Neurology

Stroke

BY: PHYSICIANS COMMITTEE FOR RESPONSIBLE MEDICINE

Overview and Risk Factors

Stroke, an infarct in the brain, is the third-leading cause of death in the United States. About 80% of strokes are ischemic in origin and generally result from occlusion of a major cerebral artery by an embolus or thrombus. Global ischemia can occur after respiratory arrest or after cardiac events such as asystole or ventricular fibrillation. Hemorrhagic strokes occur when blood from a ruptured vessel (eg, an aneurysm) compresses and damages brain tissue. Venous strokes, due to thrombosis of the venous dural sinuses, are uncommon but may be associated with hypercoagulability, dehydration, and the use of estrogen.

A transient ischemic attack (TIA) produces similar signs and symptoms, but is transitory. It often resolves completely within 30 to 60 minutes, although symptoms may last several hours. Occurrence of a TIA indicates a need for thorough neurologic and cardiovascular evaluation of stroke risk.

Warning signs of stroke include the following sudden changes:

  • Numbness (paresthesia) or weakness (paresis) of the face, arm, or leg, usually on one side of the body.
  • Confusion, difficulty speaking (dysarthria or aphasia) or understanding.
  • Visual disturbances, which may include partial or complete vision loss.
  • Dizziness and/or ataxia.
  • Severe headache with no known cause-particularly with hemorrhagic strokes.

Risk Factors

Compared with whites, African Americans and Latinos have higher incidence and mortality rates of stroke. It is currently unclear whether these differences are due to environmental or genetic causes. Other risk factors include:

Age. The risk of stroke doubles every 10 years beyond age 55.1,2

Gender. Recent studies have shown that women now have a slightly higher prevalence of stroke than men. Case-fatality rates due to stroke are also higher in women.3

Hypertension is the most important modifiable risk factor, especially for hemorrhagic stroke. Both systolic and diastolic hypertension are associated with an increased risk. (For more information, see Hypertension chapter.)

Smoking. Cigarette smoking increases risk for ischemic stroke, intracerebral hemorrhage, and subarachnoid hemorrhage. The risk is reduced to that of a nonsmoker within 2 to 5 years of smoking cessation.

Diabetes.

Hyperlipidemia.

Homocysteine. Elevated levels of homocysteine are thought to cause endothelial dysfunction, thus increasing risk for vascular disease and cerebrovascular pathology.4,5

Sedentary lifestyle. Higher levels of occupational or leisure-time physical activity protect against stroke.6 A study of women undergoing coronary angiography found that those with higher activity levels were at significantly lower risk for cardiovascular events, including stroke.7

Poor nutrition. High-fat, high-sodium diets and a lack of key nutrients such as folic acid have been associated with increased risk for stroke (see Nutritional Considerations).

Carotid stenosis. Both symptomatic and asymptomatic stenoses of the internal carotid arteries are associated with increased risk for ischemic stroke.8

Atrial fibrillation. In the Framingham Study, patients with atrial fibrillation had 5-fold greater risk of stroke than their healthy counterparts.9 Further, the attributable risk of stroke due to atrial fibrillation increased with age from 1.5% for persons aged 50 to 59 years, to 23.5% for those aged 80 to 89 years.9

Vasculitis.

Sickle cell disease.

Migraine. Studies have found that migraines with aura were strongly associated with both symptoms and actual risk of stroke and TIA.10 Hemiplegic and basilar migraines are also risk factors.

Alcohol abuse.

Drug abuse. Abuse of cocaine and amphetamines may result in hemorrhage.

Diagnosis and Treatment

Diagnosis 

Evaluation should include a detailed history of symptom onset, a thorough physical (including neurologic) examination, and imaging tests to determine whether the stroke is hemorrhagic or ischemic. Evaluation of the cardiac rhythm is also essential. Paroxysmal atrial fibrillation may easily be missed if the patient is not closely monitored.

Laboratory tests normally include a complete blood count (CBC), blood glucose level, erythrocyte sedimentation rate (elevated in temporal arteritis or other vasculitides), lipoprotein and triglyceride levels, and coagulation tests. Young patients and those without cardiovascular risk factors may have abnormal antiphospholipid antibodies (specifically lupus anticoagulant).

Computed tomography (CT) scan of the brain helps determine whether a stroke is hemorrhagic or ischemic, and is the initial study of choice. However, areas of infarct due to ischemia are often not acutely visible. CT is necessary before thrombolysis consideration, which must be given within three hours of the earliest symptom onset. Some newer, intravascular techniques may extend this brief window, but currently they are available only in tertiary care settings.

Subarachnoid hemorrhage on CT scan strongly suggests an aneurysm, although an arteriovenous malformation is also a possibility. Aneurysms and other vascular malformations can often be identified by CT scan or by magnetic resonance imaging (MRI), but cerebral angiogram (conventional or CT angiogram) is the preferred method, particularly for identification of aneurysms. MRI (diffusion– and perfusion–weighted images) is best for detecting ischemic strokes and can show damaged areas that are at risk even at the earliest stages of stroke.

Carotid duplex ultrasonagraphy, arteriography, or magnetic resonance angiography (MRA) may determine if stroke has occurred as a result of carotid occlusion. MRA is generally more accurate than carotid duplex studies.

Treatment 

Transient ischemic attack (TIA)

Because the risk of recurrent strokes is high in patients who have suffered a TIA or stroke, it is essential to identify the cause and implement therapy to reduce risk.

  • Antiplatelet therapy with aspirin or its alternatives (eg, clopidogrel, ticlopidine, or aspirin plus dipyridamole) can reduce stroke risk.
  • Warfarin should be considered if cardiac thrombi and/or atrial fibrillation are involved. Investigation for cardiac abnormalities (including right to left shunts) should be considered, particularly in young patients with stroke or TIA, or if there is a high index of suspicion for embolus.
  • Patients at high risk for stroke may require carotid endarterectomy if stenosis is over 70% on the symptomatic side. Treatment of stenosis in patients without prior ischemic symptoms remains controversial, although very high grade stenosis may warrant surgical consideration.
  • If hypercoagulability is suspected (particularly in a young individual with few other stroke risk factors), screening for known causes of hypercoagulibility is appropriate.

Ischemic stroke  

Ischemic stroke may lead to rapid (2-5 days) neurologic deterioration resulting from cerebral edema or hemorrhagic conversion of infarct, and patients may be at risk for brain herniation. Close monitoring should occur in the intensive care unit using the Glasgow coma scale, regular CT imaging, and possibly intracranial pressure monitoring.

Treatment with low-molecular-weight heparin and/or warfarin require initial ruling out of hemorrhage and baseline evaluation of the prothrombin time, partial thromboplastin time, platelet count, international normalized ratio (INR), and other tests to assess coagulation status, if indicated. 

Thrombolytic agents (eg, tissue plasminogen activator) dissolve artery–blocking clots in the brain during the critical early stages of stroke. They are of proven benefit only when administered within 3 hours of stroke onset. Later, the risk of intracerebral hemorrhage outweighs benefit).  

Antiplatelet agents (eg, aspirin, aspirin-dipyridamole, clopidogrel) should be given within 48 hours of stroke if no contraindication exists.

Some studies have also found emergency carotid endarterectomy to be effective. 

Neuroprotective agents have failed to show benefits thus far in clinical trials.

Hemorrhagic stroke 

Treatment of intracerebral hemorrhage depends on the extent of the hemorrhage and its location.

Medical or surgical decompression may be indicated.

Subarachnoid hemorrhage due to an aneurysm or arteriovenous malformation may warrant surgery, depending on the patient's age and clinical status.

A stroke-outcomes assessment should be performed daily to monitor the level of impairment.11

Many hospitals have specialized stroke-recovery units. The intensity of stroke rehabilitation efforts is associated with the degree of recovery.12 Speech therapy, physical therapy, and occupational therapy are important treatments during rehabilitation. 

Nutritional Considerations

The role of dietary factors in stroke is apparent from the disorder's pathophysiology. Because ischemic strokes are caused by atherosclerosis, they are more common in the presence of high blood cholesterol concentrations, which, in turn, are strongly linked to dietary saturated fat and cholesterol and a low fiber intake, among other contributors to cardiovascular risk. Similarly, hypertension contributes to both ischemic and hemorrhagic stroke, so diets that are high in saturated fat or sodium or low in potassium would tend to increase risk. A diet high in potassium, low in sodium, and rich in vegetables, fruits, cereal fiber, and whole grains is probably ideal for reducing stroke risk (Ding 2006).

In epidemiological studies, the following factors are associated with reduced stroke risk:

Reduced dietary fat and cholesterol. Individuals with higher blood cholesterol concentrations tend to have higher stroke risk.13,14 In women with diabetes sampled from the Nurses' Health Study, higher intakes of saturated fat and cholesterol-which raise blood cholesterol concentrations-were related to an increased risk for cardiovascular disease (CVD), including stroke.15

Diets rich in fruits, vegetables, and whole grains. Higher intakes of fruits and vegetables not only reduce fat and cholesterol intake, but also are associated with reduced risk for stroke.16 These foods provide carotenoids, vitamin C, vitamin E, and folate, all of which have been associated with reduced stroke risk in epidemiologic studies.17-22 High intake of cereal fiber was associated with lower risk for both total and hemorrhagic stroke risk in some studies,23,24 and with a lower risk of ischemic stroke in others.25

Consuming less sodium and more potassium. In addition to decreasing the risk for hypertension, lower sodium intake has been found to decrease stroke incidence and mortality.26,27 When compared with persons consuming the lowest amounts of potassium, those eating the highest amounts had the lowest stroke mortality.28,29

Maintenance of healthy body weight. The risk for stroke increases with the degree of overweight,30,31 although evidence to date is stronger for men than for women.32,33 The same dietary changes that reduce cholesterol and blood pressure also tend to reduce body weight (See Hyperlipidemia and Hypertension).

Limiting alcohol consumption. High alcohol intake (30-60 grams, or 3-6 drinks, per day) is associated with a greater risk of stroke.34,35 Consuming moderate amounts of alcohol (1-2 drinks per day) appears to reduce stroke risk,34,36 but may aggravate risk for other conditions, such as breast cancer.

After stroke occurs, adequate nutrition is an essential part of clinical care. In the FOOD Trial Collaboration, poor nutritional status was associated with worse outcomes at 6 months post stroke.37

Homocysteine. Elevated homocysteine levels are associated with heightened stroke risk. Because dietary supplementation with folic acid, pyridoxine, and vitamin B12 reduces homocysteine levels, two large supplementation trials were carried out with these vitamins. Despite the strong theoretical basis, there was no observable decrease in stroke risk (Toole 2004, Lonn 2006).

Antioxidants. Antioxidant concentrations are often low in patients with ischemic stroke, and low intake of foods rich in antioxidants is associated with elevated stroke risk. However, so far, supplementation has not been shown to significantly reduce risk.

Orders

See Basic Diet Orders.

Sodium intake less than 2 grams daily.

Nutrition consultation to instruct patient in dietary recommendations and arrange outpatient follow-up.

Physical/occupational therapy consultation for home safety evaluation.

Stroke rehabilitation and speech therapy as appropriate.

What to Tell the Family  

Stroke occurs more frequently among those of advanced age, or who have blood vessel disease, family or previous history of stroke, and poor blood pressure control. However, persons who eat diets rich in fruits, vegetables, and fiber and low in saturated fat, cholesterol, and sodium decrease their risk for stroke, as do those who quit smoking, drink alcohol minimally, and engage in regular physical activity. It is important for the patient and family to follow a similar, healthful diet in order to decrease the risk of future stroke. In addition, family members should be aware of the warning signs of stroke, and immediately call 911 if these signs occur. Timing of care is critical to treatment success. 

References

1. Brown RD, Whisnant JP, Sicks JD, et al. Stroke incidence, prevalence, and survival: secular trends in Rochester, Minnesota, through 1989. Stroke. 1996;27:373-380.

2. Whisnant JP. Modeling of risk factors for ischemic stroke. The Willis Lecture.  Stroke. 1997;28:1840-1844.

3. American Heart Association. Heart disease and stroke statistics: 2005 update. Available at: http://www.americanheart.org/downloadable/heart/
1105390918119HDSStats2005Update.pdf. Accessed June 14, 2005.

4. Wilcken DE. Novel risk factors for vascular disease: the homocysteine hypothesis of cardiovascular disease. J Cardiovasc Risk. 1998;5:217-221.

5. Boushey CJ, Beresford SA, Omenn GS, Motulsky AG. A quantitative assessment of plasma homocysteine as a risk factor for vascular disease. Probable benefits of increasing folic acid intakes. JAMA. 1995;274:1049-1057.

6. Wendel-Vos GC, Schuit AJ, Feskens EJ, et al. Physical activity and stroke. A meta-analysis of observational data. Int J Epidemiol. 2004;33:787-798. 

7. Wessel TR, Arant CB, Olson MB, et al. Relationship of physical fitness vs. body mass index with coronary artery disease and cardiovascular events in women. JAMA. 2004;292:1179-1187. 

8. Barnett HJ, Gunton RW, Eliasziw M, et al. Causes and severity of ischemic stroke in patients with internal carotid artery stenosis. JAMA. 2000. 283:1429-1436.

9. Wolf PA, Abbott RD, Kannel WB. Atrial fibrillation as an independent risk factor for stroke: the Framingham Study. Stroke. 1991;22:983-988.

10. Stang PE, Carson AP, Rose KM, et al. Headache, cerebrovascular symptoms, and stroke: the Atherosclerosis Risk in Communities Study. Neurology. 2005;64:1573-1577.

11. American Heart Association. Stroke outcomes classification.
Available at: http://www.americanheart.org/presenter.jhtml?identifier=1859.  Accessed May 30, 2005. 

12. Kwakkel G, Wagenaar RC, Koelman TW, et al.  Effects of intensity of rehabilitation after stroke: a research synthesis. Stroke. 1997;28:1550-1556.

13. Koren-Morag N, Tanne D, Graff E, Goldbourt U. Low- and high-density lipoprotein cholesterol and ischemic cerebrovascular disease: the bezafibrate infarction prevention registry. Arch Intern Med. 2002;162:993-999. 

14. Leppala JM, Virtamo J, Fogelholm R, Albanes D, Heinonen OP. Different risk factors for different stroke subtypes: association of blood pressure, cholesterol, and antioxidants. Stroke.1999;30:2535-2540. 

15. Tanasescu M, Cho E, Manson JE, Hu FB. Dietary fat and cholesterol and the risk of cardiovascular disease among women with type 2 diabetes. Am J Clin Nutr. 2004;79:999-1005. 

16. Gillman MW, Cupples LA, Gagnon D, et al. Protective effect of fruits and vegetables on development of stroke in men. JAMA. 1995;273:1113-1117.

17. Hak AE, Ma J, Powell CB, et al. Prospective study of plasma carotenoids and tocopherols in relation to risk of ischemic stroke. Stroke. 2004;35:1584-1588. 

18. Hirvonen T, Virtamo J, Korhonen P, Albanes D, Pietinen P. Intake of flavonoids, carotenoids, vitamins C and E, and risk of stroke in male smokers. Stroke. 2000;31:2301-2306. 

19. Voko Z, Hollander M, Hofman A, Koudstaal PJ, Breteler MM. Dietary antioxidants and the risk of ischemic stroke: the Rotterdam Study. Neurology. 2003;61:1273-1275. 

20. Yochum LA, Folsom AR, Kushi LH. Intake of antioxidant vitamins and risk of death from stroke in postmenopausal women. Am J Clin Nutr. 2000;72:476-483. 

21. He K, Merchant A, Rimm EB, et al. Folate, vitamin B6, and B12 intakes in relation to risk of stroke among men. Stroke. 2004;35:169-174. 

22. Bazzano LA, He J, Ogden LG, et al. Dietary intake of folate and risk of stroke in US men and women: NHANES Epidemiologic Follow-up Study. National Health and Nutrition Examination Survey. Stroke.2002;33:1183-1188. 

23. Oh K, Hu FB, Cho E, et al. Carbohydrate intake, glycemic index, glycemic load, and dietary fiber in relation to risk of stroke in women. Am J Epidemiol. 2005;161:161-169. 

24. Ascherio A, Rimm EB, Hernan MA, et al. Intake of potassium, magnesium, calcium, and fiber and risk of stroke among U.S. men. Circulation. 1998;98:1198-1204. 

25. Liu S, Manson JE, Stampfer MJ, et al. Whole grain consumption and risk of ischemic stroke in women: A prospective study. JAMA. 2000;284:1534-1540.  

26. Nagata C, Takatsuka N, Shimizu N, Shimizu H. Sodium intake and risk of death from stroke in Japanese men and women. Stroke. 2004;35:1543-1547.

27. He J, Ogden LG, Vupputuri S, Bazzano LA, Loria C, Whelton PK. Dietary sodium intake and subsequent risk of cardiovascular disease in overweight adults. JAMA. 1999;282:2027-2034. 

28. Fang J, Madhavan S, Alderman MH. Dietary potassium intake and stroke mortality. Stroke. 2000;31:1532-1537. 

29. Khaw KT, Barrett-Connor E. Dietary potassium and stroke-associated mortality. A 12-year prospective population study. N Engl J Med. 1987;316:235-240. 

30. Suk SH, Sacco RL, Boden-Albala B, et al. Abdominal obesity and risk of ischemic stroke: the Northern Manhattan Stroke Study. Stroke. 2003;34:1586-1592. 

31. Zhou BF. Effect of body mass index on all-cause mortality and incidence of cardiovascular diseases--report for meta-analysis of prospective studies open optimal cut-off points of body mass index in Chinese adults. Biomed Environ Sci. 2002;15:245-252. 

32. Rosengren A, Wilhelmsen L, Lappas G, Johansson S. Body mass index, coronary heart disease and stroke in Swedish women. A prospective 19-year follow-up in the BEDA study. Eur J Cardiovasc Prev Rehabil. 2003;10:443-450. 

33. Field AE, Coakley EH, Must A, et al. Impact of overweight on the risk of developing common chronic diseases during a 10-year period. Arch Intern Med. 2001;161:1581-1586. 

34. Mukamal KJ, Ascherio A, Mittleman MA, et al. Alcohol and risk for ischemic stroke in men: the role of drinking patterns and usual beverage. Ann Intern Med. 2005;142:11-19. 

35. Reynolds K, Lewis B, Nolen JD, Kinney GL, Sathya B, He J. Alcohol consumption and risk of stroke: a meta-analysis. JAMA. 2003;289:579-588.  

36. Klatsky AL, Armstrong MA, Friedman GD, Sidney S. Alcohol drinking and risk of hospitalization for ischemic stroke. Am J Cardiol. 2001;88:703-706. 

37. FOOD Trial Collaboration. Poor nutritional status on admission predicts poor outcomes after stroke: observational data from the FOOD trial. Stroke. 2003;34:1450-1456.

Ding EL, Mozaffarian D. Optimal dietary habits for the prevention of stroke. Semin Neurol. 2006 Feb;26(1):11-23.

Toole JF, Malinow MR, Chambless LE, Spence JD, Pettigrew LC, Howard VJ, Sides EG, Wang CH, Stampfer M. Lowering homocysteine in patients with ischemic stroke to prevent recurrent stroke, myocardial infarction, and death: the Vitamin Intervention for Stroke Prevention (VISP) randomized controlled trial. JAMA. 2004 Feb 4;291(5):565-75.

Lonn E, Yusuf S, Arnold MJ, Sheridan P, Pogue J, Micks M, McQueen MJ, Probstfield J, Fodor G, Held C, Genest J Jr; Heart Outcomes Prevention Evaluation (HOPE) 2 Investigators. Homocysteine lowering with folic acid and B vitamins in vascular disease. N Engl J Med. 2006.


Sometimes the most elegant solution is the most simple. Why plant-based nutrition? Why not? Why develop heart disease? Cancer? Diabetes? The epidemic of chronic, degenerative disease that is sweeping the western world can not only be stopped, it can be reversed. The power lies in the hands of the consumer, in the choices we make about what to put on our plates.