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"Time is Brain": Treating Stroke as an Emergency Morgan Campbell, M.D. Dr. Campbell is Assistant Professor of Medicine, Department of Neurology, University of Texas Medical School at Houston. If oxygen-rich blood is blocked from reaching the brain, brain nerve cells will die, producing damage and disability we call "stroke." Not too long ago, the treatment for most types of stroke was passive -- wait for it to be over and then manage the consequences. With this approach, most stroke victims simply died. Those who survived faced the challenge of years of rehabilitation and, often, permanent brain damage or other disability. Today, however, there are several new treatments available that help to restore blood flow to the brain and, as a result, minimize damage. What is a Stroke? A stroke happens when blood flow to the brain is blocked by a blood clot in a brain artery or because a brain blood vessel has burst. Obstruction is the more common cause. Stroke symptoms include headache, mental confusion, inability to speak, loss of consciousness and paralysis. When a stroke occurs, part or all of the brain is deprived of oxygen. Without oxygen, affected nerve cells in the brain stop functioning and begin to die within minutes. This is a disaster for the body because dead brain cells cannot be replaced. Because the brain controls the rest of the body, the death of certain brain cells often means a loss of functioning elsewhere. Stroke affects 700,000 people annually in the US. It is the third leading cause of death and the number one cause of long-term adult disability. A New Treatment and Timetable In 1996, stroke treatment changed dramatically when the FDA approved the use of a new drug called tissue plasminogen activator, or tPA, to treat stroke. tPA immediately dissolves the blood clots that cause many strokes, drasically reducing the amount of damage strokes produce. Since then, several other drugs have been developed that are similar to tPA. These include r-tPA, streptokinase, urokinase and prourokinase. Together they are known as thrombolytic drugs from the Ancient Greek word, thrombolysis, meaning "clot-dissolving." Thrombolytics, however, only work if delivered directly into the bloodstream, either through a vein or an artery (intra-arterial). Both are complicated processes, especially intra-arterial treatment, which involves assembling a medical team and performing an elaborate test called cerebral angiography. Most importantly, these drugs must be administered within a few hours of the stroke before the oxygen-deprived nerve cells suffer permanent damage. Emergency rooms and emergency medical services have to work quickly because "time is brain." In other words, the faster stroke victims are treated, the less damage to the body and, especially, to the brain. If a loved one or friend suffers a stroke, you need to make sure that he or she gets to the hospital as soon as possible. The time window for getting the best results from thrombolytic drugs is three hours from the first signs of stroke. Treating Stroke with tPA The FDA's approval of tPA in June 1996 was a major advance in stroke management.1 tPA works by traveling through the bloodstream to the clot or other blockage; it then dissolves the material causing the obstruction and allows blood flow to resume. The result is that far less brain tissue is deprived of oxygen and victims suffer less damage. But tPA and other thrombolytics can cause increased bleeding. This is the reason that they are never used to treat strokes that result from burst blood vessels. Studies demonstrated that patients given intravenous tPA within three hours of suffering a stroke were far better off three months afterward. Later studies showed that while 10-20% of all stroke victims could benefit from tPA, only 1-2% are actually getting it, or getting it in time.2,4 Today, the medical community has been gradually adjusting to view stroke as a true emergency. As in any other profession, it has proven to be a difficult and frustrating task to change long-standing beliefs and attitudes. Extensive efforts are needed to educate medical professionals, from physicians to EMS personnel, as well as the general public, about stroke awareness.5 Part of the difficulty is that in order to provide state-of-the-art stroke treatment, hospital emergency rooms and stroke treatment centers need to build a multidisciplinary support network including emergency medicine, primary care, neurology and radiology. This requires a great deal of time, money and effort.3,6,7,8 Other New Stroke Treatments Researchers are now studying a variety of other stroke treatments that may, alone or in combination with each other or with thrombolytics like tPA, further improve the outcome for those who suffer stroke. Some of these are: Intra-arterial Treatment In this experimental treatment, clot-dissolving drugs are given directly through an artery (See Figure 1).9
A significant drawback of intra-arterial therapy is that it much more difficult, compared to IV tPA, for the medical staff as it requires additional time because an angiography team or transfer to a special center may be needed. Time, of course, is of the essence in treating stroke.10 Right now, it is too early to say whether or not intra-arterial treatment will prove to be worthwhile. Endovascular Rescue Endovascular therapy involves repairing the damaged blood vessel by inserting a device called a stent which keeps the artery open (See Figure 2). Stents have been used with much success for heart arteries but positioning them in the brain arteries is much more difficult. Brain stenting is attractive because blood flow is restored without the risk of bleeding that is associated with thrombolytic medicines. We believe it may especially effective for those patients who are likely to have bleeding problems -- patients with very high blood pressure and patients who have recently had an operation.
Antiplatelet Therapy Antiplatelet therapy is one of the mainstays of stroke prevention. They work by impairing the ability of the blood to clot, thereby reducing the chances of a blood clot forming and causing a stroke. In addition to aspirin, there are several new antiplatelet agents. Aspirin is the oldest antiplatelet medication and still the most frequently prescribed. The most effective dosage of aspirin for stroke prevention has long been a subject of debate among neurologists. No single trial has established the optimal dose (the usual range is 81-325 mg per day) of aspirin but several studies strongly suggest that dosage may not, in fact, matter very much.11,16,12,14,15. Other antiplatelet drugs include ticlopidine,13 clopidogrel15 and dipyridamole (Aggrenox®).20,21,22 Sometimes, one or more of these drugs is used in combination with another therapy, such as endovascular rescue.23,24,25,26,27,28,19 For example, aspirin plus extended release dipyridamole has clearly been shown to be more effective than aspirin alone for preventive purposes. Summary Based on what we know now, the best short-term treatment for stroke caused by an obstruction is intravenous t-PA. However, this must be done as soon as possible, certainly within the first three hours of the first stroke symptoms. If you, a friend or family member suffers a stroke, the most important thing that you can do is to make sure that evaluation and treatment begins as soon as possible. Before a crisis occurs, you may want to investigate whether hospitals and emegency services in your community are equpped to give state-of-the-art stroke treatment, and, if necessary, advocate for improvement. Thrombolytic drugs such as tPA have revolutionized the treatment of stroke by giving doctors a way to intervene and limit the damage done by a stroke. In the next few years, we can expect to see the development of more and better short-term stroke therapies, as well as antiplatelet drugs and other treatments to deal with stroke prevention and the aftermath of stroke.
References 1. The National Institute of Neurologic Disorders and Stroke rt-PA Stroke Study Group. Tissue plasminogen activator for acute ischemic stroke. N Engl J Med. 1995;333:1581-1587. return 2. 1997 Heart and Stroke Statistical Update. Dallas, TX: American Heart Association; 1997. return 3. Hacke W, Kaste M, Fieschi C, et al. for the European Cooperative Acute Stroke Study Group (ECASS). Intravenous thrombolysis with recombinant tissue plasminogen activator for acute hemispheric stroke. JAMA 1995; 274:1017-1025. return 4. McDowell FH, Brott TG, Goldstein M, et al. Stroke- The first hours: emergency evaluation & treatment: consensus statement. Stroke Clinical Updates. Special Edition. Englewood, Colo: National Stroke Association; 1997. return 5. Frankel M, Kothari R. Acute ischemic stroke: a new paradigm. Emory University School of Medicine; 1998. return 6. Hacke W, Kaste M, Fieschi C, et al. Randomized double-blind placebo-controlled trial of thrombolytic therapy with intravenous altepase in acute ischaemic stroke (ECASS II). Second European-Australian Acute Stroke Study Investigators. Lancet 1998; 352:1245-1251. return 7. Generalized efficacy of t-PA for acute stroke: subgroup analysis of the NINDS t-PA Stroke Study Group. Stroke 1997; 28:2119-2125. return 8. The NINDS t-PA Stroke Study Group. Intracerebral hemorrhage after intravenous t-PA therapy for ischemic stroke. Stroke 1997; 28:2109-2118. return 9. Furlan A, Higashida R, Wechsler L, et al. Intra-arterial prourokinase for acute ischemic stroke: the PROACT II study: a randomized controlled trial. JAMA 1999; 282(21):2003-2011. return 10. Lewandowski C, Frankek M, Tomsick T, Broderick J, et al. Combined intravenous and intra-arterial rt-PA versus intra-arterial therapy of acute ischemic stroke. Stroke 1999;30:2598-2605. return 11. Antiplatelet Trialists' Collaboration. Collaborative overview of randomized trials of antiplatelet therapy: 1. Prevention of death, myocardial infarction, and stroke by prolonged antiplatelet therapy in various categories of patients. BMJ 1994; 308:81-106. return 12. Hass WK, Easton JD, Adams HP Jr, et al. A randomized trial comparing ticlopidine hydrochloride with aspirin for the prevention of stroke in high-risk patients. N Engl J Med 1989; 321:501-507. return 13. Bennett CL, Weinberg PD, Rozenberg-Ben-Dror K, et al. Thrombotic thrombocytopenic purpura associated with ticlopidine: a review of 60 cases. Ann Int Med1998; 128:541-544. return 14. CAPRIE Steering Committee. A randomized, blinded, trial of clopidogrel versus aspirin in patients at risk of ischaemic events (CAPRIE). Lancet 1996; 348:1329-1339. return 15. Diener HC, Cunha L, Forbes C, et al. European Stroke Prevention Study 2. Dipyridamole plus acetylsalicylic acid in the secondary prevention of stroke. J Neurol Sci 1996; 143:1-13. return 16. Alpers GW, Easton JD, Sacco RL. Teal P. Antithrombotic and thrombolytic therapy for ischemic stroke. Chest 1998; 114:683s-698s. return 17. Alpers GW, Tijssen J. Advances in stroke management: update 1998: Antiplatelet therapy: new foundations for optimal treatment decisions. Neurology 1999; 53(Supp 4):s25-s31. return 18. Easton JD, Diener HC, Bornstein NM, et al. Advances in stroke management: update 1998: Antiplatelet therapy: views from the experts. Neurology 1999; 53(Supp 4)s32-s37. return 19. Herbert JM, Dol F, Bernat A et al. The antiaggregating and antithrombotic activity of clopidogrel is potentiated by aspirin in several experimental models in the rabbit. Throm Haemost 1998(3); 80:512-518. return 20. Makkarr RR, Eigler NL, Frimerman A, et al. Effects of clopidogrel, aspirin and combined therapy in a porcine ex vivo model of high-shear induced stent thrombosis. Eur Heart J 1998; 10:1538-1546. return 21. Harker LA, Marzec UM, Kelly AB, et al. Clopidogrel inihibition of stent, graft, and vascular thrombogenesis with antithrombotic enhancement by aspirin in nonhuman primates. Circulation 1998; 98:2461-2469. return 22. Fifth ACCP Consensus Conference on Antithrombotic Therapy. Chest 1998; 114(5):480s. return 23. Bossavy JP, Thalamas C, Sagnard L, et al. A double-blind randomized comparison of combined aspirin and ticlopidine therapy versus aspirin or ticlopidine alone on experimental arterial thrombogenesis in humans. Blood 1998; 92:1518-1525. return 24. Steinhubl SR, Lauer MS, Mukherjee DP, et al. The duration of pretreatment with ticlopidine prior to stenting is associated with the risk of procedure-related non-Q-wave myocardial infarctions. J Am Coll Cardiol 1998; 32:1366-1370. return 25. Schomig A, et al. J Am Coll Cardiol 1998; 31(2, Supp A):99a. return 26. Schuhlen H, et al. Circulation 1998; 98(Supp):1-572. return 27. Berger P, et al. J Am Coll Cardiol 1999; 33(2, Supp A):82-1. return 28. Moses, et al. J Am Coll Cardiol 1999; 33(2, Supp A):1007-55. return |
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