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Stroke information and resources are important assets for patients. Find Prevention materials, complication minimization post stroke, and educational materials for both patients and caregivers.
Stroke information and resources are important assets for patients. Prevention materials, complication minimization post stroke, and educational materials for both patient and caregiver are available below.
Be Aware of Signs and Symptoms of Stroke
Prevention and Facts
Whether you have had a stroke or have risk factors which put you at risk of stroke, it is essential to do whatever possible to reduce that risk. Here are answers to common questions about stroke and related diseases.
Stroke is the third leading cause of death in developed countries, after heart disease and cancer. For every 100,000 people in the US, 794 have had a stroke. Each year, 400,000 patients are discharged from hospitals after a stroke. Many of these patients will be left with disabilities, unable to resume their previous lifestyle or employment. This makes the social and economic impact of stroke one of the most devastating in medicine.
Approximately 80 percent of all strokes are due to ischemic cerebral infarction, where brain tissue is injured because the blood supply is lost. 20 percent of strokes are due to bleeding into the brain because a blood vessel ruptures (hemorrhage). Cerebrovascular disease (disease of the blood vessels bringing blood to the brain) is caused by one of several processes involving the blood vessels of the brain:
Administering appropriate therapy in ischemic stroke is greatly aided by understanding why the stroke occurred. Typically, there is a suspicion of the cause when the patient first arrives and then confirmatory tests are done to prove the mechanism. Because there isn't a single cause of stroke, there isn't a single treatment. Each stroke is unique and the preventive strategies tailored to the needs of that individual patient.
The problems listed above can cause temporary neurological symptoms (a TIA or transient ischemic attack) or a permanent deficit (stroke or cerebral infarction). Low flow TIAs are usually short-lived (minutes). They are often recurrent. While they may occur as little as several times per year, they usually occur more often once per week up to several times per day. They are generally stereotyped, especially when they are due to hemodynamically significant stenotic lesions at the origin of the internal carotid artery or at the siphon portion of the internal carotid artery where collateral flow to the circle of Willis is inadequate. Symptoms usually include stereotyped hand, arm, leg, face, tongue or cheek numbness or weakness. Recurrent language, visual, or cognitive difficulty may also occur depending on the vascular territory involved.
When the stenotic lesion that obstructs flow involves the blood vessels in the back of the brain, the vertebral and the basilar arteries, the recurrent symptoms are often not stereotyped. There are many closely packed neuronal structures in the brainstem. Obstructive lesions in the distal vertebral artery or at the vertebrobasilar junction usually have disorganized dizziness that may or may not contain spinning or vertigo. It may seem that the room is tilting or the floor is coming up instead of spinning dizziness. Other symptoms may include numbness of one side of the body or face, dysarthria or diplopia. There may also be bilateral leg and arm weakness or numbness. There may be a feeling of all of low energy or a feeling of impending doom. Ischemia in the territory of the top of the basilar artery or proximal posterior cerebral artery may have all of the above recurrent symptoms as well as overwhelming drowsiness, vertical diplopia, eyelid drooping and inability to look up.
Atherosclerosis at the origin of the internal carotid artery, one of the three major extracranial vessels bringing blood to the brain, is an important cause of TIA's and stroke. The symptoms and pathological substrate of carotid artery atherosclerotic occlusive disease were first described by C. Miller Fisher in 1951. He related atherosclerotic disease at the carotid bifurcation to ischemic symptoms in the ipsilateral eye and brain. The modern era has seen an extraordinary expansion in our approach to the diagnosis and management of patients with carotid artery stenosis. A carotid bruit may be heard over the site of carotid stenosis. However, it is a poor predictor of underlying carotid stenosis with both poor sensitivity and specificity. Similarly, ocular bruits and abnormalities or asymmetries of facial pulses are not reliable predictors of carotid stenosis.
When there is 70 percent or greater narrowing of the lumen, the threat of embolic or low flow TIA or stroke is quite high. Data from the North American Symptomatic Carotid Endarterectomy trial (NASCET) suggests that even a 50 percent stenosis is important when considering a carotid endarterectomy if you have already had a symptom referable to that artery. Carotid endarterectomy is a surgical procedure to remove the plaque from the carotid artery. In the published studies, the complication rates range from 2.3% in the asymptomatic population to 6.7% in symptomatic patients. Higher complication rates, particularly in the asymptomatic patients, can nullify the benefit of surgery.
Intracranial atherothrombotic disease can produce low flow or embolic TIA. It occurs most commonly at the distal vertebral artery/vertebrobasilar junction/proximal basilar artery site. Superimposed thrombosis with thrombus propagation and embolism can result in a stroke. The siphon portion of the internal carotid artery and the middle cerebral artery stem are two other common sites of atherosclerosis. These lesions can be identified noninvasively with MR- angiography, duplex ultrasound and transcranial Doppler. These imaging modalities can also be used to follow patients and guide therapeutic decisions.
Glioblastoma and other intracranial tumors often present with transient focal neurological symptoms. The symptoms often span two different arterial territories, making a vascular lesion less likely. Focal neurological symptoms that are attributed to migraine with or without headache occur at all ages, but most often after the age of 60. Focal seizures from any cause may mimic TIAs. These most commonly arise from cavernous angioma, AVM, tumors, especially glioblastoma and old strokes. But idiopathic focal seizures do occur. They usually have positive symptoms including aura and/or shaking as opposed to weakness or sensory deficit. Rarely demyelinating lesions give rise to focal transient symptoms but they generally last for at least several days. Arteritides, other than temporal arteritis (TA), are rare. TA can cause transient monocular blindness. A sedimentation rate will suggest the diagnosis and should be obtained whenever transient monocular visual symptoms occur. Arteriovenous malformation and cavernous angioma usually produce transient focal symptoms by causing focal seizures. On occasion, arteriovenous malformations are large enough to produce transient focal symptoms on the basis of a "steal" phenomenon, where the AVM shunts blood away from normal tissue.
Treatable risk factors for atherosclerosis include hypertension, diabetes, tobacco use, hypercholesterolemia, sedentary lifestyle. Modification of these risk factors is important in the primary and secondary prevention of cardiac disease and reduces the risk of atherosclerotic ischemic stroke. Click on the individual risk factors to learn more.
Aspirin, the most commonly used antiplatelet agent, inhibits the enzyme cyclo-oxygenase reducing production of thromboxane A2, a stimulator of platelet aggregation. This interferes with thrombus formation and thereby reduces the risk of stroke. In high risk patients, there was a 31% risk reduction in nonfatal stroke. For cerebrovascular patients alone, antiplatelet therapy reduced risk of secondary stroke, MI and vascular death by 22%.
The dose of aspirin ranges between 20-1300mg in various clinical trials. The complications of aspirin increase with higher doses. The studies have not shown any evidence that higher doses of aspirin convey greater benefit. Thus the recommendations are for low dose, 50-325mg of aspirin a day.
Ticlopidine, a newer antiplatelet agent, inhibits ADP dependent fibrinogen binding. Ticlopidine has a relative risk reduction of 21% in stroke, MI, and vascular death. The common side effects of ticlopidine include rash and diarrhea. Cholestatic jaundice has occurred in a small number of patients. A rare, but serious complication of ticlopidine therapy is neutropenia which occurred in approximately 1% of patients. Thus, for the first three months of treatment, patients must undergo biweekly CBCs. Because of these complications, the relatively modest increase in efficacy of ticlopidine over aspirin, and its relatively high cost, ticlopidine is generally not considered a first line antiplatelet agent for stroke prevention but may be useful in patients who cannot tolerate aspirin.
Clopidogrel is a newer antiplatelet agent similar to ticlopidine in mechanism of action. The Clopidogrel versus Aspirin in Patients at Risk of Ischaemic Events (CAPRIE) trial compared outcome events of stroke, MI, and vascular death in 19,185 patients treated with aspirin (325 mg) or clopidogrel (75 mg) who had had a recent stroke, MI or symptomatic peripheral arterial disease. There was a relative risk reduction of 8.7% in clopidogrel treated patients. Clopidogrel does not appear to cause neutropenia.
Dipyridamole impairs platelet function by inhibiting phosphodiesterase. The recently published second European Stroke Prevention Study (ESPS-2) randomized 6602 patients who had experienced a recent transient ischemic attack or ischemic stroke to four treatment groups: 25 mg aspirin + 200 mg dipyridamole, 200 mg dipyridamole, 25 mg aspirin, and placebo, each given twice daily. 20 Dipyridamole was given as Persantin® Retard 200 mg, a sustained release tablet. In contrast to previous studies, both dipyridamole monotherapy and aspirin monotherapy had an independent and significant effect in preventing the recurrence of stroke with relative risk reductions of 16% and 18% respectively. The combination of dipyridamole plus aspirin was additive, producing a 37% relative risk reduction in stroke compared to placebo and a 23% relative risk reduction over aspirin alone
Coumadin warfarin is infrequently used in patients with carotid stenosis. For very severe stenoses, particularly in patients awaiting carotid endarterectomy, coumadin is sometimes used to maintain the patency of the lumen. Coumadin is also used in cases of carotid occlusion. Patients are often kept anticoagulated for 3-6 months to prevent propagation of thrombus in the internal carotid artery. Neither of these are proven indications for warfarin therapy. A large, multicenter, randomized, double-blind study comparing the efficacy of warfarin (INR 1.4-2.8) versus aspirin (325 mg/d) has been completed.
Below is a glossary of commonly used clinical terms used in the Stroke Service.
Stroke Support Groups
We recommend the following websites to expand our mission of stroke education.
General Stroke Sites
US Government Sites
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