1. Stroke is the fifth leading cause of death in the United States and the most common cause of serious long-term disability.
2. Completed stroke and transient ischemic attack (TIA) have the same vascular pathophysiology and are distinguished by the duration of ischemia and presence or absence of permanent tissue injury.
3. TIA is defined as a transient episode of neurologic dysfunction caused by focal brain, spinal cord, or retinal ischemia without acute infarction. Diffusion-weighted MRI has revealed that many events that fit the former definition of vascular symptoms lasting <24 hours were, in fact, associated with acute infarction, therefore this tissue-based definition of TIA is now most widely used.
1. The onset of stroke is typically sudden, and symptoms vary according to the site of ischemia.
2. History is directed at distinguishing stroke and TIA from other causes of sudden focal deficits such as migraine and focal seizures.
3. Underlying factors in the history that suggest the possible cause of stroke are
a. Heart disease, including atrial fibrillation, and peripheral arterial disease.
b. Atherosclerotic risk factors (hypertension, diabetes, hypercholesterolemia, smoking, sedentary lifestyle, family history of stroke, and atherosclerotic disease).
c. History suggesting thrombophilia, cranial or cervical trauma, or neck, face, and head pain that suggest arterial dissection; history of fever, chills, cardiac symptoms, or drug abuse that suggest endocarditis.
4. When acute thrombolytic or endovascular therapies are being considered, the precise time of symptom onset and problems that might contraindicate such therapies should be determined.
1. Most cases of focal cerebral ischemia are caused by blockage of a cerebral artery. The most common causes of occlusion are as follows:
a. Embolism of thrombotic material from the heart chambers or valves or from another source such as the aorta
b. Atherosclerosis in a large or medium artery, particularly a carotid artery, causes either stenosis with reduction of distal blood flow or local thrombosis leading to artery-to-artery embolism to a cerebral vessel
c. Mural thickening and luminal stenosis and, ultimately, occlusion of small cerebral vessels, typically the result of chronic exposure to hypertension (HTN), diabetes mellitus (DM), and hyperlipidemia
2. Less common causes of vascular occlusion include cervical arterial dissection; arteritis of small and large vessels; vasospasm; thrombophilia; and embolism of material other than thrombus, such as fat, air, tumor, amniotic fluid, or intravascular medical devices. The main disorders underlying stroke are listed in Table 6-1, but most are infrequent compared to the big three: cardioembolism, large vessel atherosclerosis, and small vessel disease.
Table 6-1 Some Causes of Stroke | ||||||||||||||||||||||||||||
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1. The outcome of an individual ischemic event depends on the location, magnitude, and duration of the ischemia, hence ultimately on the size and location of
the completed stroke. The outcome after stroke can be improved by the early use of an intravenous thrombolytic agent and by early revascularization with endovascular clot retrieval.
2. The risk of a completed stroke after a TIA depends on the mechanism of the TIA and the success of appropriate acute and preventive therapies. The ABCD2 score has been used to predict the risk of stroke in the days after TIA (Table 6-2). Predictive power is enhanced by consideration of dual TIAs, ie, recent prior TIA, and brain MRI and carotid imaging. The ABCD2 score is commonly used by emergency departments to triage patients with TIA.
Table 6-2 ABCD2 Score for Predicting Early Stroke Risk After TIA | ||||||||||||||||||||||||||||||||||||||||||||||||||||||
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1. The examiner should note the temperature, blood pressure (BP), and cardiac rhythm, the quality of carotid pulses and the presence of bruits, and the quality of heart sounds and presence of murmur and any findings that might suggest a special mechanism, such as splinter hemorrhages (endocarditis) or petechiae (thrombotic thrombocytopenic purpura and other causes).
2. The neurologic examination should define the localization and clinical stroke syndrome. This allows prediction of the vessel involved and the mechanism of vascular occlusion.
1. Middle cerebral artery (MCA) territory syndrome: Contralateral gaze paresis, hemiparesis, and hemisensory loss, often with contralateral visual field loss, and cortical signs (aphasia with left hemispheric lesions; neglect with right).
2. MCA branch (partial) syndromes: Nonfluent aphasia (Broca aphasia if perisylvian and transcortical motor aphasia if sparing the perisylvian area) if involving anterior division branches and fluent aphasia (Wernicke aphasia if perisylvian and transcortical sensory aphasia if sparing the perisylvian area) if involving
posterior division branches of the left MCA. (In fact, many posterior strokes cause nonfluent aphasia, especially acutely.)
3. Anterior cerebral artery (ACA) syndrome: Predominant leg weakness and sensory deficits, sparing of vision. Bilateral frontal signs suggest a common origin of the two anterior cerebral arteries.
4. Posterior cerebral artery (PCA) syndrome: Contralateral homonymous hemi- or quadrantanopsia, typically with intact motor and somatosensory function or with associated cortical deficits.
a. Memory loss from medial temporal infarction
b. Alexia without agraphia from dominant visual cortex and splenium of corpus callosum infarction
c. Agnosias, such as color naming and recognition disorders and prosopagnosia (facial recognition disorder), from infarction of the inferior temporo-occipital cortex
5. Mid-basilar artery syndrome suggesting atherosclerotic stenosis or occlusion of the mid-basilar artery with pontine (dysarthria, horizontal diplopia, vertigo, quadriparesis) and cerebellar dysfunction.
6. Top-of-the-basilar syndrome suggesting embolic occlusion of the distal basilar artery with midbrain (decreased arousal; vertical and horizontal diplopia; bilateral ptosis; unequal and irregular poorly reactive pupils), thalamic, and occipital dysfunction.
7. Lacunar syndromes usually indicate occlusion of a small cerebral vessel (eg, pure motor or pure sensory syndromes without visual loss or cortical findings [aphasia or neglect]) or isolated hemiparesis with ataxia. Dysarthria is common with many deep infarcts, such as lacunar infarcts in the pons or the internal capsule.
8. Borderzone (watershed) infarcts occur when a large region of the cerebrum is subjected to reduced blood flow either from proximal vascular occlusion or from global reduction in perfusion due to systemic hypotension.
a. Anterior watershed stroke typically produces the “man-in-a-barrel” syndrome characterized by leg and proximal upper extremity weakness with relative sparing of the distal upper extremities from infarction of the ACA and MCA border zone in the high frontal convexity.
b. The posterior watershed stroke may produce Balint syndrome (simultanagnosia, optic ataxia, and ocular apraxia) from infarction of the MCA and PCA border zone in the parieto-occipital region.
1. The goals of acute neuroimaging after stroke are as follows:
a. To define the site and location of an established infarct and the extent of ischemic tissue at risk
b. To identify the site of an acute vascular occlusion
c. To identify potential sources of the embolus
d. To identify hemorrhage or unexpected lesions mimicking acute cerebral infarction
2. Computed tomography (CT) and CT angiography
a. Noncontrast CT dependably identifies acute hemorrhage. It is insensitive to infarction within hours of stroke onset. However, subtle changes are sometimes detected: “dense MCA sign” of thrombus in the MCA stem, sylvian fissure dot sign indicating thrombus in the more distal MCA branches, or hypodensity, loss of gray-white differentiation, and sulcal effacement all of
which indicated early infarction. With MCA stem occlusion, loss of gray-white differentiation is most commonly seen in the basal ganglia capsular region and insula (“insular ribbon sign”).
b. CT angiography evaluates the patency of cerebral vessels from the aortic arch through the neck and intracranially.
c. CT perfusion techniques provide acute information about the size of established infarct and of hypoperfused tissue at risk of infarction.
3. MRI and MRA
a. The diffusion-weighted imaging (DWI) sequence of MRI is far more sensitive than CT for detecting early infarction. Acute infarction becomes bright on this sequence within minutes of tissue infarction. Correlation with low signal on apparent diffusion coefficient images differentiates acute infarction from other causes of bright signal on DWI.
b. MRA defines flow in the cerebral vessels from the aortic arch to the proximal intracranial arterial branches.
c. MRI perfusion techniques provide information about the size of established infarct and of hypoperfused tissue at risk.
4. Conventional angiography (digital subtraction angiography (DSA)
a. DSA is more sensitive and specific than either CTA or MRA and remains the gold standard for diagnostic vascular imaging; although sometimes used solely for diagnostic reasons, conventional angiography is now routine for the application of acute endovascular therapies.
5. Carotid duplex ultrasound
a. Carotid ultrasound includes Doppler assessment of blood flow velocities and anatomic imaging by gray scale and color flow techniques.
b. It is widely available, noninvasive, and, in good hands, it reliably defines and quantifies most proximal atherosclerosis carotid lesions.
c. Doppler waveforms can also give indirect information about upstream and downstream stenoses that are outside of the field of carotid ultrasound.
6. Transcranial Doppler ultrasound (TCD)
a. TCD allows imaging of the flow of the major vessels of the circle of Willis, the proximal middle, anterior, and posterior cerebral arteries; the ophthalmic artery; and the vertebral and basilar arteries. Information about direction, velocity, and turbulence of flow allows identification of stenosis or vasospasm of intracranial vessels and assessment of pathways of collateralization. Embolic signals may also be detected.
b. High flow velocities suggest vascular narrowing from stenosis or vasospasm, or elevated flow, as in generalized high-flow states, such as arteriovenous malformations. Because ultrasound is safe and noninvasive, it can be used serially for repeated examinations. Its most valuable application has been serial evaluation of the severity of cerebral vasospasm after subarachnoid hemorrhage (SAH).
1. Electrocardiogram (ECG), chest radiograph (CXR), glucose, electrolytes, blood urea nitrogen (BUN), creatinine, complete blood count (CBC) with platelets, and prothrombin time ([PT], international normalized ratio [INR]), and an activated partial thromboplastin time (aPTT) should be part of the initial evaluation to help determine the cause of the event and to provide information critical to the planning of acute therapy.
2. If fever or cardiac murmur is present, or if there are other reasons to suspect endocarditis, then C-reactive protein (CRP) or erythrocyte sedimentation rate (ESR), blood cultures, and echocardiogram are important to pursue this diagnosis.
3. If there is reason to suspect drug abuse, toxicology screening is valuable.
4. In the postacute phase, echocardiography, cardiac rhythm monitoring, further definition of the cerebral vasculature and laboratory tests directed at stroke risk factors are indicated as follows:
a. Fasting serum glucose and HgA1C; total, low-density lipoprotein (LDL), and high-density lipoprotein (HDL) cholesterol; and triglycerides.
b. High-sensitivity CRP elevation and hyperhomocysteinemia have been identified as a modifiable risk factor for atherosclerosis.
c. Patients in whom hypercoagulability is suspected should be evaluated for underlying cancer, and, in some cases, with IgG and IgM antiphospholipid antibodies, ß-2 glycoprotein 1 antibodies, lupus anticoagulant assay including, dilute Russell viper venom test, screening for factor V Leiden, prothrombin G20210A mutation, and levels and activities of proteins C and S and antithrombin III.
d. Where aortic atheroma, valvular or left atrial appendage visualization, or definition of a patent foramen ovale (PFO) will alter secondary preventive therapy, transesophageal echocardiography should be considered, because the sensitivity of transthoracic echocardiography is low for lesions at these sites.
1. Cerebral perfusion depends on the mean systemic arterial pressure (MAP) based on the basic hemodynamic relationship CBF = (MAP − CVP)/CVR, where CBF = cerebral blood flow, MAP = mean arterial pressure, CVP = cerebral venous pressure, and CVR = cerebrovascular resistance).
2. Areas of brain distal to narrowed or occluded arteries may be supplied by collateral vessels. When fully dilated (ie, autoregulated to maximize CBF), flow in these vessels becomes passively dependent on the MAP. Therefore, it is desirable to maintain MAP high in the setting of acute stroke.
3. It is common for patients with acute stroke to have acute BP elevations on presentation.
a. In general BP should not be lowered, unless
1) BP lowering is necessary to fulfill criteria for safe thrombolysis (see the section on Intravenous Thrombolysis and Tables 6-3 and 6-4), or unless acute medical issues demand it:
a) Acute myocardial infarction
b) Aortic dissection
c) Hypertensive crisis with end-organ involvement (congestive heart failure, acute renal failure, hypertensive encephalopathy)
b. A threshold above which BP should be treated acutely has not been established outside of these complications; however, consensus guidelines from the American Stroke Association suggest that therapy should be withheld unless diastolic BP is above 120 mm Hg or systolic BP is above 220 mm Hg. Lowering by 15% is reasonable when BP exceeds this level.
c. Patients with excessive BP elevation who are otherwise suitable for IV thrombolysis (alteplase [tPA] or tenecteplase [TNK]) should be treated acutely to achieve tolerable BP for therapy (systolic BP < 185, diastolic BP < 110). The antihypertensive goals and regimen modeled after the practice in the National Institute of Neurological Disorders and Stroke trial of intravenous (IV) tPA and recommended by the American Stroke Association are shown in Table 6-3.
Table 6-3 Acute Antihypertensive Therapy for Administration of Intravenous Tissue Plasminogen Activator | |||||
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Table 6-4 Indications and Contraindications for IV tPA or TNK for Acute Ischemic Stroke | |||||||
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1. Patients may be monitored with pulse oximetry and given supplemental oxygen for desaturation to less than 95%.
2. Both hyperthermia and hyperglycemia may increase the size of the ultimate infarct in experimental models and some clinical studies; therefore, patients should receive antipyretic medications and external cooling, if needed, to maintain normal body temperature and insulin to avoid excessive glucose elevation.
1. All patients who present within 3 hours of onset of stroke symptoms should be considered for IV thrombolytic therapy with tPA or TNK.
2. Patients who can be treated within 3 to 4.5 hours should be considered for IV thrombolytic therapy if they do not meet these added exclusion criteria: older than 80 years, NIHSS more than 25, taking oral anticoagulants, history of both prior stroke and DM.
3. Indications and contraindications for IV thrombolysis are listed in Table 6-4.
4. For suitable patients, an IV thrombolytic agent should be given as soon as the essential evaluation can be completed. The dose of tPA is 0.9 mg/kg to a maximum total dose of 90 mg. Ten percent of this dose is given as a bolus over about 1 to 2 minutes. The remainder is infused over 1 hour. The dose of TNK is 0.25 mg/kg to a maximum of 25 mg, given as a single bolus. It is advised that emergency departments establish protocols for administration to speed up preparation and minimize errors.Related posts:
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