Sudden onset of a neurologic deficit from a vascular mechanism: 85% are ischemic; 15% are primary hemorrhages [subarachnoid (Chap. 19) and intraparenchymal]. An ischemic deficit that resolves rapidly is termed a transient ischemic attack (TIA); 24 h is a commonly used boundary between TIA and stroke whether or not a new infarction has occurred, although most TIAs last between 5 and 15 min. Recently proposed new definitions classify all brain infarctions as strokes regardless of duration of symptoms. Stroke is the leading cause of neurologic disability in adults; 200,000 deaths annually in the United States. Much can be done to limit morbidity and mortality through prevention and acute intervention.
Ischemic stroke is most often due to embolic occlusion of large cerebral vessels; source of emboli may be heart, aortic arch, or other arterial lesions such as the carotid arteries. Small, deep ischemic lesions are most often related to intrinsic small-vessel disease (lacunar strokes). Low-flow strokes are seen with severe proximal stenosis and inadequate collaterals challenged by systemic hypotensive episodes. Hemorrhages most frequently result from rupture of aneurysms or small vessels within brain tissue. Variability in stroke recovery is influenced by collateral vessels, blood pressure, and the specific site and mechanism of vessel occlusion; if blood flow is restored prior to significant cell death, the pt may experience only transient symptoms, i.e., a TIA.
Abrupt and dramatic onset of focal neurologic symptoms is typical of ischemic stroke. Pts may not seek assistance on their own because they are rarely in pain and may lose appreciation that something is wrong (anosognosia). Symptoms reflect the vascular territory involved (Table 18-1). Transient monocular blindness (amaurosis fugax) is a particular form of TIA due to retinal ischemia; pts describe a shade descending over the visual field.
TABLE 18-1 ANATOMIC LOCALIZATION IN STROKE
Lacunar Syndromes (Small-Vessel Strokes)
Most common are:
• Pure motor hemiparesis of face, arm, and leg (internal capsule or pons)
• Pure sensory stroke (ventral thalamus)
• Ataxic hemiparesis (pons or internal capsule)
• Dysarthria—clumsy hand (pons or genu of internal capsule).
Vomiting and drowsiness occur in some cases, and headache in about one-half. Signs and symptoms are often not confined to a single vascular territory. Etiologies are diverse but hypertension-related is the most common (Table 18-2). Hypertensive hemorrhages typically occur in the following locations:
TABLE 18-2 CAUSES OF INTRACRANIAL HEMORRHAGE
• Putamen: Contralateral hemiparesis often with homonymous hemianopia.
• Thalamus: Hemiparesis with prominent sensory deficit.
• Pons: Quadriplegic, “pinpoint” pupils, impaired horizontal eye movements.
• Cerebellum: Headache, vomiting, gait ataxia.
A neurologic deficit that evolves gradually over 5–30 min strongly suggests intracerebral bleeding.
Principles of management are outlined in Fig. 18-1. Stroke needs to be distinguished from potential mimics, including seizure, migraine, tumor, and metabolic derangements.
FIGURE 18-1 Medical management of stroke and TIA. Rounded boxes are diagnoses; rectangles are interventions. Numbers are percentages of stroke overall. ABCs, airway, breathing, circulation; BP, blood pressure; CEA, carotid endarterectomy; ICH, intracerebral hemorrhage; SAH, subarachnoid hemorrhage; TIA, transient ischemic attack.
• Imaging. After initial stabilization, an emergency noncontrast head CT scan is necessary to differentiate ischemic from hemorrhagic stroke. With large ischemic strokes, CT abnormalities are usually evident within the first few hours, but small infarcts can be difficult to visualize by CT. CT or MR angiography (CTA/MRA) and perfusion may help reveal vascular occlusions and tissue at risk for infarction. Diffusion-weighted MRI has a high sensitivity for identifying ischemic stroke even minutes after onset.
ACUTE ISCHEMIC STROKE Treatments designed to reverse or lessen tissue infarction include: (1) medical support, (2) thrombolysis and endovascular techniques, (3) antiplatelet agents, (4) anticoagulation, and (5) neuroprotection.
MEDICAL SUPPORT Optimize perfusion in ischemic penumbra surrounding the infarct.
• Blood pressure should never be lowered precipitously (exacerbates the underlying ischemia), and only in the most extreme situations should gradual lowering be undertaken (e.g., malignant hypertension with bp > 220/120 or, if thrombolysis planned, bp > 185/110 mmHg).
• Intravascular volume should be maintained with isotonic fluids as volume restriction is rarely helpful. Osmotic therapy with mannitol may be necessary to control edema in large infarcts, but isotonic volume must be replaced to avoid hypovolemia.
• In cerebellar infarction (or hemorrhage), rapid deterioration can occur from brainstem compression and hydrocephalus, requiring neurosurgical intervention.
THROMBOLYSIS AND ENDOVASCULAR TECHNIQUES
• Ischemic deficits of <3 h duration, with no hemorrhage by CT criteria, may benefit from thrombolytic therapy with IV recombinant tissue plasminogen activator (Table 18-3).
TABLE 18-3 ADMINISTRATION OF INTRAVENOUS RECOMBINANT TISSUE PLASMINOGEN ACTIVATOR (rtPA) FOR ACUTE ISCHEMIC STROKE (AIS)a
• Based on recent data, IV rtPA is used in some centers for deficits of 3–4.5 h duration, but is not yet approved for this window in the U.S. and Canada.
• Ischemic stroke from large-vessel intracranial occlusion results in high rates of morbidity and mortality; pts with such occlusions may benefit from intraarterial thrombolysis (<6 h duration) or embolectomy (<8 h duration) administered at the time of an urgent cerebral angiogram at specialized centers.
• Aspirin (up to 325 mg/d) is safe and has a small but definite benefit in acute ischemic stroke.
• Trials do not support the use of heparin or other anticoagulants acutely for pts with acute stroke.
• Hypothermia is effective in coma following cardiac arrest but has not been adequately studied in pts with stroke. Other neuroprotective agents have shown no benefit in human trials despite promising animal data.
STROKE CENTERS AND REHABILITATION
• Pt care in comprehensive stroke units followed by rehabilitation services improves neurologic outcomes and reduces mortality.
ACUTE INTRACEREBRAL HEMORRHAGE
• Noncontrast head CT will confirm diagnosis.
• Rapidly identify and correct any coagulopathy.
• Nearly 50% of pts die; prognosis is determined by volume and location of hematoma.
• Stuporous or comatose pts generally are treated presumptively for elevated ICP. Treatment for edema and mass effect with osmotic agents may be necessary; glucocorticoids not helpful.
• Neurosurgical consultation should be sought for possible urgent evacuation of cerebellar hematoma; in other locations, data do not support surgical intervention.
EVALUATION: DETERMINING THE CAUSE OF STROKE
Although initial management of acute ischemic stroke or TIA does not depend on the etiology, establishing a cause is essential to reduce risk of recurrence (Table 18-4); particular attention should be on atrial fibrillation and carotid atherosclerosis as these etiologies have proven secondary prevention strategies. Nearly 30% of strokes remain unexplained despite extensive evaluation.
TABLE 18-4 CAUSES OF ISCHEMIC STROKE
Clinical examination should be focused on the peripheral and cervical vascular system. Routine studies include CXR and ECG, urinalysis, CBC/platelets, electrolytes, glucose, ESR, lipid profile, PT, PTT, and serologic tests for syphilis. If a hypercoagulable state is suspected, further studies of coagulation are indicated.
Imaging evaluation may include brain MRI (compared with CT, increased sensitivity for small infarcts of cortex and brainstem); MR or CT angiography (evaluate patency of intracranial vessels and extracranial carotid and vertebral vessels); noninvasive carotid tests (“duplex” studies, combine ultrasound imaging of the vessel with Doppler evaluation of blood flow characteristics); or cerebral angiography (“gold standard” for evaluation of intracranial and extracranial vascular disease). For suspected cardiogenic source, cardiac echocardiogram with attention to right-to-left shunts, and 24-h Holter or long-term cardiac event monitoring indicated.
PRIMARY AND SECONDARY PREVENTION OF STROKE
Atherosclerosis is a systemic disease affecting arteries throughout the body. Multiple factors including hypertension, diabetes, hyperlipidemia, and family history influence stroke and TIA risk (Table 18-5). Cardioembolic risk factors include atrial fibrillation, MI, valvular heart disease, and cardiomyopathy. Hypertension and diabetes are also specific risk factors for lacunar stroke and intraparenchymal hemorrhage. Smoking is a potent risk factor for all vascular mechanisms of stroke. Identification of modifiable risk factors and prophylactic interventions to lower risk is probably the best approach to stroke overall.
TABLE 18-5 RISK FACTORS FOR STROKE
Platelet antiaggregation agents can prevent atherothrombotic events, including TIA and stroke, by inhibiting the formation of intraarterial platelet aggregates. Aspirin (50–325 mg/d) inhibits thromboxane A2, a platelet aggregating and vasoconstricting prostaglandin. Aspirin, clopidogrel (blocks the platelet ADP receptor), and the combination of aspirin plus extended-release dipyridamole (inhibits platelet uptake of adenosine) are the antiplatelet agents most commonly used. In general, antiplatelet agents reduce new stroke events by 25–30%. Every pt who has experienced an atherothrombotic stroke or TIA and has no contraindication should take an antiplatelet agent regularly because the average annual risk of another stroke is 8–10%. The choice of aspirin, clopidogrel, or dipyridamole plus aspirin must balance the fact that the latter are more effective than aspirin but the cost is higher.
In pts with atrial fibrillation, the choice between anticoagulant or aspirin prophylaxis is determined by age and risk factors; the presence of any risk factor tips the balance in favor of anticoagulation (Table 18-6).
TABLE 18-6 CONSENSUS RECOMMENDATION FOR ANTITHROMBOTIC PROPHYLAXIS IN ATRIAL FIBRILLATION
Anticoagulation Therapy for Noncardiogenic Stroke
Data do not support the use of long-term warfarin for preventing atherothrombotic stroke for either intracranial or extracranial cerebrovascular disease.
Carotid endarterectomy benefits many pts with symptomatic severe (>70%) carotid stenosis; the relative risk reduction is ~65%. However, if the perioperative stroke rate is >6% for any surgeon, the benefit is lost. Endovascular stenting is an emerging option; there remains controversy as to who should receive a stent or undergo endarterectomy. Surgical results in pts with asymptomatic carotid stenosis are less robust, and medical therapy for reduction of atherosclerosis risk factors plus antiplatelet medications is generally recommended in this group.
For a more detailed discussion, see Smith WS, English JD, Johnston SC: Cerebrovascular Diseases, Chap. 370, p. 3270, in HPIM-18.