- Pathophysiology
- Clinical Features
- Ischemic Stroke
- Lacunar Syndromes (Small-Vessel Strokes)
- Intracranial Hemorrhage
- Evaluation: Determining the Cause of Stroke
- Primary and Secondary Prevention of Stroke
- Risk Factors
- Antiplatelet Agents
- Embolic Stroke
- Anticoagulation Therapy for Noncardiogenic Stroke
- Carotid Revascularization
Sudden onset of a neurologic deficit from a vascular mechanism: ∼85% are ischemic; ∼15% are primary hemorrhages (subarachnoid [Chap. 20 Subarachnoid Hemorrhage] and intraparenchymal). An ischemic deficit that resolves rapidly without radiologic evidence of an infarction is termed a transient ischemic attack (TIA); 24 h is a commonly used boundary between TIA and stroke, although most TIAs last between 5 and 15 min. Stroke is a leading cause of neurologic disability in adults; ∼150,000 deaths annually in the United States. Much can be done to limit morbidity and mortality through prevention and acute intervention.
Ischemic stroke can be due to embolic occlusion of large cerebral vessels; source of emboli may be heart, aortic arch, or other arteries such as the internal carotids. Small, deep ischemic lesions are most often related to intrinsic small-vessel disease (lacunar strokes). Low-flow strokes are occasionally 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. 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 19-1 Anatomic Localization in Stroke). Transient monocular blindness (amaurosis fugax) is a particular form of TIA due to retinal ischemia; pts describe a shade descending over the visual field and the ipsilateral carotid artery is often implicated.
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 with increased intracranial pressure (ICP), and headache is common. Signs and symptoms are often not confined to a single vascular territory. Etiologies are diverse but hypertension is the most common cause (Table 19-2 Causes of Intracranial Hemorrhage). Hypertensive hemorrhages typically occur in the following locations:
- Putamen: contralateral hemiparesis often with homonymous hemianopia
- Thalamus: hemiparesis with prominent sensory deficit
- Pons: quadriplegia, “pinpoint” pupils, impaired horizontal eye movements
- Cerebellum: headache, vomiting, gait ataxia
A neurologic deficit that evolves gradually over 30-90 min strongly suggests intracerebral bleeding.
| TREATMENT | ||
StrokePrinciples of management are outlined in Fig. 19-1. Medical Management of Stroke and TIA. Stroke needs to be distinguished from potential mimics, including seizure, migraine, tumor, and metabolic derangements.
ACUTE ISCHEMIC STROKETreatments designed to reverse or lessen tissue infarction include: (1) medical support, (2) intravenous thrombolysis, (3) endovascular revascularization, (4) antiplatelet agents, (5) anticoagulation, and (6) neuroprotection. MEDICAL SUPPORTOptimize perfusion in ischemic penumbra surrounding the infarct.
INTRAVENOUS THROMBOLYSIS
ENDOVASCULAR REVASCULARIZATION
ANTIPLATELET AGENTS
ANTICOAGULATION
NEUROPROTECTION
STROKE CENTERS AND REHABILITATION
ACUTE INTRACEREBRAL HEMORRHAGE
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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 19-4 Causes of Ischemic Stroke); particular attention should be on atrial fibrillation and carotid atherosclerosis because these etiologies have proven secondary prevention strategies. Nearly 30% of strokes remain unexplained despite extensive evaluation.
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, and PTT. 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 ultrasound; 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 cardiac telemetry (including long-term cardiac event monitoring) indicated.
Primary and Secondary Prevention of Stroke
Atherosclerosis is a systemic disease affecting arteries throughout the body (Table 19-5 Recommendations on Chronic Use of Antithrombotics for Various Cardiac Conditions). Multiple factors including hypertension, diabetes, hyperlipidemia, and family history influence stroke and TIA risk. Cardioembolic risk factors include atrial fibrillation/flutter, 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.
Platelet antiaggregation agents can prevent atherothrombotic events, including TIA and stroke, by inhibiting formation of intraarterial platelet aggregates. Aspirin (50-325 mg/d) inhibits thromboxane A2, a platelet aggregating and vasoconstricting prostaglandin. Aspirin, clopidogrel (blocks the platelet adenosine diphosphate [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 high. The choice of aspirin, clopidogrel, or dipyridamole plus aspirin must balance the fact that the latter are marginally more effective than aspirin but the cost is higher. In pts with minor stroke or TIA, a short course (21-90 d) of aspirin in combination with clopidogrel reduces events; long-term dual antiplatelet medications are ineffective and have higher rates of hemorrhagic complications.
In pts with atrial fibrillation and stroke, anticoagulants are generally the treatment of choice.
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 questionable. Endovascular stenting is another option, especially in those aged <70 years. 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 pending ongoing trial results.