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Office UrgenciesAcute neurologic symptoms—TIA, migraine, or something else?GREGORY L. HENRY, MD, Clinical Professor, Department of Emergency Medicine, University of Michigan Medical School, Ann Arbor; and past president, American College of Emergency Physicians.S. CLAIBORNE JOHNSTON, MD, PhD, Director, University of California-San Francisco Medical Center Stroke Service; and Associate Professor of Neurology and Epidemiology in Residence, UCSF, San Francisco.What diagnostic studies need your immediate attention? What is the patient's short-term stroke risk? These experts outline a rational approach to this often underestimated emergency.
A transient ischemic attack (TIA) is a potent harbinger of stroke. In one series conducted between March 1997 and February 1998, 10.5% of more than 1700 Californians who were identified in the emergency department (ED) as having a TIA had a stroke in the 90 days following the TIA. Approximately half of these occurred in the first 2 days after the TIA.1 In an analysis performed as part of the Oxford (England) Community Stroke Project in 2003, the 7- and 30-day stroke risks from the onset of a first-ever TIA were 8.6% and 12%, respectively.2 Even more ominous, among patients who had a nonretinal TIA associated with a 70% to 99% stenosis of the internal carotid artery, the 90-day stroke risk was 25% in one series.3 The implications are enormous in light of estimates that as many as 500,000 Americans come to medical attention each year because of TIAs. The number of patients who ignore or do not notice a TIA is unknown.4 Based on these data—especially the evidence of elevated stroke risk during the first few days after a TIA—stroke specialists reiterate that symptoms suggesting a TIA should be considered an emergency and be evaluated promptly. But patients' (and sometimes clinicians') understanding of the nature and implications of a TIA is a barrier to timely evaluation and treatment. In a 2003 telephone survey of more than 10,000 American adults, just over 8% could define the term TIA and describe one symptom of an attack. Of those respondents who said they had been told by a clinician that they had had a TIA, only 64% had seen a clinician within 24 hours of the episode.5 How can primary care practitioners raise awareness among their patients about the serious nature of TIAs? The results of a 2000 study suggest that they may need to take these episodes more seriously themselves. In a practice audit conducted in 27 primary care practices in the eastern United States, one third of patients with a first-ever TIA or stroke who were initially evaluated in the office of their primary care practitioners were not admitted to the hospital and had no further diagnostic tests. The investigators also concluded that anticoagulants were underused among patients with atrial fibrillation.6 When a patient presents to the ED with a completed stroke, medicine has a limited amount to offer. The patient's best hope of restoring function lies in rehabilitative services. But patients who had a TIA have potentially preventable and treatable disease. It is a paradox that the patient with the least severe physical findings may have the most to gain from rapid assessment and therapy. WHAT DOES THE NATURE OF A "SPELL" REVEAL?Patients report various types of neurologic episodes that may correspond to clinical entities ultimately identified as a TIA, seizure, atypical migraine, or syncope. The range of possible symptoms caused by a TIA is enormous, and TIA mimics are plentiful. The characteristics of a TIA are a reflection of the site at which ischemia occurs and, as explained in a recent review, at least 17 such sites exist on each side of the brain.7 The possible symptoms produced by these areas of ischemia include, but are not limited to numbness of face, hand, or leg, with or without weakness; paralysis; slurred speech; dizziness; double vision; hemianopia; transient monocular blindness; imbalance; aphasia; confusion; head pain.7 Determining the cause of these or similar symptoms can be difficult and complicated. Nonetheless, a few diagnostic pearls are sometimes helpful. TIA Suspect a TIA when you can relate specific symptoms to a discrete area of the brain. For example, unilateral weakness suggests involvement of the motor areas of the cortex, and numbness or tingling in a limb suggests sensory area involvement. In contrast, bilateral or "all-over" weakness or tingling is usually associated with conditions other than a TIA. Keep in mind, however, that weakness, a common symptom of TIA, is rare with other causes of neurologic spells.1 Problems with speech or word-finding, of course, suggest ischemia in the speech centers. Incoordination results if the cerebellum is affected, and brain stem nuclei involvement may lead to vertigo or dizziness. Patients with multiple TIAs tend to have ischemic compromise in the same area of the brain and, hence, similar symptoms from attack to attack. Seizure Suspect a seizure rather than a TIA when you observe or the patient reports postictal symptoms such as jerky limb movements or flashing lights. A seizure, unlike a TIA, often includes some tonic-clonic motor activity, which a bystander may have observed. Syncope A cardiac arrhythmia is more likely than a TIA to cause syncope. In fact, most patients with syncope, especially young ones, have simple faints and do not have serious cardiac or neurologic disease. Dyspnea, chest pain, and palpitations preceding loss of consciousness are clues to a cardiac etiology. If syncope occurs in the course of a TIA, it is usually accompanied by a more typical TIA symptom, such as one-sided weakness or a visual disturbance. Migraine Symptom onset in migraine is usually gradual. A sensory symptom, for example, may begin in the thumb, then progress gradually to involve the hand, then the face. Slow, stepwise symptom progression is unusual in a patient with TIA but typical of migraine without headache. "Positive" symptoms, such as scintillating scotomata, are common with migraine but very rare with TIA. A history of migraine is very helpful. Importance of observer reportsVery often, the patient does not understand or accurately remember what happened during the episode in question. Consider it a strong clue to a TIA when a patient tells you, "I don't know why I'm here. Whatever it was, it's all better now." Anyone who observed the episode can play a valuable role and might report helpful information such as momentary drooping of the facial muscles or difficulty in grasping a coffee mug. The observer will also be able to reveal whether the patient had tonic-clonic movements, lost control of bladder and bowel function, or lost consciousness. Depending on what areas of the brain were involved, the patient may not be able to tell you how long the episode lasted. The observer can usually provide a more accurate estimate of the attack's duration. In a patient with a syncopal or near-syncopal type of attack, the duration of symptoms and the pulse rate are the most valuable observations that a bystander can make. Observations in the TIA aftermathThe clinician usually sees a neurologically intact, asymptomatic patient in the wake of a TIA. According to contemporary definition, a TIA must resolve within 24 hours. In general, they rarely last more than a few hours. Sometimes call a longer-lasting TIA is called a reversible ischemic neurologic deficit (RIND). TIA symptoms to predict stroke riskSome TIA symptoms are more likely than others to precede stroke. Sudden-onset weakness is one of the most common TIA symptoms and one of the most important harbingers of stroke. A speech impairment is similarly ominous. A stroke is more likely following a TIA of more than 10 minutes' duration or in someone with diabetes or who is 60 or older. In contrast, isolated vertigo or numbness is less strongly predictive of imminent stroke.8 TIAs involving the retina seem to carry less risk of subsequent stroke than other types of TIA. ASSESSMENTA first TIA is an emergency. Your goal should be to initiate an appropriate evaluation as quickly as possible, bearing in mind the high stroke risk during the first 24 to 48 hours after the event. All of these patients require prompt carotid and cranial imaging. The goal of the assessment is to answer the following questions: • Does the patient have a cardiac arrhythmia? • Is a structural lesion such as a valvular defect or a thrombus present? • Is there evidence of an arterial blockage that can be cleared? In practice, approximately 15% to 20% of patients have one of these conditions, and definitive therapy can be initiated. For the remainder, aspirin is often the treatment of choice. Although the patient may come to a primary care office initially, it is often more expedient to direct the patient to the ED, as the required testing will be done at the hospital. Make sure the patient understands the importance of waiting and completing the assessment, even if the symptoms resolve. The next week may be too late. Occasionally, a patient who had an attack on a Friday, for example, may not try to reach you until Monday morning. This patient has already passed though the period of peak stroke risk but still needs a complete evaluation within several days. Physical examination and laboratory testsThe physical examination may reveal clues to disorders other than TIA. As part of the examination, listen to the neck for bruits. However, the results should not determine whether you order carotid imaging because all patients with a first TIA are candidates for such studies. Similarly, cardiac auscultation may reveal a valve or rhythm problem, but an ECG, and perhaps prolonged cardiac monitoring, will also be necessary. Be alert to signs of residual neurologic damage, which may support a diagnosis of TIA and reveal important information about the site of the ischemia or suggest another diagnosis entirely. Laboratory studies usually do not provide crucial information in this setting. If you suspect hypoglycemia or hyponatremia, the standard tests may be useful. Depending on the patient's medical history, the characteristics of the spell, the findings on the physical examination, and your clinical intuition, liver function tests and determination of electrolyte and cardiac troponin levels may be appropriate. As one author recently noted, the diagnostic yield from some of these tests may be quite low overall, but the consequences of missing a condition such as diabetes in the acute situation could be grave.9 An ECG is recommended for all patients with TIA, and atrial fibrillation is a significant finding. An ECG may also reveal evidence of a recent MI that could account for the patient's symptoms. Depending on the findings and your clinical suspicions, Holter monitoring may be advisable. In some facilities, patients with a first TIA are admitted to a telemetry ward for 24 hours of observation. These precautions are worth considering because a brief ECG conducted in the ED may be too brief to pick up important clues or record significant events, such as a run of paroxysmal atrial fibrillation. The costs of observation are outweighed by benefits of rapid action in case of stroke. Note that documentation of paroxysmal atrial fibrillation is an indication for anticoagulation. Cardiac echocardiography is done when signs, symptoms, or physical findings hint at a cardiac embolus or a valve problem. Imaging studiesAll patients with suspected TIA are candidates for cranial and carotid imaging. Debates continue among researchers about the benefits of one technology over another. But in practice, the goal is to get studies done by whatever means are available. Brain imaging In about 1% of patients who present with a suspected TIA, the CT or MRI scan reveals another serious source of symptoms such as a brain tumor, multiple sclerosis, or a subdural hematoma.10 In others, evidence of a brain infarct may be seen, even in patients in whom symptoms have resolved—and these patients may be at greater risk of deteriorating. Some evidence shows that MRI, especially diffusion-weighted MRI, is more likely than a CT to reveal areas of focal ischemia.11,12 Vascular testing The possibility of internal carotid artery stenosis can be explored by one of several means. Doppler ultrasonography and MRI angiography are approximately equally effective, with sensitivities exceeding 80% for stenoses that exceed 70% of the lumen diameter. CT angiography is less widely available and has not been as rigorously evaluated as ultrasonography and MRI. MRI angiography and/or CT angiography of the intracranial arteries and cervical vertebral arteries may show vessel dissection or stenosis. The study of choice should be the one that will direct your surgeon to act. Preliminary treatment during assessmentAspirin will be the treatment of choice for the majority of patients with TIA, and this can begin during the assessment (although no studies have confirmed its benefit so soon after the event). The risk of brain hemorrhage after aspirin administration is thought to be lower in patients with TIA than in those who have had a stroke. Depending on the outcome of the workup, therapy may be continued indefinitely. Although a patient's BP is often elevated in the aftermath of a TIA, it is inappropriate to take aggressive antihypertensive measures in the emergency setting. Do not lower BP acutely in a TIA patient. Elevated BP is a response to poor perfusion during a TIA, and lowering it abruptly worsens perfusion in this situation. If present, hypertension should be managed gradually and slowly. Oxygen therapy has not proven useful in patients recovering from a TIA. Dilation of blood vessels in the brain depends on blood carbon dioxide levels, not oxygen levels. Should the patient be admitted?Usually, a patient who has just had a TIA should be admitted for the initial workup, both to facilitate monitoring and to ensure rapid care in the event of a stroke during the 24 to 48 hours after the TIA. Admission is usually unnecessary for patients with recurrent TIA who are on an appropriate regimen. INTERVENTION AND PREVENTIONAt least 80% of patients who have a first TIA are candidates for aspirin therapy. Aspirin reduces the risk of subsequent stroke and cardiovascular events by more than 20%. For a patient with a first TIA, other antiplatelet agents have no demonstrable benefits over those offered by aspirin. The usual aspirin dosage is 81 mg/d. As demonstrated in trials conducted more than a decade ago in patients with stroke or TIA, higher dosages have no clear benefit, and the possibility of side effects, notably bleeding, increases.13 What is the next therapeutic step when a patient has a subsequent TIA? Increasing the aspirin dosage is usually not recommended, again because higher dosages have not been shown to be beneficial. Other treatment options include the combination of aspirin and extended-release dipyridamole (Aggrenox). In a 1996 study, this agent was more effective than aspirin in reducing subsequent stroke risk in patients with a history of TIA or stroke, but the combined outcome of stroke and death was similar to that of aspirin.14 The antiplatelet agents clopidogrel (Plavix) and ticlopidine (Ticlid) can also be used as second-line treatments in patients with a history of TIA who have another event while on aspirin prophylaxis. In the Clopidogrel versus Aspirin in Patients at Risk of Ischaemic Events (CAPRIE) study, clopidogrel displayed a marginal benefit over aspirin in the prevention of the combined end points of stroke, MI, and vascular death in patients with recent stroke, among other conditions.15 The usual dosage of clopidogrel in this situation is 75 mg/d. Other studies have had similar results, with clopidogrel showing a slight advantage over aspirin. The combination of aspirin and clopidogrel has demonstrated efficacy in patients with unstable angina and suspected MI. In the Clopidogrel in Unstable Angina to Prevent Recurrent Events (CURE) trial, the combination of aspirin and clopidogrel yielded a 20% risk reduction in the primary outcome measure of cardiovascular death, nonfatal MI, and stroke.16 Nonetheless, cardiac and ischemic events differ in many ways. For example, patients who have had a stroke are far more likely to have another than to have an MI. Until more data are available, experts advise caution in using aspirin and clopidogrel in combination to prevent strokes in patients with a history of TIA.17 Ticlopidine has effects similar to those of clopidogrel, but concerns about the risk of neutropenia, thrombotic thrombocytopenic purpura, and other blood dyscrasias have limited its use in recent years. The risk of thrombotic thrombocytopenic purpura in users of ticlopidine is estimated at about 1 in 4000, and the condition is fatal in about 20% of those.18 The usual dosage of ticlopidine is 250 mg bid, taken with food. Oral anticoagulation has no clearly defined role in reducing stroke risk after TIA in patients without a known source of cardiac embolism, such as atrial fibrillation, a mural thrombus, or an artificial valve. Warfarin is no more effective than aspirin in these patients. Patients with atherosclerotic carotid diseaseImmediate endarterectomy is recommended for patients with symptomatic anatomically correctable carotid stenoses of 70% to 99% demonstrated by Doppler ultrasound or another method. According to American Heart Association (AHA) guidelines, the procedure can be considered in patients with less serious stenoses in the range of 50% to 69%, but benefits from operation on such stenoses have proved more elusive. Patients with stenoses of less than 50% are not candidates, as endarterectomy is unlikely to be beneficial. Concerns that conducting this procedure too soon would cause cerebral hemorrhages are likely to be unfounded in patients with TIA. Patients with cardiac embolismOral anticoagulation is essential to prevent stroke in patients with a documented cardiac emboli source. The following international normalized ratios (INRs) and durations of therapy are recommended in the AHA guidelines on preventing stroke in patients with prior TIA: • Nonvalvular atrial fibrillation: INR 2 to 3 (target 2.5); lifelong therapy • Left ventricular thrombus, recent MI: INR 2 to 3 (target 2.5) for 6 months • Prosthetic heart valve: INR 3 to 4 (target 3.5); lifelong therapy. Just-released guidelines from the American College of Physicians and the American Academy of Family Physicians highlight an important change in approach to this common condition: conversion to sinus rhythm is no longer considered a primary goal of treatment, as the risks of antiarrhythmic medications may outweigh their benefits. Instead, therapy emphasizes 2 key approaches in patients with atrial fibrillation: • Chronic anticoagulation therapy General risk factor reductionRisk factor reduction is a crucial part of stroke prevention in a patient who has had a TIA, and a comprehensive cardiac risk evaluation is required.20 Patients with diabetes are a special concern, because higher blood glucose levels seem to be associated with an elevated risk of stroke as well as larger strokes. The AHA guidelines specify the following steps to reduce stroke risk in patients with a history of TIA: • Smoking cessation • Maintenance of BP at less than 140/90 mm Hg (less than 130/80 mm Hg if target organ damage is present) • Maintenance of glycosylated hemoglobin A1C of less than 7% • Maintenance of LDL cholesterol at less than 100 mg/d; if triglycerides are greater than or equal to 200 mg/dL, then non-HDL cholesterol should be less than 130 mg/dL. • Consumption of no more than 2 alcoholic beverages a day • Body mass index of 18.5 to 24.9 kg/m2 • 30 to 60 minutes of physical activity at least 3 to 4 times a week.20 A recent review of the literature that included 7 randomized, controlled trials and 8 comparison groups has reiterated the importance of BP reduction for preventing strokes in patients with a history of TIA or stroke. Although no effect was seen on vascular or all-cause mortality, BP-lowering was associated with a reduced risk of all stroke, nonfatal stroke, MI, and total vascular events. ACE inhibitors and diuretics had strong effects and were even more effective when used together. The greater the difference in BP between the control and treatment groups, the greater was the reduction in stroke risk.21 Another recent trial suggests that aggressive BP treatment in patients with bilateral carotid blockages of greater than 70% may actually increase stroke risk. These patients comprise a small fraction of patients with TIA.22
PRODUCED BY MARY DESMOND PINKOWISHDr Henry and Dr Johnston disclose that they have no financial involvement with any companies doing business in this field.
REFERENCES 1. Johnston SC, Gress DR, Browner WS, et al. Short-term prognosis after emergency department diagnosis of TIA. JAMA. 2000;284:2901-2906. 2. Lovett JK, Dennis MS, Sandercock PA, et al. Very early risk of stroke after a first transient ischemic attack. Stroke. 2003;34:138-140. 3. Streifler JY, Eliasziw M, Benvente OR, et al. The risk of stroke in patients with first-ever retinal vs hemispheric transient ischemic attacks and high-grade carotid stenosis: North American Symptomatic Carotid Endarterectomy Trial. Arch Neurol. 1995;52:246-249. 4. Johnston SC. Transient ischemic attack. N Engl J Med. 2002;347:1687-1692. 5. Johnston SC, Fayad PB, Gorelick PB, et al. Prevalence and knowledge of transient ischemic attack among US adults. Neurology. 2003;60:1429-1434. 6. Goldstein LB, Bian J, Samsa GP, et al. New transient ischemic attack and stroke: outpatient management by primary care physicians. Arch Intern Med. 2000;160:2941-2946. 7. Fisher CM. Transient ischemic attacks. N Engl J Med. 2002;347:1642-1643. 8. Johnston SC, Sidney S, Bernstein AL, et al. A comparison of risk factors for recurrent TIA and stroke in patients diagnosed with TIA. Neurology. 2003;60:280-285. 9. Bamford J. Assessment and investigation of stroke and transient ischaemic attack. J Neurol Neurosurg Psychiatry. 2001;70(suppl 1):I3-I6. 10. Douglas VC, Johnston CM, Elkins J, et al. Head computed tomography findings predict short-term stroke risk after transient ischemic attack. Stroke. 2003;34:2894-2898. 11. Kidwell CS, Alger JR, Di Salle F, et al. Diffusion MRI in patients with transient ischemic attacks. Stroke. 1999:30:1174-1180. 12. Crisostomo RA, Garcia MM, Tong DC. Detection of diffusion-weighted MRI abnormalities in patients with transient ischemic attack: correlation with clinical characteristics. Stroke. 2003;34:932-937. Epub 2003 Mar 13. 13. Peters RJ, Mehta SR, Fox KA, et al. Effects of aspirin dose when used alone or in combination with clopidogrel in patients with acute coronary syndromes: observations from the Clopidogrel in Unstable angi– na to prevent Recurrent Events (CURE) study. Circulation. 2003;108:1682-1687. Epub 2003 Sep 22. Available at: http://circ.ahajournals.org/cgi/content/full/108/14/1682 . Accessed February 2, 2004. 14. Diener HC, Cunha L, Forbes C, et al. European Stroke Prevention Study. 2. Dipyridamole and acetylsalicylic acid in the secondary prevention of stroke. J Neurol Sci. 1996;143:1-13. 15. CAPRIE Steering Committee. A randomised, blinded, trial of clopidogrel versus aspirin in patients at risk of ischaemic events (CAPRIE). Lancet. 1996;348-1329-1339. 16. Yusuf S, Zhao F, Mehta SR et al and the Clopidogrel in Unstable Angina to Prevent Recurrent Events Trial investigators. Effects of clopidogrel in addition to aspirin in patients with acute coronary syndromes without ST-segment elevation. N Engl J Med. 2001;345:494-502. 17. Albers GW, Amarenco P. Combination therapy with clopidogrel and aspirin: can the CURE results be extrapolated to cerebrovascular patients? Stroke. 2001;32:2948-2949. 18. Wolf PA, Clagett GP, Easton JD, et al. Preventing ischemic stroke in patients with prior stroke and transient ischemic attack: a statement for healthcare professionals from the Stroke Council of the American Heart Association. Stroke. 1999;30:1991-1994. 19. Snow V, Weiss KB, LeFevre M, et al. Management of newly detected atrial fibrillation: a clinical practice guideline from the American Academy of Family Physicians and the American College of Physicians. Ann Intern Med. 2003;139:1009-1017. 20. Adams RJ, Chimowitz MI, Alpert JS, et al. Coronary risk evaluation in patients with transient ischemic attack and ischemic stroke: a scientific statement for healthcare professionals from the Stroke Council and the Council on Clinical Cardiology of the American Heart Association/American Stroke Association. Stroke. 2003;34:2310-2322. 21. Rashid P, Leonardi-Bee J, Bath P. Blood pressure reduction and secondary prevention of stroke and other vascular events: a systematic review. Stroke. 2003;34:2741-2748. 22. Rothwell PM, Howard SC, Spence JD, et al. Relationship between blood pressure and stroke risk in patients with symptomatic carotid occlusive disease. Stroke. 2003;34:2583-2590.
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