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A stroke is a neurologic injury caused by an abnormality of the blood vessels supplying the central nervous system. Although strokes may occur in the spinal cord, they are uncommon and this chapter will focus on strokes that involve the brain. In the United States each year, about 800,000 individuals have a stroke and 130,000 die from a stroke, that is, a stroke every 40 seconds and death from stroke every 4 minutes. Stroke is the fifth leading cause of death in the United States and a very important cause of prolonged disability. Although strides have been made in the prevention and treatment of stroke in the last 25 years, the economic, social, and psychological costs of stroke remain huge.
Many medical conditions and behaviors predispose to stroke. These include hypertension, diabetes, obesity, hyperlipidemia, sedentary life style, smoking, cardiac disease, and heavy alcohol use. Prevention of stroke is very important and can be accomplished by physicians attending to these stroke risk factors, advising patients about their lifestyles and habits, and prescribing appropriate medications. Primary prevention is prevention of a first stroke, whereas secondary prevention is prevention of stroke recurrence. Second and third strokes are most often due to the same stroke subtype as the initial stroke. Identification of stroke etiology, therefore, is the most important step in avoiding recurrence.
VASCULAR ANATOMY
The nature of neurologic symptoms and signs helps to localize dysfunction to a particular area of the brain and a particular vascular supply. Intimate knowledge of the vascular anatomy of the brain, therefore, is necessary. The cerebral vasculature is divided into the anterior and posterior circulations, with the anterior (carotid) circulation supplying the cerebral hemispheres except for the medial temporal lobes and a portion of the occipital lobes, and the posterior (vertebrobasilar) circulation supplying the brainstem, thalami, cerebellum, and the posterior portions of the cerebral hemispheres (Fig. 14-1).
ANTERIOR CIRCULATION
The right common carotid artery (CCA) branches from the innominate artery. The left CCA arises directly from the aorta. The CCA divides in the neck into the internal carotid artery (ICA) and the external carotid artery. The ICA travels behind the pharynx, entering the skull where it forms an S-shaped curve—the carotid siphon. This portion of the ICA gives rise to the ophthalmic artery. The ICA then penetrates the dura and gives off the anterior choroidal and posterior communicating arteries before bifurcating into the anterior cerebral (ACA) and middle cerebral arteries (MCA).
The ACA supplies the anterior medial cerebral hemispheres, the caudate nuclei, and the basal frontal lobes. The anterior communicating artery connects the two ACAs. The MCA courses laterally, giving off lenticulostriate artery branches to the basal ganglia and internal capsule. The MCA trifurcates into small anterior temporal branches and large superior and inferior divisions. The superior division supplies the lateral cerebral hemispheres superior to the sylvian fissure, whereas the inferior division supplies the temporal and inferior parietal lobes.
The anterior choroidal artery arises from the ICA after the ophthalmic and posterior communicating arteries. It courses along the optic tract giving off branches to the globus pallidus and posterior limb of the internal capsule and then supplies the medial temporal lobe and the lateral geniculate body.
FIGURE 14-1. Schematic diagram of the vascular territories of the brain. [coronal section. ACA, anterior cerebral artery; MCA, middle cerebral artery; PCA, posterior cerebral arteries.]
POSTERIOR CIRCULATION
The first branch of each subclavian artery is the vertebral artery (VA). The VA enters the spinal column via the transverse foramina of C5 or C6 and runs within the intravertebral foramina, exiting to course behind the atlas before piercing the dura mater to enter the foramen magnum. The intracranial VAs join to form the basilar artery at the ponto-medullary junction.
The intracranial VA gives off posterior and anterior spinal artery branches, penetrating arteries to the medulla, and the posterior inferior cerebellar artery (PICA). The basilar artery then runs in the midline along the clivus giving off bilateral anterior inferior cerebellar artery and superior cerebellar artery (SCA) branches before dividing at the pontomesencephalic junction into the posterior cerebral arteries (PCA). Small penetrating arteries arise at the basilar artery bifurcation to supply the medial portions of the midbrain and thalami.
The vascular supply of the brainstem includes large paramedian arteries and smaller, short circumferential arteries that penetrate the basal portions of the brainstem into the tegmentum. Long circumferential arteries course around the brainstem and give off branches to the lateral tegmentum. The PCA gives off penetrating arteries to the midbrain and thalamus, courses around the cerebral peduncles, and then supplies the occipital lobe and inferior surface of the temporal lobe.
The circle of Willis connects the anterior circulations of each side through the anterior communicating artery, and the posterior and anterior circulations of each side through the posterior communicating artery (Fig. 14-2).
KEY POINTS
●Each carotid artery supplies two-fifths of the brain; the vertebrobasilar circulation, one-fifth.
●The anterior circulation supplies mainly the cerebrum, whereas the posterior circulation supplies the brainstem, cerebellum, thalami, and the visual cerebral cortex.
BRAIN ISCHEMIA
About 80% of strokes are ischemic whereas 10% each are due to subarachnoid and intracerebral hemorrhages. Ischemic strokes are divided into thrombotic, embolic, and systemic hypoperfusion mechanisms.
THROMBOSIS
Thrombosis refers to obstructed blood flow due to a localized occlusive process within one or more vessels. The most common vascular pathology is atherosclerosis, in which fibrous tissue and lipid materials form plaques that encroach on the lumen. Atherosclerosis affects mostly the large cervical and intracranial arteries. Less commonly, a clot forms within the lumen due to a primary hematologic problem, for example, polycythemia, thrombocytosis, or hypercoagulability. Vessel wall pathologies leading to thrombosis include vasoconstriction, fibromuscular dysplasia, and arterial dissection. Thrombosis of penetrating intracranial arteries is most often the consequence of hypertension, with hypertrophy of the media and deposition of fibrinoid material. Microatheromas can obstruct the penetrating artery origins.
FIGURE 14-2. Arteries of the circle of Willis. [ACA, anterior cerebral artery; AICA, anterior inferior cerebellar artery; ICA, internal carotid artery; MCA, middle cerebral artery; PCA, posterior cerebral arteries; PICA, posterior inferior cerebellar artery; SCA, superior cerebellar artery.]
EMBOLISM
An embolus occurs when clot material formed elsewhere within the vascular system lodges in a vessel and blocks blood flow. The material arises proximally, mostly from the heart; from major arteries such as the aorta, ICAs, and VAs; and from systemic veins. Cardiac sources of embolism include the heart valves, endocardium, and clots or tumors within the atrial or ventricular cavities. Artery-to-artery emboli are composed of clot, platelet clumps, or fragments of plaques. They may begin in large arteries and occur in the context of arterial dissection. Thrombi originating in systemic veins travel to the brain through cardiac defects such as an atrial septal defect or a patent foramen ovale, a process termed paradoxical embolism. Occasionally, air, fat, cholesterol crystals, bacteria, and foreign bodies enter the vascular system and embolize to brain vessels.
SYSTEMIC HYPOPERFUSION
Decreased blood flow to brain tissue may be caused by low systemic perfusion pressure. The most common causes are cardiac pump failure (most often due to myocardial infarction or arrhythmia) and systemic hypotension (due to blood loss or hypovolemia). The lack of perfusion is more generalized than in localized thrombosis or embolism and affects the brain diffusely and bilaterally. Poor perfusion is most critical in border zone or so-called watershed regions at the periphery of the major vascular supply territories, for example, between the ACA and MCA or between the MCA and PCA.
KEY POINTS●Ischemia can be due to a localized process within an artery (thrombosis), blockage of an artery by emboli arising proximally, or a general decrease in blood flow (systemic hypoperfusion).
●Emboli most often come from the heart, aorta, and proximal portions of the neck or intracranial arteries.
●Atherosclerosis most often affects the large cervical and intracranial arteries.
COMMON ISCHEMIC STROKE SYNDROMES
Clinical localization often involves matching patterns of clinical deficits with corresponding vascular localizations.
ANTERIOR CIRCULATION
1.Left cerebral hemisphere strokes lead to
a.Right hemiparesis: often arm, hand, and face > leg
b.Right hemisensory loss
c.Aphasia
d.In large lesions, conjugate deviation of the eyes to the left; right hemianopia or hemi-inattention
e.When caused by ICA occlusive disease, transient left monocular visual loss may also occur.
2.Right cerebral hemisphere strokes cause
a.Left hemiparesis: often arm, hand, and face > leg
b.Left hemisensory loss
c.Poor drawing and copying
d.Neglect of the left visual field
e.In large lesions, conjugate deviation of the eyes to the right, left hemianopia
f.When the signs are due to ICA occlusive disease, transient right monocular visual loss may accompany the brain signs.
These cerebral hemispheric lesions are most often caused by carotid artery occlusion, embolism to the MCA or its branches, or basal ganglionic intracerebral hemorrhages.
POSTERIOR CIRCULATION
1.Lateral medullary stroke (Wallenberg syndrome, usually due to intracranial VA occlusion) causes
a.Ipsilateral facial pain, or reduced pain and temperature sensation on the ipsilateral face, or both
b.Loss of pain and temperature in the contralateral limbs and body
c.Ipsilateral Horner syndrome
d.Nystagmus
e.Incoordination of the ipsilateral arm
f.Leaning and veering while sitting or walking, with gait ataxia
g.In deep lesions, dysphagia and hoarseness
2.Bilateral pontine base and often medial tegmentum stroke (usually due to basilar artery occlusion, or pontine hemorrhage) causes
a.Quadriparesis
b.Unilateral or bilateral conjugate gaze paresis; sometimes internuclear ophthalmoplegia or sixth nerve palsy
c.When the medial tegmentum is involved bilaterally, coma
3.Cerebellar infarction (usually due to embolism to the PICA or SCA, or cerebellar hemorrhage) causes
a.Gait ataxia; often inability to walk
b.Dysarthria
c.Ipsilateral arm dysmetria
4.Left PCA territory stroke causes
a.Right homonymous hemianopia
b.At times, amnesia
c.Alexia without agraphia when the splenium of the corpus callosum is involved
5.Right PCA territory stroke causes
a.Left homonymous hemianopia
b.At times, left-sided visual neglect
PCA territory infarcts are most often caused by embolism arising from the heart, aorta, or VAs.
LACUNAR SYNDROMES
Lacunar strokes are most often due to occlusion of a penetrating artery. Similar to large-vessel strokes, they produce a fairly limited range of presentations. Lacunar strokes may occur in either the anterior or the posterior circulations. Classic lacunar stroke syndromes include the following:
Pure motor lacune: weakness of the contralateral arm, face, and leg without sensory, visual, or cognitive or behavioral signs. Common locations of lacunes producing pure motor stroke include the corona radiata, posterior limb of the internal capsule, and pons.
Sensorimotor lacune: combination of motor and sensory lacunes. This syndrome is due to infarction in the ventral posterior thalamus and adjacent posterior limb of the internal capsule.
Dysarthria—clumsy hand syndrome: slurred speech and clumsiness of the contralateral hand. The most common location of a lacune producing this syndrome is in the base of the pons.
Ataxic hemiparesis: weakness and ataxia of the contralateral limbs, often greater in the leg and foot than in the arm and hand. The most common locations for lacunes producing ataxic hemiparesis are the base of the pons, the posterior limb of the internal capsule, and the corona radiata.
ARTERIAL DISSECTION
Dissection of the carotid or vertebral arteries may lead to ischemic stroke. Carotid dissection typically presents with severe retro-orbital headache ipsilateral to the lesion. Strokes involve the anterior circulation and occur either by thrombosis of the ICA or more commonly by an embolus arising from the dissection. On physical examination, patients with carotid artery dissection may have an ipsilateral Horner’s syndrome due to the involvement of the ascending oculosympathetic tract. Perspiration is preserved because those fibers ascend with the external carotid artery. VA dissection may be produced by neck manipulation or trauma and is commonly associated with ipsilateral neck pain and stroke in the posterior circulation.
DIAGNOSTIC EVALUATION
After taking a thorough history, performing a general examination emphasizing the heart and blood vessels, and performing a neurologic examination, the next step in evaluation of a patient with a suspected stroke is usually a brain image. Computed tomography (CT) and magnetic resonance imaging (MRI) scans are used to separate brain infarction from hemorrhage. Figure 14-3 shows a deep brain hemorrhage. Figure 14-4 shows a brain infarction on CT scan. MRI with diffusion-weighted imaging is more sensitive to acute brain infarction than is CT (Fig. 14-5).
FIGURE 14-3. Intracerebral hemorrhage. A computed tomographic scan showing a right basal ganglionic hemorrhage due to hypertension. The hemorrhage has extended into the right frontal horn of the lateral ventricle.
FIGURE 14-4. Computed tomographic scan of the head demonstrates a wedge-shaped hypodensity in the distribution of a branch of the left middle cerebral artery.
The symptoms and signs, when combined with brain imaging, should allow localization to the left or right anterior circulation, the posterior circulation, or to a lacunar syndrome. In patients with cerebral infarction, the heart, aorta, and neck and intracranial arteries and their branches should be imaged. This can be performed using echocardiography, extracranial and transcranial ultrasound, CT angiography (CTA), or MR angiography (MRA). In patients in whom the signs localize to the anterior circulation, vascular imaging of the ICAs should be emphasized, whereas in posterior circulation cases, the VAs and their intracranial branches should be emphasized. In cases of suspected arterial dissection, CTA, or MRA with fat-suppressed imaging (“fat sats”), to evaluate the cervical carotid and vertebral arteries should be obtained. The blood should be checked for abnormalities of erythrocytes, leukocytes, and coagulation by ordering a complete blood count, platelet count, and prothrombin time reported as an international normalized ratio. Intensive investigation for coagulopathy may be required for some patients.
FIGURE 14-5. Bright signal is seen on an MRI with diffusion-weighted imaging (DWI), indicating a recent infarction.
KEY POINTS
●The course of symptom development and results of brain imaging should allow separation of ischemia from hemorrhage, and in case of ischemia, identification of the most likely stroke mechanism: thrombosis, embolism, or systemic hypoperfusion.
●Cardiac, brain, and vascular imaging should help to identify stroke etiology.
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