk of a stroke is related to high blood pressure. When the blood pressure is controlled, the stroke risk may decrease about 40%, which also reduces the heart attack rate by about 27% and heart failure by 54%.
Once a person is in the recovery phase, an active stroke rehabilitation program may take many months, often six months to a year to get the maximum recovery from a stroke.
Prevention of strokes -
1. Diet - fruits and vegetables are often rich in potassium along with a healthy diet, as well as potassium supplementation if needed.
2. Eating fish two or three times a week provides omega-3 fatty acids that may help lower stroke and heart attack rates. Those eating salmon, tuna (baked or broiled) or herring four times a week were seen to have a 27% lower risk of stroke than those who ate it once a month. Those eating fried fish or fish burgers more than once a week had a 40% higher risk of stroke.
3. Exercise thirty minutes a day (moderate to vigorous) - by accumulating several activities including housework, walking stairs, or taking brisk walks. Exercise lowers blood pressure, reduces blood clots, and can cut the stroke rate in half.
4. Those who are overweight or obese have at least a 30% or about 50% higher risk for stroke respectively compared to normal weight men. Exercise helps maintain a healthy weight and also treats diabetes actively.
5. Talk to your doctor to see if daily aspirin would be helpful for you.
Strokes and Transient Neurological Attacks - TIAs
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The difference between a transient ischemic attack (TIAs)2 and ischemic stroke attacks is that the symptoms resolve in less than 24 hours. The underlying cause can be identical for TIA and stroke; thus, early diagnosis and treatment is needed. Symptoms are usually easy to diagnosis but often difficult to distinguish a TIA from a stroke early. 3
Patients are not always helpful, as they can be affected with neurological deficits, and symptoms are often indistinguishable from each other.
Accurate diagnosis is vital, and a diagnosis is important, as the risk of a stroke in days or weeks following a TIA is high, with an average risk of about 11% at 90 days after a TIA when carefully monitored and followed following a TIA diagnosis. TIA treatment is complex, as it requires an Emergency Department evaluation, hospitalization, and sometimes stroke prevention if the diagnosis is missed, as there are competing conditions, such as migraine and vasovagal syncope. The differential may include Meniere's disease, hyperventilation, cardiac syncope, hypoglycemia, or orthostatic hypotension. Also, following a TIA, it may be a harbinger of an increased risk for dementia (especially vascular dementia), as well as a potential risk for stroke or myocardial infarction.
- The implications of this are as follows:
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A TNA - transient neurological attack - may be non-focal and treated in a benign way, and there's no consistent evaluation plan or guidelines for prognostic information.
No matter what the cause of the TNA/TIA events are, greater attention needs to be exerted in order to find who is at greater risk through a more complete evaluation, especially to rule out underlying contributing diseases.4
The goal is to assess the stroke risk by using a validated ABCD.
- Only identifying the potential cause of a TNA/TIA can reduce the risk of subsequent stroke and vascular dementia. These investigations are justified. The following are to be considered:
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1. Brain imaging
2. Carotid imaging
3. Electrocardiogram
4. Careful history and physical examination
5. Cholesterol panel, glucose, hemoglobin A1c
6. Assessment for vascular risk factors
Cardiac Monitoring and Echocardiogram
A vague diagnosis is unacceptable.
Treatment and preventive practices are recommended for all patients with TIA, including anti-platelet drugs, such as aspirin, Dipyridamole, clopidogrel, a statin and an antihypertensive program, using agents as necessary.
Hospitalization may be indicated, especially when there is a non-focal TNA because of a shorter stroke risk versus patients with high risk for a stroke.
Those with a TIA/TNA with sudden onset symptoms without an underlying etiology need a diagnosis, if possible to help plan future follow-up care, especially adding preventive lifestyle measures.
There is an association between an elevated non-fasting triglyceride blood level associated with increased risk of myocardial infarction, ischemic heart disease and death, and arteriosclerotic events.5 In this study of 13,956 participants, it was shown that non-fasting triglyceride levels were associated with an increased risk of ischemic strokes.Stroke Assesment and Treatments
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There is a National Institutes of Health Stroke Scale that is often used for assessment. An irregular pulse may suggest atrial fibrillation or elevated blood pressure, or a hypertensive encephalopathy (brain dysfunction), and this precludes thrombolysis if blood pressures are over 185/110. A carotid bruit suggests carotid artery narrowing or stenosis.
Laboratory tests: Blood glucose for hypoglycemia, CBC, prothrombin time, and a partial thromboplastin time (PTT), especially if thrombolytic therapy is being considered, and an EKG to rule out atrial fibrillation or an acute myocardial infarction. Strokes may be complicated by myocardial ischemia or arrhythmias or a heart attack, and monitoring for these for twenty-four hours is recommended. Perform an echocardiogram if infective endocarditis is suspected.
Imaging: A cerebral infarction cannot be distinguished from a hemorrhage based on symptoms, and either a CAT scan or MRI is required to differentiate these two entities. Non-contrast CTs are more available and less expensive and can be sensitive for diagnosis of acute hemorrhage, but MRI has a higher sensitivity for acute ischemic changes. When intra-arterial thrombolysis or mechanical clot retrieval is considered, CT or MRI angiography is useful to identify the site of arterial occlusion. They provide complete visualization from the aortic arch to the Circle of Willis and beyond.
Intravenous thrombolysis: The National Institute of Neurological Disorders and Stroke Recombinant Tissue Plasminogen Activator (NINDSrt-PA) Stroke Study demonstrated the efficacy of intravenous rt-PA within three hours of the onset of stroke symptoms. Maximal total dose is 90 mg. Thirty one to fifty percent had a favorable neurological or functional outcome at three months versus 20-38% in those who received a placebo. The mortality rates were similar in both groups. Symptomatic intracranial hemorrhage occurred in 6%. More studies that treated with rt-PA six hours after onset of symptoms failed to find benefit from thrombolysis versus treatment at three hours, but benefits are greatest when started as early as possible. The incidence of intracranial hemorrhage increases with age.
Additional Treatments:
Aspirin. Two large studies have shown that between 160 to 300 mg per day initiated within 48 hours after the onset of the stroke and continued for two weeks or until discharge reduced the death rate and dependency at discharge or at six months. This was probably due to reducing the risk of recurrent ischemic strokes. The benefits were small, as one needed to treat 77 patients to obtain one patient with an improved outcome. The safety profile was good. Aspirin should be withheld during the first twenty-four hours.5
The Role of Anticoagulant Therapy
Six meta-analysis studies involving 21,966 patients found no evidence of the value of anticoagulants, either heparin, low molecular weight, thrombin inhibitors, or oral anticoagulants in the acute phase, improved functional outcome. Also, there was no proven functional improvement using anticoagulants with acute cardioembolic strokes, as well.
- Prevention of complications:
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1. Nutrition is a major problem; although, routine use of oral nutritional supplements or tube feedings to prevent or treat under nutrition in hospitalized stroke patients resulted in long-term functional outcome.
2. Prevention of deep venous thrombosis and pulmonary emboli, which are increased risks, especially with age and stroke severity (often with leg paralysis). A lot is dependent on stroke severity. Anticoagulants did not improve overall functional outcomes; although, unfractionated heparin or a low-molecular weight heparin has been recommended in patients at high risk for deep vein thrombosis, especially for immobile patients.
3. Patients with large supratentorial infarcts, which are space occupying with brain edema, are at higher risk for uncal herniation between the second and fifth days with high case mortality up to 78%. There is no proven effective medical treatment thus far.
4. Surgical treatment for space occupying lesions in the region of the middle cerebral artery in the first 48 hours after stroke onset reduced fatal mortalities to 22% versus 78% in the medical management group and decreased disability to 57% from 79%.
5. It is important to control hypertension, hypercholesterolemia with statin therapy, as well as control diabetes, promote smoking cessation, and use of carotid endarterectomy for stenosis when indicated. - Even in the United States, only a small percentage of patients receive rt-PA intravenous due to the restriction of the three-hour time window after onset of symptoms. There have been no conclusive studies proving intravenous thrombolysis recanalizes occluded arteries. There has been recanalization of an occluded middle cerebral artery two hours after thrombolysis in up to one-third of patients.
Newer technology is being developed. Improved function and less disability have been seen when the thrombolytic therapy was directed against the site of the occlusion. This could be a more rapid treatment and improved recanalization.
Other essential early treatments: - 1. Control high blood pressure.
2. Control high glucose levels.
3. Reduce body temperature in the first few hours, as these factors lead to a higher mortality.
4. Check cholesterol. Treat if elevated (see a cardiologist).
The Debate on Whether Lowering the Blood Pressure Affects Cerebral Profusion
The current consensus recommends withholding anti-hypertensive therapy during the acute phase unless the diastolic blood pressure exceeds 120 mmHg of mercury or a systolic over 220mmHg of mercury. Patients with such blood pressures are not candidates for rt-PA thrombolysis therapy. Try to maintain systolic pressure under 188mmHg and diastolic at less than 105mmHg of mercury.
Ways of Neuroprotection
There are many strategies known, but only rt-PA and aspirin have been shown to be clearly effective.
Hypothermia has been shown to reduce infarct volume and improve neurologic outcomes in animal models and improved functional outcomes in randomized clinical patient trials with global cerebral ischemia after cardiac arrest, but results were not consistent with traumatic brain injury.
In conclusion
After a clinical evaluation, and if less than three hours, rt-PA should be considered after clearance with either a CAT scan or an MRI to rule out the chances of a hemorrhagic stroke. Aspirin should be started after twenty-four hours, 300 mg daily for the first two weeks and then a lower dose, and dypridamole is considered for secondary prevention. Aggressive management of cardiovascular diabetic hypertensive risk factors, smoking cessation, hypertension control and statins for lipid disorders are warranted.
Contraindications to Thrombolysis
Onset greater than three hours, intravenous hemorrhage by CT or MRI, head trauma or stroke in prior three months, myocardial infarction in less than three months, GI or other hemorrhage, major surgery two weeks earlier, history of intracranial hemorrhage, systolic blood pressure greater than 185 or diastolic greater than 110mmHg of mercury. Also, evidence of active bleeding, oral anticoagulation therapy with an INR greater than 1.7, prior use of heparin 48 hours with prolonged PTT, and a platelet count less than 100,000 per cubic mm, blood sugar less than 30 mg/dl.
Acute Cardioembolic Stroke6
Anticoagulants were shown to increase intracerebral bleeding and did not reduce death or disability in acute cardioembolic stroke. In a randomized control trial comparing anticoagulants (unfractionated heparin, low-molecular-weight heparin, or heparinoids) with other treatments or placebo given within 48 hours of the onset of a stroke were assessed. There were 4,624 patients in the series, of which 3797 had atrial fibrillation, and 827 had other cardioembolic sources.
The results of the study showed that anticoagulants did not differ significantly from placebo or aspirin for death or disability and recurrent strokes or all strokes, but they did increase the risk of symptomatic intracranial bleeding. Thus, there was no major difference between the anticoagulant placebo and aspirin for death or disability from stroke, but they did increase the risk for intracranial bleeding.
Of note is that short-term anticoagulation is commonly used for ischemic strokes - some ten years ago heparin was commonly used. Paciaroni and colleagues have shown that there were no benefits of anticoagulation when given within hours of an ischemic stroke, but did increase the risk for hemorrhagic complications. They felt that short-term anticoagulation for reducing the risk for recurrent ischemic stroke, and there was no net benefit in mortality or disability.
The prophylactic use of heparins for deep venous thrombosis still remains somewhat uncertain in non- ambulatory patients, and this is still being investigated. A lower dose for prophylaxis is more effective than compression devices, but those with cardioembolic transischemic attacks may also benefit in short-term anticoagulation, as the risk for recurrence is particularly high for patients, and the risk for brain hemorrhages should be substantially lower in the absence of major brain infarction.
The Role of Exercise and Your Brain
Doing aerobic exercise increases the blood flow to the brain, which can help brain cell nourishment and can improve brain function and cognition.
There are summary searches, showing the growth of new brain cell neurons in the hippocampus area of the brain, which controls learning and memory. Walking twenty to thirty minutes a day is a good exercise.
Researchers say specialized treadmill may help stroke patients re-learn how to walk. A "specialized treadmill can help stroke patients learn to walk correctly again,"7 ..."seven stroke patients who did what's called locomotor treadmill training with partial body-weight support, which uses a treadmill outfitted with a harness. By securing patients to a harness to support a portion of their body weight while they walk on the treadmill helped patients re-learn how to walk in a safe and controlled way. Early intervention is vital for success. Patients started on the treadmill as soon as possible during the acute period of recovery after their stroke."
Vigorous walking for about an hour a day five times a week can chop a dozen years off the biological age of persons 64 and older.8
Physical activity can extend a patient's functional independence, suggested Roy Shephard, MD, PhD., of the University of Toronto and colleagues.9
The researchers found that "a loss of at least four to five mL/kg/min" of oxygen "per decade continues into advanced old age," limiting "the amount of activity a patient could participate in without becoming fatigued."
In patients over 64, vigorous walking boosted "maximal oxygen intake by about 25 percent within three months." Moreover, those individuals had an "increase in maximal oxygen intake of six mL/kg/min, or a decrease of about 12 years of biological age." Physical activity "also hastens recovery from injuries, and any additional muscle power may prevent falls."
- References
1 - van Worp, H. B. and van Gijn, J., "Acute Ischemic Stroke."N Engl J Med, 357: 572-9, 2007.
- 2
- S. Claiborne Johnson, MD, PhD, "Transient Neurological Attack, A Useful Concept" JAMA, 2007;298(24):2912-2913.
- 3
- Koudstaalp, P. J., Gentsma, I. G., Van, G. I. J. N. J, "Clinical Disagreement on the Diagnosis of Transient Ischemic Attack: Is the Patient or the Doctor to Blame?" Stroke, 1989, 2002, 300-30
- 4
- Michiel J. Bos, MD, MSc; Marie Josee E. van Rijn, MD, PhD; Jacqueline C. M. Witteman, PhD; Albert Hofman, MD, PhD; Peter J. Koudstaal, MD, PhD; Monique M. B. Breteler, MD, PhD, "Incidence in Prognosis of Transient Neurological Attacks," JAMA, 2007;298(24):2877-2885.
- 5
- Freiberg, JI, Tybjarg-Hansen, A, Jensen, JS, Nordestgaard, BG, MD, DMSc, "Non-fasting Triglycerides and Risk of Ischemic Stroke in the General Population," JAMA, 2008; 300(18): 2142-2152.
- 6
- Paciaroni M, and Agnelli, G, Micheli, S, Caso, V, "Efficacy and Safety of Anticoagulant Treatment in Acute Cardioembolic Stroke: A Meta-analysis of Randomized Controlled Trials." Stroke, 2007; 38: 423-30
- 7
- Karen J. McCain, PT, DPT, NCS, Fabian E. Pollo, PhD, Brian S. Baum, MS, Scott C. Coleman, MS, Shawn Baker, PT, DPT, Patricia S. Smith, PT, PhD, NCS, Locomotor Treadmill Training With Partial Body-Weight Support Before Overground Gait in Adults With Acute Stroke: A Pilot Study Archives of Physical Medicine and Rehabilitation Volume 89, Issue 4, Page A9 (April 2008)
- 8
- M. Hamer and Y. Chida, Walking and primary prevention: a meta-analysis of prospective cohort studies British Journal of Sports Medicine 2008;42:238-243
- 8
- Roy Shephard, MD, PhD, Maximal oxygen intake and independence in old age, BR J Sports Med. 2009 May;43(5):342-6. Epub 2008 Apr 10
First appeared September 27, 2009