Transient Ischemic Attack Case File
Eugene C. Toy, MD, Gabriel M. Aisenberg, MD
Case 36
A 72-year-old man is seen in the emergency department because of the acute onset of a right facial droop, right arm weakness, and some difficulty speaking. These symptoms started 6 hours ago while he was sitting at the breakfast table. He had no headache, no loss of consciousness, and no abnormal involuntary movements. Two weeks ago, he had a transient painless loss of vision in his left eye, which resolved spontaneously within a few hours. His medical history is significant for long-standing hypertension and a myocardial infarction 4 years previously, which was treated with percutaneous angioplasty. His medications include a daily aspirin (81 mg), metoprolol, and simvastatin. He does not smoke. When you see him in the emergency department, his symptoms have nearly resolved. He is afebrile, heart rate is 62 beats per minute (bpm), and blood pressure (BP) is 135/87 mm Hg. The right corner of his mouth droops, with slight flattening of the right nasolabial fold, but he is able to fully elevate his eyebrows. His strength is 4/5 in his right arm and hand, and the rest of his neurologic examination, including cerebellar testing and gait, are normal. He has no carotid bruits; his heart rhythm is regular with no murmur but with an S4 gallop. The remainder of his physical examination is normal. Laboratory studies, including renal function, liver function, lipid profile, glucose, and complete blood count (CBC), are normal. Within a few hours, all of the patient’s symptoms have resolved.
▶ What is the most likely diagnosis?
▶ What is your next step in the care of this patient?
ANSWERS TO CASE 36:
Transient Ischemic Attack
Summary: A 72-year-old man presents with
- Acute onset of right facial droop and right arm weakness and some difficulty speaking, which resolves within hours
- No headache, decreased consciousness, or abnormal involuntary movements
- Previous transient painless loss of vision in his left eye that resolved spontaneously within a few hours
- Known atherosclerotic disease but no carotid bruits
Most likely diagnosis: Transient ischemic attack (TIA) most likely caused by atheroembolism from the left internal carotid artery.
Next step: Perform urgent noncontrast computed tomography (CT) of the head.
ANALYSIS
Objectives
- Describe the most common mechanisms for ischemic stroke: carotid stenosis, cardioembolism, and small-vessel disease. (EPA 2, 10)
- Understand the evaluation of a stroke patient with the goal of secondary prevention. (EPA 1, 3)
- Differentiate patients best managed with medical therapy from those who benefit from carotid endarterectomy (CEA). (EPA 4)
Considerations
Patients who present with acute focal neurologic deficits require rapid evaluation for suspected stroke. The saying is, “Time is brain tissue.” An efficient but thorough neurologic examination should include cranial nerve testing, somatic motor strength, somatic sensory testing, speech and language assessment, and cerebellar testing, including gait. Neurologic scoring should be done on a standardized manner such as the National Institute of Health Stroke Scale. Emergency laboratory work, such as glucose, CBC, electrolytes, and coagulation profile, and electrocardiography (ECG) are important. Noncontrast CT of the brain is necessary to differentiate between ischemic stroke and hemorrhagic stroke, which cannot be definitively distinguished clinically. If CT shows no hemorrhage and no large multilobar infarction (> one-third of the cerebral hemisphere), patients with the clinical diagnosis of acute ischemic attack may receive thrombolytics (intravenous recombinant tissue plasminogen activator [tPA]) as long as it can be delivered within 3 hours (some patients may be treated with intravenous thrombolytics up to 4.5 hours) of the onset of symptoms; this is associated with a reduction in mortality and disability. Thus, rapid triaging of patients with possible TIA/stroke is critical.
This 72-year-old man presented more than 6 hours after the onset of symptoms and has had resolution of neurologic deficits, consistent with a suspected diagnosis of TIA. He has established atherosclerotic coronary disease but no known carotid artery disease. He denies headache, which is important because migraine headache may be associated with neurologic deficits; it would be rare for an elderly man to have the first presentation of migraine headache. Various neurologic diseases, such as multiple sclerosis, may be characterized by complete resolution of neurologic deficits, but the symptoms usually last longer than 24 hours. He does not have abnormal motor activity, which might suggest seizure disorder.
If the noncontrast CT excludes acute intracranial pathology, the patient should be counseled about secondary prevention of future ischemic events; this includes risk factor reduction through antiplatelet and statin therapy, BP control, smoking cessation, and noninvasive imaging of the carotid arteries to determine the extent of stenosis. With the patient’s symptoms, if there is more than 70% stenosis of the left internal carotid artery, the possibility of left CEA should be discussed.
APPROACH TO:
Transient Ischemic Attack and Prevention of Stroke
DEFINITIONS
AMAUROSIS FUGAX: Transient monocular blindness that often is described as a gray shade being pulled down over the eye caused by retinal ischemia, most often due to emboli originating from the carotid artery.
CEREBROVASCULAR ACCIDENT (CVA): Also known as stroke. Acute onset of a focal neurologic deficit due to a cerebral infarction or hemorrhage. CVAs are widely subdivided into ischemic and hemorrhagic.
TRANSIENT ISCHEMIC ATTACK: Transient neurologic deficit caused by focal brain, spinal cord, or retinal ischemia, without acute infarction.
CLINICAL APPROACH
Pathophysiology
Transient ischemic attacks, often called “ministrokes,” typically refer to the sudden onset of a focal neurologic deficit, with spontaneous resolution within 24 hours (usually within the first hour). However, current definition of TIA focuses on a biological end point (tissue injury) rather than an arbitrary time cutoff. Recent understanding is that there is risk of tissue infarction, even when focal symptoms resolve within less than 24 hours, which may be visualized on brain magnetic resonance imaging (MRI) with diffusion-weighted or perfusion-weighted imaging.
Not all transient focal neurologic events actually represent ischemia, however. The differential diagnosis includes classic migraine, postictal paralysis, seizures, certain infections, prolonged hypoglycemia, cerebral hemorrhage, or even slow-evolving intracranial processes such as subdural hematoma, abscess, or tumors, which can suddenly produce symptoms because of edema or hemorrhage or can result in seizure activity. However, clinical evaluation and imaging studies of the brain should be sufficient to exclude most or all of these diagnoses.
TIAs are produced by temporary ischemia to a vascular territory, usually caused by thrombosis or embolism and less commonly by vasculitis, hematologic disorders such as sickle cell disease, or vasospasm. By far, the most common causes of stroke or TIA are carotid atherosclerosis (large-vessel disease); cardioembolism, usually to branches of the middle cerebral artery (medium-size vessel disease); or lipohyalinosis affecting the small lenticulostriate arteries (small-vessel disease).
Clinical Presentation
The focal neurologic symptoms produced by ischemia depend on the area of the cerebral circulation involved and may include (1) amaurosis fugax, (2) hemiparesis, (3) hemianesthesia, (4) aphasia, or (5) dizziness/vertigo as a result of vertebrobasilar insufficiency. The significance of a TIA is not the symptoms it produces because by definition it is self-resolved, but the risk for future events it portends. The highest-risk patients for stroke are those with previous ischemic events such as TIA; that is, it can be looked on as a warning sign of recurrent stroke, which may be disabling. Table 36–1 shows the ABCD2 scoring system, which can be used to triage patients with TIA to assess their risk for recurrent events within the first 3 months (most of them occur within the first 2 days).
The workup for a TIA begins with a history and physical examination (see Table 36–2). Pertinent historical factors include time of onset, course, duration of symptoms, atherosclerotic risk factors, and relevant medical history (ie, atrial fibrillation). Physical examination should begin with BPs in all four extremities and should include a fundoscopic examination. In this patient, the first symptom was amaurosis fugax due to cholesterol emboli, called Hollenhorst plaques, which often can be seen lodged in the retinal artery. Auscultation for carotid bruits, cardiac murmurs, assessment of cardiac rhythm, evidence of embolic events to other parts of the body, and a complete neurologic examination should also be performed.
A noncontrast CT scan (or some institutions prefer MRI) of the brain also must be performed initially. Noncontrast CT scans of the brain are very sensitive in detecting acute cerebral hemorrhage but are relatively insensitive to acute ischemic strokes, particularly when the area of the stroke is less than 5 mm in diameter or is located in the region of the brainstem or if the stroke is less than 12 hours old. Further imaging with magnetic resonance may be considered. Laboratory data that should always be obtained include CBC, fasting lipid profile, and serum glucose level. Other laboratory data, such as an erythrocyte sedimentation rate in elderly populations to evaluate for temporal arteritis, should be tailored to the patient. Generally, a 12-lead ECG must be obtained to evaluate for atrial fibrillation. An echocardiogram can be useful to evaluate for valvular or mural thrombi, along with a bubble study to assess for a connection between the atria. Finally, imaging of the extracranial vasculature to detect severe carotid artery stenosis is essential to guide further stroke prevention therapy. Carotid Doppler ultrasound and magnetic resonance angiography are effective noninvasive imaging studies and are often used as first-line diagnostic tools.
Treatment
Stroke prevention begins with antiplatelet therapy, and aspirin should be used in all cases unless there is a contraindication to its use. Aspirin should be started within 48 hours of a TIA or stroke. However, if tPA is used, it is best to wait 24 hours after administration of the tPA to start aspirin therapy. Use of clopidogrel or combination aspirin and dipyridamole may be slightly superior to aspirin for stroke prevention but at a substantially higher cost. Combination therapy with aspirin and clopidogrel has not been shown to provide greater benefit in stroke prevention but does produce a higher rate of bleeding complications.
For patients with TIA/stroke as a consequence of carotid atherosclerosis, medical management includes antiplatelet agents and aggressive risk reduction via BP control, treatment of hyperlipidemia and diabetes, and smoking cessation. In the acute phase of an ischemic event, when a patient has neurologic symptoms, hypertension is not to be dropped significantly since arterial BP that is too low may underperfuse the brain tissue beyond a blockage (this concept is recognized as permissive hypertension). Acute BP management is recommended only when systolic BP > 220 mm Hg, diastolic BP > 120 mm Hg, or tPA will be administered (goal of systolic BP < 185 mm Hg and diastolic BP < 110 mm Hg). Blood glucose should be maintained between 140 and 180 mg/dL during a stroke, as tight glucose control shows a mortality benefit poststroke.
As a part of future stroke risk reduction, after 24 hours, if the patient is stable neurologically, antihypertensive therapy can be restarted in patients with known hypertension. Patients with a TIA who are stable several days after the event and are found to have elevated BP pressure (≥ 140/90 mm Hg) should be treated to a goal BP of < 140 mm Hg systolic and < 90 mm Hg diastolic. High-intensity statin therapy should be initiated for all TIA patients to reduce the risk of stroke and other cardiovascular events. These patients should also undergo screening for diabetes with hemoglobin A1C, fasting glucose measurement, or glucose tolerance test, and they should be treated based on the American Diabetic Association guidelines. Patients who are obese (body mass index > 30 kg/m2) should be encouraged to implement lifestyle modifications to lose weight. While the effect of weight loss on stroke prevention is unclear, weight loss can help control other risk factors. Last, smoking cessation is an extremely important step to take in reducing the risk of a stroke, as primary prevention, as well as after a TIA.
For patients with cardioembolic stroke as a result of atrial fibrillation, long-term anticoagulation with warfarin (Coumadin) reduces the risk of systemic embolization by approximately 70%. Newer oral anticoagulants (dabigatran, apixaban, rivaroxaban, and edoxaban) have recently been approved for patients with atrial fibrillation and are comparable in efficacy to warfarin with lower risk of cerebral bleeding. The risk of stroke among patients with atrial fibrillation can be predicted using the CHADS2-Vasc score. For patients with small-vessel disease-producing lacunar infarctions, BP control and antiplatelet agents are the mainstays of therapy.
For TIA patients found to have carotid artery stenosis, in addition to medical therapy as described previously, patients should be evaluated for carotid artery endarterectomy (open surgery to remove plaques), carotid artery angioplasty (percutaneous intervention where inflation of a balloon is used to open the artery), or stenting.
Surgical endarterectomy for severe carotid artery stenosis has successfully reduced the long-term risk of stroke in both symptomatic and asymptomatic patients. For patients who suffer a TIA or stroke and have an ipsilateral carotid artery stenosis greater than 70%, CEA reduces the rate of stroke and is highly recommended. For symptomatic patients with stenosis of 50% to 69%, CEA can reduce the future stroke risk, but it is recommended on a case-by-case basis, taking the patient’s characteristics into account. For asymptomatic patients with greater than 60% stenoses, endarterectomy reduces the risk of stroke as well, but to a much lesser degree than symptomatic patients. It should be noted that the surgery is not without risk and can actually cause significant morbidity and mortality from a postsurgical stroke; therefore, the surgery should be performed in a center with very low surgical morbidity and mortality.
In asymptomatic patients, carotid surgery should only be performed when there is relatively low comorbidity and a long life expectancy in order to gain the most benefit. Carotid artery stenting (CAS) is available for patients with carotid stenosis, but like endarterectomy, it also carries a risk of embolization and stroke. Stenting may be considered as an alternative to surgery for symptomatic patients who are high-risk surgical candidates or for patients with anatomy that would prevent open surgery. In patients over the age of 70 years, endarterectomy is associated with better outcomes. In younger patients, endarterectomy and stenting are considered equal in terms of periprocedural complications. For carotid stenosis of less than 50%, neither CAS nor CEA is recommended.
CASE CORRELATION
- See also Case 8 (Atrial Fibrillation/Mitral Stenosis) and Case 38 (Headache/ Temporal Arteritis).
COMPREHENSION QUESTIONS
36.1 A previously healthy 75-year-old man is being seen in the office for an episode of weakness that he reports occurred 2 weeks previously. He states that he had weakness of the left arm and left leg that lasted for 4 hours and slowly resolved over the rest of day. His arm and leg also felt “heavy” and had some numbness. He denies having similar episodes in the past. On physical examination, his BP is 140/90 mm Hg. He is found to have a right carotid bruit on auscultation. A duplex ultrasound demonstrates a 75% stenosis of the right carotid artery. Which of the following is the best therapy for this patient at this time?
A. Aspirin plus clopidogrel
B. Warfarin (Coumadin)
C. Carotid endarterectomy
D. Carotid artery stenting
E. Tissue plasminogen activator
36.2 One year ago, a 24-year-old woman had an episode of diplopia of 2 weeks’ duration. The symptoms resolved completely. Currently, she complains of left arm weakness but no headache. Which of the following is the most likely diagnosis?
A. Recurrent TIAs
B. Subarachnoid hemorrhage
C. Complicated migraine
D. Multiple sclerosis
36.3 A 67-year-old woman is being seen in the office for the acute onset of dizziness. She says she was sitting on the couch watching TV when the episode came on, and the room was spinning. She feels nauseous. Her history includes a stroke 2 years ago that left some right-sided weakness. Which of the following arteries is most likely to be affected in today’s presentation?
A. Vertebrobasilar
B. Carotid
C. Aorta
D. Middle cerebral
36.4 A 62-year-old man who works at an automobile assembly line has noticed that he feels pain, fatigue, and numbness in his right arm while working for the last several months. This morning at work, he noticed vertigo, then light-headedness, then lost consciousness for a few seconds. The BP in his right arm is 30 mm Hg lower than that in his left arm. What is the most likely diagnosis?
A. Left middle cerebral artery stroke
B. Lacunar infarction involving right internal capsule
C. Stenosis of right subclavian artery due to atherosclerosis
D. Multiple sclerosis
ANSWERS
36.1 C. This patient has symptomatic carotid disease, which includes symptoms such as TIAs and small, nondisabling ischemic strokes. A patient who presents with symptomatic carotid disease and stenosis between 70% and 99% should receive a CEA. It has been found that patients over the age of 70 fare better with a CEA than stenting alone (answer D). When symptomatic patients present with stenosis between 50% and 69%, management depends on gender. Women tend to have better outcomes with optimal medical management, whereas men have improved outcomes with CEA. Medical therapy such as antiplatelet medication (answer A) or anticoagulation (answer B) is not as effective as CEA in this circumstance. Tissue plasminogen activator (tPA) (answer E) is indicated for thromobotic strokes within 4.5 hours of onset of symptoms and not appropriate in this patient’s setting.
36.2 D. Multiple neurologic deficits separated in space and time in a young patient are suggestive of multiple sclerosis. The symptoms lasting longer than 24 hours as well as the patient’s age make TIAs (answer A), even if recurrent, less likely to be the cause of her symptoms. A subarachnoid hemorrhage (answer B) will often present with a “thunder clap headache” or “the worst headache” of the patient’s life and is usually an isolated event. A complicated migraine (answer C) can include symptoms such as changes in vision and arm weakness but with or before the onset of the headache.
36.3 A. Vertigo and dizziness can be seen in vertebrobasilar insufficiency. Transient monocular blindness or amaurosis fugax is associated with internal carotid (answer B) pathology. Face weakness, dysarthria, and hemiplegia greater in the upper extremity are associated with pathology in the middle cerebral artery (answer D). A problem of the aorta (answer C) would lead to global brain ischemia as well as multiorgan insufficiency.
36.4 C. The patient likely has subclavian steal: the phenomenon of flow reversal in the vertebral artery ipsilateral to a hemodynamically significant stenosis of the subclavian artery. The neurologic symptoms can be caused by vertebrobasilar ischemia, hence the problems with vertigo. The difference in BP in both arms strongly suggests this diagnosis. Left middle cerebral artery stroke (answer A) would lead to speech difficulties and right hemiplegia. Lacunar infarcts involving the right internal capsule (answer B) would lead to transient left-sided arm/leg weakness or sensory deficits and not vertigo. Multiple sclerosis (answer D), which is a demyelinating disease affecting the white matter of the brain, can lead to a variety of deficits, including vertigo, weakness, and diplopia; however, there is no difference in BP in the arms with MS.
CLINICAL PEARLS
▶ The most common causes of cerebral infarction are carotid atherosclerotic stenosis, cardioembolism, and small-vessel disease such as lipohyalinosis.
▶ Cerebral infarction, TIA, and amaurosis fugax all may be symptoms of carotid stenosis.
▶ In symptomatic patients with severe stenosis > 70%, CEA is superior to medical therapy in stroke prevention, provided the surgical risk is low (< 6%).
▶ For other patients, stroke prevention consists mainly of antiplatelet agents (aspirin, clopidogrel) and risk factor modification, for example, lowering BP, controlling hypercholesterolemia, and smoking cessation.
REFERENCES
Brott TG, Brown RD Jr, Meyer FB, et al. Carotid revascularization for prevention of stroke: carotid endarterectomy and carotid artery stenting. Mayo Clin Proc. 2004;79:1197-1208.
Kernan WN, Ovbiagele B, Black HR, et al. Guidelines for the prevention of stroke in patients with stroke or transient ischemic attack: a guideline for healthcare professionals from the American Heart Association/American Stroke Association. Stroke. 2014;45:2160-2236.
Mantese VA, Timaran CH, Chiu D, et al. The Carotid Revascularization Endarterectomy Versus Stenting Trial (CREST): stenting versus carotid endarterectomy for carotid disease. Stroke. 2010; 41(10 suppl):S31-S34.
Pulsinelli WA. Ischemic cerebrovascular disease. In: Goldman L, Bennett JC, eds. Cecil’s Textbook of Medicine. 21st ed. Philadelphia, PA: Saunders; 2000:2099-2109.
Smith WS, English JD, Johnston SC. Cerebrovascular diseases. In: Jameson JL, Fauci AS, Kasper SL, et al, eds. Harrison’s Principles of Internal Medicine. 20th ed. New York, NY: McGraw Hill; 2018:2259-2586.
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