Cerebrovascular Disease
Steven R. Bailey
INTRODUCTION
Disease of the cerebrovascular system reflects intrinsic alterations of blood flow that occur because of ischemia, hemorrhage, or mass effect. This chapter provides an overview of the clinically important aspects regarding ischemic and hemorrhagic stroke.
Cerebrovascular disease and stroke remain the fifth leading cause of death and the most frequent causes of disability in the United States and the world. In the United States, there are an estimated 795,000 new or recurrent strokes each year, with 147,810 stroke-related deaths reported in 2018.1
PATHOGENESIS
Stroke is due to the interruption of blood flow to the brain tissue because of blockage of an artery or hemorrhage from an artery resulting in vascular spasm and compression. Ischemic stroke accounts for over 70% of all strokes,2 and can be secondary to multiple etiologies including intracerebral atherosclerosis, embolization of plaque/thrombus from an extracerebral vessel, or cardioembolic events. Rare events that are not discussed in greater detail include arteriovenous malformations, vasculitis, and venous sinus thromboses.
One of the most common arterial causes of ischemic stroke is an embolus of an atherosclerotic plaque, with or without thrombus, that originates from arteries within the neck, aortic arch, or intracranial vessels. Inflammation and ulceration of these large vessels occurs as part of the systemic atherosclerotic process involving the heart, peripheral aorta, and cerebral vessels. Occasionally, the carotid artery may progress to complete occlusion; however, in the setting of an intact circle of Willis, this rarely causes a stroke as the primary lesion. More commonly, ulceration and exposure of the lipid-rich core of the atherosclerotic lesion initiates a thrombus that most commonly embolizes to the internal carotid arteries, distal to the bifurcation of the common carotid artery.
Intracranial atherosclerosis, as an etiology of ischemic stroke, shows marked geographic and racial disparities. It is the etiology of ischemic stroke in only 10% to 15% of White patients, typically in diabetic patients who are heavy smokers. This rate increases in Black individuals and is as high as 30% to 50% of Asian patients.3 Not only is the likelihood of stroke higher in Black as compared to White individuals but they also have a larger burden of intracerebral atherosclerosis.4 As discussed later, therapy for intracranial occlusion is far more challenging than are large vessel embolic events.
CLINICAL PRESENTATION
Patients suffering a stroke most often present with facial asymmetry, alteration of speech, or arm weakness. This has given rise to the pneumonic “FAST,” which stands for facial asymmetry, arm weakness, speech changes, and time to call 911, as promoted by the American Stroke Association. This was modified to include changes in balance, especially gait-related and eye changes with diplopia or visual changes. This has given rise to the BEFAST mnemonic because it is estimated to identify more than 95% of patients who present with an acute stroke syndrome.
Middle Cerebral Artery Stroke
The middle cerebral artery (MCA) is the most commonly affected vascular distribution. It is divided into four anatomic segments, M1, M2, M3, and M4. M1 supplies the horizontal segment of the MCA that is responsible for blood flow to the basal ganglia.5 The basal ganglia control emotions, executive function, motor control, and motor learning. The M2 or Sylvian segment supplies blood to the parietal lobe, the insula, inferolateral temporal lobe, and the superior temporal lobe. Branches from this segment supply areas of the brain that process sound and integrate experience and emotion. The M3 (opercular) segment nourishes the surface of the frontoparietal and temporal operculum and extends to the sylvian fissure. The M4 (cortical) segment supplies the surface of the sylvian fissure extending over the cortex.
An MCA infarction typically results in contralateral hemiparesis, facial paralysis, and sensory loss of the face and upper extremity. Gaze preferences toward the side of the lesion may be seen. The lower extremity is less commonly involved. Other findings of an MCA stroke include dysarthria, aphasia, and hemispheric neglect.
The Anterior Cerebral Artery Stroke
The anterior cerebral arteries (ACAs) supply the medial segments of the sylvian fissure forward. It often divides into two branches, A1 and A2. The central artery supplies the caudate nucleus, corpus callosum, and anterior putamen. The cortical branches supply the frontal and olfactory lobes via the orbital branches, parietal lobe from the parietal branches, and
cingulate, superior, central, and paracentral gyri. The ACA runs above the optic chiasm and pituitary glands.
cingulate, superior, central, and paracentral gyri. The ACA runs above the optic chiasm and pituitary glands.
An ACA infarct is a rare event, seen in only 3% of all strokes. Typical symptoms include contralateral hemiplegia that is worse in the leg than in the arm (crural hemiparesis). The eye fields may deviate away from the side of hemiplegia. Sensory loss is minimal. Reduced verbal expression or mutism can resemble aphasia.
Posterior Cerebral Artery Stroke
Posterior cerebral artery (PCA) blood flow is related to multiple interconnected vessels. PCA is divided into four segments, P1, P2, P3, and P4. The posterior circulation is supplied by the vertebral, basilar, posterior inferior cerebellar, anterior inferior cerebellar, and superior cerebellar arteries. The PCA supplies the lower part of the optic tract radiations.
Stroke in the posterior circulation is associated with symptoms of diplopia vertigo, visual field defects, dysphagia, memory impairment, and altered consciousness. Unilateral PCA infarction may result in contralateral homonymous hemianopia with sparing of macular vision. Less severe involvement may result in quadrantanopia. Aggressive behavior, hypersomnolence hallucinations, and aggressive behavior or pure sensory stroke may be presenting symptoms as well.
Differential Diagnosis of Acute Stroke
Patients with systemic infections, brain tumors, seizure disorders, metabolic disorders (ie, hypoglycemia or hyponatremia), positional vertigo, or conversion disorders may manifest neurologic symptoms that simulate stroke. Features that suggest non-stroke etiologies include younger age, mild symptoms, no history of vascular risk factors, and arrival to the emergency room by personal transportation rather than by emergency medical services.
The clinical diagnosis of an individual suffering a stroke can be difficult, and in more than 30% of cases, the neurologic symptoms are not due to an acute cerebrovascular event but are due to other etiologies.6 Neurologic symptoms that can resemble a stroke may be due to systemic infection, seizure, brain tumor, toxic or metabolic disorders (hyponatremia or hypoglycemia), positional vertigo, or psychiatric problems such as a conversion disorder.
Hemorrhagic Stroke
Intracerebral hemorrhage (ICH) is most often the result of hypertension or vascular abnormalities resulting in the rupture of smaller penetrating arteries in contrast to ischemic stroke due to large vessel occlusion. ICH accounts for 10% to 20% of strokes worldwide, but varies widely across social and ethnic strata. In low-income countries, the rates of ICH are nearly double compared to that in high-income countries (22 vs 10 per 100,000 person-years7). Non-modifiable risk factors include, age, sex, ethnicity, chronic kidney disease, and cerebral amyloid angiopathy. Rates vary widely across races, with Asian and Black individuals having rates much higher than do Whites and Hispanics. The rates are higher in men than in women. The greatest disparity is seen with age. The rate of ICH increases from 37.2 per 100,000 person-years in men aged 55 to 74 years to 176.3 per 100,000 person-years in men aged 75 to 94 years.8 Cerebral microbleeds increase with age and are more common in men. These are associated with an increased risk of warfarin-associated ICH as well as spontaneous ICH.
Cardioembolic Stroke
Cardioembolic stroke is increasing in frequency, because treatments for hypertension and hyperlipidemia decrease other causes of ischemic stroke. Importantly, cardioembolic strokes are associated with larger strokes than are other etiologies of ischemic stroke.10 A number of risk factors are associated with cardioembolic stroke including atrial fibrillation, patent foramen ovale, recent myocardial infarction, systolic heart failure, infective endocarditis, prosthetic heart valve, and aortic arch atheroma. Rare causes include atrial myxoma, papillary fibroelastoma, and mitral calcification.
Types of Stroke
Hemorrhagic stroke often presents differently than does ischemic stroke.11 As the putamen is the most common location for ICH, the most common symptoms are the development over many minutes or a few hours of headache, nausea, and vomiting. Although vomiting may occur in 50% of hemispheric ICH, almost all of cerebellar ICHs have this symptom. Seizures that occur in 10% of patients with ICH are seen in up to 50% of patients with lobar hemorrhage. Decreased level of consciousness may occur because of increased intracranial pressure. Stupor or coma in the setting of ICH defines a subset with involvement of the brainstem reticular activation system.
Cardioembolic strokes typically present with neurologic defects that are maximal at onset and are more likely to affect the cerebral cortex in contrast to small vessel or lacunar strokes with slower progression of symptoms. The involvement of the cerebral cortex is more likely to result in aphasia or visual field defects. Approximately 50% of cardioembolic strokes involve multiple vascular segments.12
DIAGNOSTIC APPROACH
Referral to Stroke Center
It is recommended by the American Heart Association (AHA)/American Stroke Association (ASA) 2019 guidelines that the early management of patients for potential stroke occurs within a regional system of care.6 Patients at high clinical suspicion should be referred to a certified stroke center capable of administering thrombolytic therapy (ie, intravenous tissue plasminogen activator [IV t-PA]). The benefit, in the setting of multiple thrombolytic-capable facilities, of referring to a center that has mechanical thrombectomy capability is uncertain at this time.
The treatment of stroke should begin with a determination of symptom onset, because this is critical for decisions
regarding therapy and prognosis. If the time of symptom onset is unknown, the time the patient was last known to be normal without new neurologic symptoms should be used as the time of onset.
regarding therapy and prognosis. If the time of symptom onset is unknown, the time the patient was last known to be normal without new neurologic symptoms should be used as the time of onset.
An expeditious neurologic assessment should be performed for all patients with suspected stroke. The most common tool is the National Institutes of Health Stroke Scale (NIHSS), which reviews 11 categories including level of consciousness, gaze, visual, facial palsy, motor function of arms and legs, ataxia, language, dysarthria, extinction, and inattention. Vertigo is associated with vertebrobasilar artery system occlusion, and may be either central or peripheral. A focused physical examination is also important as part of the initial evaluation. Vital signs, breathing, circulation, and airway need to be assessed. Patients with respiratory compromise due to elevated intracranial pressure are at increased risk for aspiration and asphyxiation, and they should be evaluated for the need for endotracheal intubation.
Reversible causes of neurologic defects should be excluded. Blood glucose using a finger stick should be determined immediately. Other laboratory testing including complete blood count and platelets, troponin, prothrombin time, international normalized ratio, and activated partial thromboplastin time may be indicated, but should not delay the start of thrombolytic therapy. Additional laboratory testing can be deferred until the acute stroke management has occurred.
Diagnostic Modalities
The clinical diagnosis of stroke is based on clinical presentation, but confirmed with imaging. The imaging tools available include computed tomography (CT) without contrast, computed tomography angiography (CTA), CT perfusion, CT venography, magnetic resonance imaging (MRI), magnetic resonance angiography (MRA), magnetic resonance perfusion, ultrasonography, nuclear medicine, and invasive angiography. CT imaging is readily available and non-contrast CT imaging studies do not increase the risk of renal dysfunction. Conversely, imaging using contrast—iodinated and gadolinium—can result in renal injury.
The initial imaging performed for patients with suspected stroke is CT without contrast, which is excellent at excluding hemorrhage. The identification of ischemic stroke by non-contrast CT varies with the age of infarction. In the hyperacute phase (<12 hours) non-contrast CT is most valuable for excluding hemorrhage. Occasionally a thrombus can be detected because of high attenuation in the images. In the acute phase (12-24 hours), the findings are subtle: loss of gray/white matter interface due to increased water content secondary to cell edema. The subacute phase (24 hours to 5 days) demonstrates edema due to altered blood vessels with well-defined margins and mass effect. Old strokes are visualized by non-contrast CT as volume loss of parenchyma and hypoattenuation due to encephalomacia.13 The non-contrast CT image can be used in risk assessment and decisions regarding thrombolytic therapy. The ASPECTS (Alberta Stroke Program Early CT Score) scale is a 10-point quantitative score used to assess early ischemic changes on non-contrast head CT. A score of less than 7 is associated with worse outcomes.14
CTA is performed by injection of IV contrast, typically into an antecubital vein, to better identify vessel thrombosis or occlusion, aneurysm, and dissection. Reconstructions of three-dimensional (3D) images and maximal intensity projections can assist with determination of clot length and distal stenosis.
MRI with or without gadolinium plays an important role in stroke imaging. MRI has higher soft-tissue contrast imaging ratios than does CT, particularly in the hyperacute and acute phases of stroke, with changes seen as early as 3 hours. Multiple protocols may be used, including fluid-attenuated inversion recovery (FLAIR), T2-weighted imaging (T2WI), T1-weighted imaging (T1WI), and diffusion-weighted imaging (DWI). DWI utilizes the impairment of mitochondrial function resulting in a shift of water into the cell, causing restricted water motion, and is considered the best sequence to detect brain infarctions as early as minutes after onset. It has a sensitivity ranging from 88% to 100% and a specificity of 95% to 100%, with an accuracy of 95%.15 MRA is similar to CTA, but is more time consuming to obtain, is not available in every center, and is typically used for patients allergic to iodinated contrast material.
MANAGEMENT
Medical Approach
In the setting of an acute stroke, medical management consists of a focused history to determine timing of onset of stroke and assessment of indications and contraindications to thrombolytic therapy or mechanical thrombectomy (Algorithm 81.1). The current goal for door-to-needle time is 60 minutes or less. Within this goal is a door-to-initial physician contact (<2.5 minutes), door-to-stroke team (within 5 minutes), door-to-CT/MRI acquisition (within 25 minutes), door-to-CT/MRI interpretation (within 45 minutes), and door-to-needle time of less than 60 minutes. If there is a decision to perform mechanical thrombectomy, the door-to-device time should be less than 90 minutes. Innovative protocols such as direct door-to-CT can yield even shorter times to definitive therapy.
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