Stroke is the leading cause of serious, long-term disability. Of those who survive a stroke, 50% to 70% are functionally independent, and 15% to 30% live with permanent disability. Twenty-six percent require long-term care after 3 months.³ Common long-term disabilities include hemiparesis, inability to walk, complete or partial dependence for activities of daily living (ADLs), aphasia, and depression. In addition to the physical, cognitive, and emotional impact of the stroke on the stroke survivor, the stroke affects the lives of the stroke victim’s caregiver and family.⁴ A stroke is a lifelong change for both the stroke survivor and the family.

Pathophysiology of Stroke

Anatomy of Cerebral Circulation

Blood is supplied to the brain by two major pairs of arteries: the internal carotid arteries (anterior circulation) and the vertebral arteries (posterior circulation). The carotid arteries branch to supply most of the frontal, parietal, and temporal lobes; the basal ganglia; and part of the diencephalon (thalamus and hypothalamus). The major branches of the carotid arteries are the middle cerebral and anterior cerebral arteries. The vertebral arteries join to form the basilar artery, which branches to supply the middle and lower parts of the temporal lobes, occipital lobes, cerebellum, brainstem, and part of the diencephalon. The main branch of the basilar artery is the posterior cerebral artery. The anterior and posterior cerebral circulation is connected at the circle of Willis by the anterior and posterior communicating arteries (Fig. 58-1). (Fig. 56-9 illustrates the arteries at the base of the brain.) Genetic variations in this area are common, and all connecting vessels may not be present.

FIG. 58-1 Cerebral arteries and the circle of Willis. The top of the temporal lobe has been removed to show the course of the middle cerebral artery.

Regulation of Cerebral Blood Flow

The brain requires a continuous supply of blood to provide the oxygen and glucose that neurons need to function. Blood flow must be maintained at 750 to 1000 mL/min (55 mL/100 g of brain tissue), or 20% of the cardiac output, for optimal brain functioning. If blood flow to the brain is totally interrupted (e.g., cardiac arrest), neurologic metabolism is altered in 30 seconds, metabolism stops in 2 minutes, and cellular death occurs in 5 minutes.

The brain is normally well protected from changes in mean systemic arterial blood pressure (BP) over a range from 50 to 150 mm Hg by a mechanism known as cerebral autoregulation. This involves changes in the diameter of cerebral blood vessels in response to changes in pressure so that the blood flow to the brain stays constant. When cerebral ischemia occurs, cerebral autoregulation may be impaired, and it is often dependent on changes in BP. Carbon dioxide is a potent cerebral vasodilator, and changes in arterial carbon dioxide levels have a dramatic effect on cerebral blood flow (increased carbon dioxide levels increase cerebral blood flow, and decreased carbon dioxide levels decrease cerebral blood flow). Very low arterial oxygen levels (partial pressure of arterial oxygen less than 50 mm Hg) or increases in hydrogen ion concentration also increase cerebral blood flow.

Factors that affect blood flow to the brain include systemic BP, cardiac output, and blood viscosity. During normal activity, oxygen requirements vary considerably, but changes in cardiac output, vasomotor tone, and distribution of blood flow normally maintain adequate blood flow to the head. Cardiac output has to be reduced by one third before cerebral blood flow is reduced. Changes in blood viscosity affect cerebral blood flow, with decreased viscosity increasing flow.

Collateral circulation may develop over time to compensate for a decrease in cerebral blood flow. An area of the brain can potentially receive blood supply from another blood vessel even if blood supply from the original vessel has been cut off (e.g., because of thrombosis). In other words, the vessels in the brain make an “alternate route” for blood flow to reach damaged areas. Individual differences in collateral circulation partly determine the degree of brain damage and functional loss when a stroke occurs. For example, the bloodstreams of the internal carotid system and the basilar system meet in the posterior communicating arteries. In normal situations the pressure of the arteries is equal and blood will not mix. However, if one of the vessels is blocked, blood will flow from the intact artery to the damaged one, preventing a CVA.

Intracranial pressure (ICP) also influences cerebral blood flow. Increased ICP causes brain compression and reduced cerebral blood flow. One of your major goals when caring for a stroke patient is to reduce secondary injury related to increased ICP (see Chapter 57).

Risk Factors for Stroke

The most effective way to decrease the burden of stroke is prevention and teaching, especially about risk factors. Risk factors can be divided into nonmodifiable and modifiable. Stroke risk increases with multiple risk factors.

Nonmodifiable Risk Factors

Nonmodifiable risk factors include age, gender, ethnicity or race, and family history or heredity. Stroke risk increases with age, doubling each decade after 55 years of age. Two thirds of all strokes occur in individuals older than 65 years, but stroke can occur at any age. Strokes are more common in men, but more women die from stroke than men. Because women tend to live longer than men, they have more opportunity to suffer a stroke.¹

Gender Differences

Stroke

Men	Women
• Stroke is more common in men than in women. • In most age-groups, more men than women will have a stroke in a given year. • Men are more likely to have a thrombotic stroke. • Men are more likely to have an embolic stroke. • Men have a better chance of surviving a stroke than women do.	• At all ages, more women than men die from strokes. • Women are more likely to have a hemorrhagic stroke. • Women with atrial fibrillation have an increased risk for stroke. • Oral contraceptive use and pregnancy contribute to stroke risk. • tPA is used less frequently to treat women who have strokes.

tPA, Recombinant tissue plasminogen activator.

African Americans have a higher incidence of stroke and a higher death rate from stroke than whites. This may be related in part to a higher incidence of hypertension, obesity, and diabetes mellitus in African Americans.

Cultural & Ethnic Health Disparities

Stroke

African Americans

• Have a higher incidence of strokes than whites.

• The rate of first strokes is almost twice that of whites.

• Are three times more likely than whites to have an ischemic stroke and four times more likely to have a hemorrhagic stroke.

• High incidence of strokes may be related to their increased rates of hypertension, diabetes mellitus, and sickle cell anemia.

• Have a higher incidence of smoking and obesity than whites, which are two risk factors for stroke.

• Are twice as likely to die from a stroke as whites.

Other Ethnicities

• Hispanics, Native Americans, and Asian Americans have a higher incidence of strokes than whites.

• Diabetes (an important risk factor for strokes) is common among Hispanics.

• Native Americans are more likely than whites to have at least two risk factors for stroke.

Genetic risk factors are important in the development of all vascular diseases, including stroke. A person with a family history of stroke has an increased risk of having a stroke. Genes encoding products involved in lipid metabolism, thrombosis, and inflammation are believed to be potential genetic factors for stroke.

Modifiable Risk Factors

Modifiable risk factors are those that can potentially be altered through lifestyle changes and medical treatment, thus reducing the risk of stroke. Modifiable risk factors include hypertension, heart disease, diabetes mellitus, smoking, excessive alcohol consumption, obesity, sleep apnea, metabolic syndrome, lack of physical exercise, poor diet, and drug abuse.

Hypertension is the single most important modifiable risk factor, but it is still often undetected and inadequately treated. Increases in systolic and diastolic BP independently increase the risk of stroke. Stroke risk can be reduced by up to 50% with appropriate treatment of hypertension.1–3

Heart disease, including atrial fibrillation, myocardial infarction, cardiomyopathy, cardiac valve abnormalities, and cardiac congenital defects, is also a risk factor for stroke. Atrial fibrillation is responsible for about 20% of all strokes.¹ The incidence of atrial fibrillation increases with age.

Diabetes mellitus is a significant risk factor for stroke. The risk for stroke in people with diabetes mellitus is five times higher than in the general population.¹

Increased serum cholesterol and smoking are risk factors for stroke. Smoking nearly doubles the risk of stroke. The risk associated with smoking decreases substantially over time after the smoker quits. After 5 to 10 years of no tobacco use, former smokers have the same risk of stroke as nonsmokers.⁵

The effect of alcohol on stroke risk appears to depend on the amount consumed. Women who drink more than one alcoholic drink per day and men who drink more than two alcoholic drinks per day are at higher risk for hypertension, which increases their chance of stroke. Illicit drug use, especially cocaine use, has been associated with stroke risk.¹

Abdominal obesity increases ischemic stroke risk in all ethnic groups. In addition, obesity is also associated with hypertension, high blood glucose, and elevated blood lipid levels, all of which increase the risk of stroke.¹ An association of physical inactivity and increased stroke risk is present in both men and women, regardless of ethnicity. Benefits of physical activity can occur with even light to moderate regular activity and may be related to the beneficial impact of exercise on other risk factors. Nutrition teaching is important for the individual at risk for stroke, since a diet high in fat and low in fruits and vegetables may increase stroke risk.

The early forms of birth control pills that contained high levels of progestin and estrogen increased a woman’s chance of experiencing a stroke, especially if the woman also smoked heavily. Newer, low-dose oral contraceptives have lower risks for stroke except in those individuals who are hypertensive and smoke.

Other conditions that may increase the risk for strokes include migraine headaches, inflammatory conditions, and hyperhomocysteinemia. Sickle cell disease is another known risk factor for stroke.

Transient Ischemic Attack

Another risk factor associated with stroke is a past history of a transient ischemic attack (TIA). A TIA is a transient episode of neurologic dysfunction caused by focal brain, spinal cord, or retinal ischemia, but without acute infarction of the brain. Clinical symptoms typically last less than 1 hour. In the past, TIAs were operationally defined as any focal cerebral ischemic event with symptoms lasting less than 24 hours. However, it is important to teach the patient to seek treatment for any stroke symptoms, since there is no way to predict if a TIA will resolve or if it is in fact the development of a stroke.⁶ In general, one third of individuals who experience a TIA do not experience another event, one third have additional TIAs, and one third progress to stroke.⁷

TIAs may be due to microemboli that temporarily block the blood flow. TIAs are a warning sign of progressive cerebrovascular disease. The signs and symptoms of a TIA depend on the blood vessel that is involved and the area of the brain that is ischemic. If the carotid system is involved, patients may have a temporary loss of vision in one eye (amaurosis fugax), transient hemiparesis, numbness or loss of sensation, or a sudden inability to speak. Signs of a TIA involving the vertebrobasilar system may include tinnitus, vertigo, darkened or blurred vision, diplopia, ptosis, dysarthria, dysphagia, ataxia, and unilateral or bilateral numbness or weakness.

TIAs should be treated as medical emergencies. Teach people at risk for TIA to seek medical attention immediately with any stroke-like symptom and to identify the time of symptom onset.⁸

Types of Stroke

Unlike a TIA, where ischemia occurs without infarction, a stroke results in infarction and cell death. Strokes are classified as ischemic or hemorrhagic based on the cause and underlying pathophysiologic findings (Fig. 58-2 and Table 58-2).

TABLE 58-2

TYPES OF STROKE

Gender and Age	Warning and Onset	Prognosis
Ischemic
*Thrombotic*
Men more than women Oldest median age	Warning: TIA (30%-50% of cases) Onset: Often during or after sleep	Stepwise progression, signs and symptoms develop slowly, usually some improvement, recurrence in 20%-25% of survivors.
*Embolic*
Men more than women	Warning: TIA (uncommon) Onset: Lack of relationship to activity, sudden onset	Single event, signs and symptoms develop quickly, usually some improvement, recurrence common without aggressive treatment of underlying disease.
Hemorrhagic
*Intracerebral*
Slightly higher in women	Warning: Headache (25% of cases) Onset: Activity (often)	Progression over 24 hr. Poor prognosis, fatality more likely with presence of coma.
*Subarachnoid*
Slightly higher in women Youngest median age	Warning: Headache (common) Onset: Activity (often), sudden onset, most commonly related to head trauma	Usually single sudden event, fatality more likely with presence of coma.

TIA, Transient ischemic attack.

Ischemic Stroke

An ischemic stroke results from inadequate blood flow to the brain from partial or complete occlusion of an artery. Nearly 80% of strokes are ischemic.¹ A TIA attack is usually a precursor to ischemic stroke. Ischemic strokes are further divided into thrombotic and embolic strokes.

Thrombotic Stroke.

A thrombotic stroke occurs from injury to a blood vessel wall and formation of a blood clot (see Fig. 58-2, A). The lumen of the blood vessel becomes narrowed and, if it becomes occluded, infarction occurs. Thrombosis develops readily where atherosclerotic plaques have already narrowed blood vessels. Thrombotic stroke, which is the result of thrombosis or narrowing of the blood vessel, is the most common cause of stroke, accounting for about 60% of strokes.¹ Two thirds of thrombotic strokes are associated with hypertension or diabetes mellitus, both of which accelerate atherosclerosis. In 30% to 50% of individuals, thrombotic strokes are preceded by a TIA.

The extent of the stroke depends on rapidity of onset, the size of the damaged area, and the presence of collateral circulation. Most patients with ischemic stroke do not have a decreased level of consciousness in the first 24 hours, unless it is due to a brainstem stroke or other conditions such as seizures, increased ICP, or hemorrhage. Ischemic stroke symptoms may progress in the first 72 hours as infarction and cerebral edema increase.

Embolic Stroke.

Embolic stroke occurs when an embolus lodges in and occludes a cerebral artery, resulting in infarction and edema of the area supplied by the involved vessel (see Fig. 58-2, B). Embolism is the second most common cause of stroke, accounting for about 24% of strokes.¹ Most emboli originate in the endocardial (inside) layer of the heart, with plaque breaking off from the endocardium and entering the circulation. The embolus travels upward to the cerebral circulation and lodges where a vessel narrows or bifurcates (splits). Heart conditions associated with emboli include atrial fibrillation, myocardial infarction, infective endocarditis, rheumatic heart disease, valvular prostheses, and atrial septal defects. Less common causes of emboli include air and fat from long bone (e.g., femur) fractures.

The patient with an embolic stroke commonly has severe clinical symptoms that occur suddenly. Embolic strokes can affect any age-group. Rheumatic heart disease is one cause of embolic stroke in young to middle-aged adults. An embolus arising from an atherosclerotic plaque is more common in older adults.

Warning signs are less common with embolic than with thrombotic stroke. The embolic stroke often occurs rapidly, giving little time to accommodate by developing collateral circulation. The patient usually remains conscious, although he or she may have a headache. Prognosis is related to the amount of brain tissue deprived of its blood supply. The effects of the emboli are initially characterized by severe neurologic deficits, which can be temporary if the clot breaks up and allows blood to flow. Smaller emboli then continue to obstruct smaller vessels, which in turn involve smaller portions of the brain with fewer deficits noted. Recurrence of embolic stroke is common unless the underlying cause is aggressively treated.

Hemorrhagic Stroke

Hemorrhagic strokes account for approximately 15% of all strokes and result from bleeding into the brain tissue itself (intracerebral or intraparenchymal hemorrhage) or into the subarachnoid space or ventricles (subarachnoid hemorrhage or intraventricular hemorrhage).¹

Intracerebral Hemorrhage.

Intracerebral hemorrhage is bleeding within the brain caused by a rupture of a vessel and accounts for about 10% of all strokes (see Fig. 58-2, C). The prognosis of patients with intracerebral hemorrhage is poor, with the 30-day mortality rate at 40% to 80%. Fifty percent of the deaths occur within the first 48 hours.¹

Hypertension is the most common cause of intracerebral hemorrhage (Fig. 58-3). Other causes include vascular malformations, coagulation disorders, anticoagulant and thrombolytic drugs, trauma, brain tumors, and ruptured aneurysms. Hemorrhage commonly occurs during periods of activity. Most often there is a sudden onset of symptoms, with progression over minutes to hours because of ongoing bleeding.

FIG. 58-3 Massive hypertensive hemorrhage rupturing into a lateral ventricle of the brain.

Manifestations include neurologic deficits, headache, nausea, vomiting, decreased level of consciousness (in about 50% of patients), and hypertension. The extent of the symptoms varies depending on the amount, location, and duration of the bleeding. A blood clot within the closed skull can result in a mass that causes pressure on brain tissue, displaces brain tissue, and decreases cerebral blood flow, leading to ischemia and infarction.

Approximately half of intracerebral hemorrhages occur in the putamen and internal capsule, central white matter, thalamus, cerebellar hemispheres, and pons. Initially, patients experience a severe headache with nausea and vomiting. Clinical manifestations of putaminal and internal capsule bleeding include weakness of one side (including the face, arm, and leg), slurred speech, and deviation of the eyes. Progression of symptoms related to a severe hemorrhage includes hemiplegia, fixed and dilated pupils, abnormal body posturing, and coma. Thalamic hemorrhage results in hemiplegia with more sensory than motor loss. Bleeding into the subthalamic areas of the brain leads to problems with vision and eye movement. Cerebellar hemorrhages are characterized by severe headache, vomiting, loss of ability to walk, dysphagia, dysarthria, and eye movement disturbances.

Hemorrhage in the pons is the most serious because basic life functions (e.g., respiration) are rapidly affected. Hemorrhage in the pons can be characterized by hemiplegia leading to complete paralysis, coma, abnormal body posturing, fixed pupils (small in size), hyperthermia, and death.

Subarachnoid Hemorrhage.

Subarachnoid hemorrhage (SAH) occurs when there is intracranial bleeding into the cerebrospinal fluid–filled space between the arachnoid and pia mater membranes on the surface of the brain.⁹ SAH is commonly caused by rupture of a cerebral aneurysm (congenital or acquired weakness and ballooning of vessels). Aneurysms may be saccular or berry aneurysms, ranging from a few millimeters to 20 to 30 mm in size, or fusiform atherosclerotic aneurysms. The majority of aneurysms are in the circle of Willis. Other causes of SAH include trauma and illicit drug (cocaine) abuse. About 40% of people who have a hemorrhagic stroke due to a ruptured aneurysm die during the first episode. Fifteen percent die from subsequent bleeding.⁹ The incidence increases with age and is higher in women than men.

The patient may have warning symptoms if the ballooning artery applies pressure to brain tissue, or minor warning symptoms may result from leaking of an aneurysm before major rupture. In general, cerebral aneurysms are viewed as a “silent killer,” since individuals do not have warning signs of an aneurysm until rupture has occurred.

Safety Alert

• Sudden onset of a severe headache that is different from a previous headache and typically the “worst headache of one’s life” is a characteristic symptom of a ruptured aneurysm.

Loss of consciousness may or may not occur. The patient’s level of consciousness may range from alert to comatose, depending on the severity of the bleed. Other manifestations include focal neurologic deficits (including cranial nerve deficits), nausea, vomiting, seizures, and stiff neck. Despite improvements in surgical techniques and management, many patients with SAH die. Survivors may be left with significant morbidity, including cognitive difficulties.

Complications of aneurysmal SAH include rebleeding before surgery or other therapy is initiated and cerebral vasospasm (narrowing of the blood vessels), which can result in cerebral infarction. Cerebral vasospasm is most likely due to an interaction between the metabolites of blood and the vascular smooth muscle. During the lysis of subarachnoid blood clots, metabolites are released. These metabolites can cause endothelial damage and vasoconstriction. In addition, release of endothelin (a potent vasoconstrictor) may play a major role in the induction of cerebral vasospasm after SAH. Patients with SAH who are at risk for vasospasm are often kept in the intensive care unit for 14 days until the threat of vasospasm is reduced. Peak time for vasospasm occurs 6 to 10 days after the initial bleed.

Clinical Manifestations of Stroke

The neurologic manifestations do not significantly differ between ischemic and hemorrhagic stroke. The reason for this is that destruction of neural tissue is the basis for neurologic dysfunction caused by both types of stroke. The clinical manifestations are related to the location of the stroke. Specific manifestations related to the type of stroke are discussed in the previous section. The general clinical manifestations of ischemic and hemorrhagic stroke are discussed together here.

A stroke can affect many body functions, including motor activity, bladder and bowel elimination, intellectual function, spatial-perceptual alterations, personality, affect, sensation, swallowing, and communication. The functions affected are directly related to the artery involved and area of the brain it supplies (Table 58-3). Manifestations related to right- and left-brain damage differ somewhat and are shown in Fig. 58-4.

TABLE 58-3

STROKE MANIFESTATIONS RELATED TO ARTERY INVOLVEMENT

Artery	Deficit
Anterior cerebral	Motor and/or sensory deficit (contralateral), sucking or rooting reflex, rigidity, gait problems, loss of proprioception and fine touch
Middle cerebral	Dominant side: Aphasia, motor and sensory deficit, hemianopsia Nondominant side: Neglect, motor and sensory deficit, hemianopsia
Posterior cerebral	Hemianopsia, visual hallucination, spontaneous pain, motor deficit
Vertebral	Cranial nerve deficits, diplopia, dizziness, nausea, vomiting, dysarthria, dysphagia, and/or coma

An additional assessment question that you need to ask is the time of the onset of symptoms. This is important for all types of stroke, especially ischemic strokes, since the time can affect treatment decisions.

Motor Function

Motor deficits are the most obvious effect of stroke. Motor deficits include impairment of (1) mobility, (2) respiratory function, (3) swallowing and speech, (4) gag reflex, and (5) self-care abilities. Symptoms are caused by the destruction of motor neurons in the pyramidal pathway (nerve fibers from the brain that pass through the spinal cord to the motor cells). The characteristic motor deficits include loss of skilled voluntary movement (akinesia), impairment of integration of movements, alterations in muscle tone, and alterations in reflexes. The initial hyporeflexia (depressed reflexes) progresses to hyperreflexia (hyperactive reflexes) for most patients.

Motor deficits after a stroke follow certain specific patterns. Because the pyramidal pathway crosses at the level of the medulla, a lesion on one side of the brain affects motor function on the opposite side of the body (contralateral). The arms and legs of the affected side may be weakened or paralyzed to different degrees depending on which part of and to what extent the cerebral circulation was compromised. A stroke affecting the middle cerebral artery leads to a greater weakness in the upper extremity than the lower extremity. The affected shoulder tends to rotate internally, and the hip rotates externally. The affected foot is plantar flexed and inverted. An initial period of flaccidity may last from days to several weeks and is related to nerve damage. Spasticity of the muscles, which follows the flaccid stage, is related to interruption of upper motor neuron influence.

Communication

The left hemisphere is dominant for language skills in right-handed persons and in most left-handed persons.¹⁰ Language disorders involve expression and comprehension of written and spoken words. The patient may experience aphasia, which may be receptive aphasia (loss of comprehension), expressive aphasia (inability to produce language), or global aphasia (total inability to communicate). Aphasia occurs when a stroke damages the dominant hemisphere of the brain.

Dysphasia refers to impaired ability to communicate. However, in most settings the terms aphasia and dysphasia are used interchangeably, with aphasia often being the more common term used. (Dysphasia should not be confused with the similarly pronounced dysphagia, which is difficulty swallowing.)

Patterns of aphasia may differ, since the stroke affects different portions of the brain. Aphasia may be classified as nonfluent (minimal speech activity with slow speech that requires obvious effort) or fluent (speech is present but contains little meaningful communication) (Table 58-4). Most types of aphasia are mixed, with impairment in both expression and understanding. A massive stroke may result in global aphasia. Many stroke patients also experience dysarthria, a disturbance in the muscular control of speech. Impairment may involve pronunciation, articulation, and phonation. Dysarthria does not affect the meaning of communication or the comprehension of language, but it does affect the mechanics of speech. Some patients experience a combination of aphasia and dysarthria.

TABLE 58-4

TYPES OF APHASIA

Type	Characteristics
Broca’s	• A type of nonfluent aphasia. • Damage to frontal lobe of brain. • Frequently speak in short phrases that make sense but are produced with great effort. • Often omit small words such as “is,” “and,” and “the.” • May say, “Walk dog,” meaning, “I will take the dog for a walk,” or “book book two table,” for “There are two books on the table.” • Typically understand speech of others fairly well. • Often aware of their difficulties and can become easily frustrated.
Wernicke’s	• A type of fluent aphasia. • Damage occurs in left temporal lobe, although it can result from damage to right lobe. • May speak in long sentences that have no meaning, add unnecessary words, and even create made-up words. • May say, “You know that smoodle pinkered and that I want to get him round and take care of him like you want before.” • Often difficult to follow what person is trying to say. • Usually have great difficulty understanding speech. • Often unaware of their mistakes.
Global	• A type of nonfluent aphasia. • Results from damage to extensive portions of language areas of brain. • Have severe communication difficulties. • May be extremely limited in ability to speak or comprehend language.
Other	• Results from damage to different language areas in brain. • Some people may have difficulty repeating words and sentences even though they can speak and they understand the meaning of the word or sentence. • Others may have difficulty naming objects even though they know what the object is and what its use is.

Diagnostic Studies for Stroke

When manifestations of a stroke occur, diagnostic studies are done to (1) confirm that it is a stroke and not another brain lesion and (2) identify the likely cause of the stroke (Table 58-5). Tests also guide decisions about therapy.

TABLE 58-5

DIAGNOSTIC STUDIES
Stroke

Diagnosis of Stroke (Including Extent of Involvement)

• Computed tomography (CT) scan

• CT angiography (CTA)

• Magnetic resonance imaging (MRI)

• Magnetic resonance angiography (MRA)

• CT/MRI perfusion and diffusion imaging

Cerebral Blood Flow

• Cerebral angiography

• Carotid angiography

• Digital subtraction angiography

• Transcranial Doppler ultrasonography

• Carotid duplex scanning

Cardiac Assessment

• Electrocardiogram

• Chest x-ray

• Cardiac markers (troponin, creatine kinase-MB)

• Echocardiography (transthoracic, transesophageal)

Additional Studies

• Complete blood count, including platelets

• Coagulation studies: prothrombin time, activated partial thromboplastin time

• Electrolytes, blood glucose

• Renal and hepatic studies

• Lipid profile

• Cerebrospinal fluid analysis *

^*A lumbar puncture to obtain cerebrospinal fluid is avoided if increased intracranial pressure is suspected.

Important diagnostic tools for patients who have experienced a stroke are a noncontrast computed tomography (CT) scan or magnetic resonance imaging (MRI).¹² These tests can rapidly distinguish between ischemic and hemorrhagic stroke and help determine the size and location of the stroke. Serial CT scans may be used to assess the effectiveness of treatment and to evaluate recovery. Once the individual suspected of TIA or stroke arrives in the emergency department, it is important to rapidly assess and diagnose the patient (usually through a noncontrast head CT or MRI).¹² Rapid access to these diagnostic tools is important, since the results will determine treatment options for the patient.

CT angiography (CTA) provides visualization of cerebral blood vessels. It can be performed after or at the same time as the noncontrast CT scan. CTA can provide an estimate of perfusion and detect filling defects in the cerebral arteries. Magnetic resonance angiography (MRA) can detect vascular lesions and blockages, similar to CTA. CT/MRI perfusion and diffusion imaging may also be done.

Cardiac imaging is also recommended because many strokes are caused by blood clots from the heart. Angiography can identify cervical and cerebrovascular occlusion, atherosclerotic plaques, and malformation of vessels. Cerebral angiography is a definitive study to identify the source of SAH. Risks of angiography include dislodging an embolus, causing vasospasm, inducing further hemorrhage, and provoking an allergic reaction to contrast media.

Intraarterial digital subtraction angiography (DSA) reduces the dose of contrast material, uses smaller catheters, and shortens the length of the procedure compared with conventional angiography. DSA involves the injection of a contrast agent to visualize blood vessels in the neck and the large vessels of the circle of Willis. It is considered safer than cerebral angiography because less vascular manipulation is required.

Transcranial Doppler (TCD) ultrasonography is a noninvasive study that measures the velocity of blood flow in the major cerebral arteries. TCD is effective in detecting microemboli and vasospasm and is ideal for the patient suspected of having an SAH. Carotid duplex scanning is used not only to detect the cause of the stroke, but also to stratify patients for either medical management or carotid intervention if they have carotid stenoses.

A lumbar puncture may be done to look for evidence of red blood cells in the cerebrospinal fluid if an SAH is suspected but the CT does not show hemorrhage. A lumbar puncture is avoided if the patient is suspected of having an obstruction in the foramen magnum or other signs of increased ICP because of the danger of herniation of the brain downward, leading to pressure on cardiac and respiratory centers in the brainstem and potentially death.

If the suspected cause of the stroke includes emboli from the heart, diagnostic cardiac tests should be done. Blood tests are also done to help identify conditions contributing to stroke and to guide treatment (see Table 58-5).

The LICOX system may be used as a diagnostic tool to evaluate the progression of stroke. LICOX measures brain oxygenation and temperature (see discussion in Chapter 57 on p. 1365 and Fig. 57-10). Secondary brain injury adds significantly to mortality risk and poor functional outcome after a stroke.

Collaborative Care for Stroke

Preventive Therapy

Primary prevention is a priority for decreasing morbidity and mortality risk from stroke (Table 58-6). The goals of stroke prevention include health promotion for a healthy lifestyle and management of modifiable risk factors to prevent a stroke. Health promotion focuses on (1) healthy diet, (2) weight control, (3) regular exercise, (4) no smoking, (5) limitation on alcohol consumption, and (6) routine health assessments. Patients with known risk factors such as diabetes mellitus, hypertension, obesity, high serum lipids, or cardiac dysfunction require close management.

TABLE 58-6

COLLABORATIVE CARE
Stroke