Stroke.

Stroke is essentially a disease of the cerebral vasculature in which a failure to supply oxygen to brain cells, which are the most susceptible to ischemic damage, leads to their death. The syndromes that lead to stroke compose two broad categories: ischemic and hemorrhagic stroke. Ischemic strokes account for approximately 80% of strokes, whereas hemorrhagic strokes account for the remaining 20%.¹²⁸

Transient ischemic attack.

Symptoms of a transient ischemic attack (TIA) include the focal deficits of an ischemic stroke within a clearly vascular distribution, but TIAs are reversible defects because no cerebral infarction ensues. The causes of TIAs can be thrombotic and embolic and could result from a cerebral vasospasm. By definition, the effects of TIAs must resolve in less than 24 hours. Since 35% of patients who have had a TIA will have a stroke within five years, they should have a complete evaluation for cerebrovascular disease and sources of embolism.¹⁶⁷ The treatment of TIAs depends on the source of the emboli or thrombi and can include anticoagulation therapy and/or surgery.

Embolic stroke.

Cerebral embolic strokes are the most common subtype of ischemic stroke. Embolic strokes usually are characterized by an abrupt onset, although they also can be associated with stuttering symptoms. Usually no heralding events occur, such as TIAs or previous small strokes evolving into larger strokes.⁸³ A warning with microemboli that cause smaller events are uncommon, and the usual clue to a possible embolic source is a completed stroke.¹²⁸ The source of approximately 40% of embolic strokes is unknown, even after the common sources have been evaluated extensively. Most embolic strokes of known cause occur after emboli that are cardiac in origin.²⁷ The second most common sources of emboli are atherothrombotic lesions that result in artery-to-artery embolisms. These lesions can be in the aorta, the carotid and vertebrobasilar systems, and, less frequently, smaller arteries.

Sources of emboli

Pathophysiology.

Atherosclerotic plaque formation is greatest at the branching points of major vessels and forms in areas of turbulent flow. Chronic hypertension is a common precursor, and damage to the intimal wall may be followed by lymphocyte infiltration. Foam cells then develop, and the first stage of atherosclerosis is formed. Calcification and narrowing with resultant turbulent flow follow. In this setting of turbulent flow, plaque ulceration can become a site for thrombus formation. If the thrombus forms and is degraded rapidly, a transient ischemic phenomenon can occur, which is the setting of a TIA. Classically, the symptoms of internal carotid disease include amaurosis fugax and monocular blindness. If the clot does not break up or lyse, a cerebral infarction can occur. The size and severity of the infarction depends on available collateral circulation and the size of the occluded vessel. In patients with extensive atherosclerotic disease, however, a limited amount of collateral circulation is available, and the sparing from collateral circulation may be limited.

Atherothrombotic disease.

The most common site for the development of atherosclerosis and the subsequent development of atherothrombosis that leads to TIAs and stroke in the anterior circulation is the origin of the carotid artery and in the posterior circulation is the top of the basilar artery. Other sites of atherosclerosis include the carotid siphon and the stems (bases) of the middle cerebral artery, anterior cerebral artery, and origin of the basilar artery.⁵¹ The atheromatous plaques are sources of emboli that can cause distal symptoms in a TIA or stroke. These embolic events are similar events from other embolic sources. Table 1-2 lists common stroke syndromes, and Figs. 1-1 to 1-3 explain the anatomy of these strokes. Atherosclerotic disease is screened most readily by carotid Doppler ultrasonography and transcranial Doppler imaging. Magnetic resonance angiography (MRA) and carotid and cerebral angiography can further elucidate lesions, which can be treated surgically or medically.

Table 1-2 Common Stroke Syndromes

Figure 1-1 Circle of Willis and cerebral circulation.

Figure 1-2 Medial view of brain with anterior and posterior cerebral artery circulation and areas of cortical function.

Figure 1-3 Lateral view of brain with middle cerebral artery and its branches and areas of cortical function.

Lacunar syndrome.

A lacunar stroke occurs in one of the perforating branches of the circle of Willis, the middle cerebral artery stem, or the vertebral or basilar arteries. The occlusion of these vessels results from the atherothrombotic or lipohyalinotic blockage of one of these arteries. The development of disease in these arteries correlates closely with the presence of chronic hypertension and diabetic microvascular disease.^107,128 These are small vessels, 100 to 300 μm in diameter, that branch off the main artery and penetrate into the deep gray or white matter of the cerebrum.¹⁰⁷ The resulting infarcts are from 2 mm to 3 cm in size and account for roughly 20% of all strokes. These types of strokes usually evolve over a few hours and sometimes can be heralded by transient symptoms in lacunar TIAs. Lacunar strokes can cause recognizable syndromes (Table 1-3). The basic lacunar syndromes are (1) pure motor hemiparesis from an infarct in the posterior limb of the interior capsule or pons, (2) pure sensory stroke from an infarct in the ventrolateral thalamus, (3) ataxic hemiparesis from an infarct in the base of the pons or the genu of the internal capsule, and (4) pure motor hemiparesis with motor apraxia resulting from an infarct in the genu of the anterior limb of the internal capsule and the adjacent white matter in the corona radiata. Recovery from a lacunar stroke often can be dramatic, and in some individuals, near complete or complete resolution of deficits can occur in several weeks or months. In patients who have had multiple lacunar infarcts, a syndrome characterized by emotional instability, slow abulia (impairment in or loss of volition), and bilateral pyramidal signs known as pseudobulbar palsy will develop. This diagnosis is based on the symptoms and the use of computerized tomography (CT) or magnetic resonance imaging (MRI). MRI is especially useful in this situation for detecting small lesions in the deep brain structures or brainstem; the ability of CT to see lesions clearly in these areas is limited.²⁹

Table 1-3 Lacunar Stroke Syndromes and Their Anatomical Sites

Hemorrhagic conversion.

As a sequela of an embolic or ischemic infarction, a purely ischemic infarct may convert into a hemorrhagic lesion. Thrombi can migrate, lyse, and reperfuse into an ischemic area, leading to small hemorrhages (petechial hemorrhages) because the damaged capillaries and small blood vessels no longer maintain their integrity. These damaged areas then can coalesce (combine) and form a hemorrhage into ischemia.⁸³ These conversions are more common in large infarcts, such as an occluded middle cerebral artery, or in a large infarction in the distribution of a lenticulostriate artery. In patients who have large infarcts with possibility of hemorrhage, anticoagulation therapy is not used because of the risk of hemorrhagic conversion. These types of hemorrhages have characteristics in common with hemorrhagic strokes.

Hypertensive bleed.

Hypertensive cerebral hemorrhages usually occur in four sites: the putamen and internal capsule, the pons, the thalamus, and the cerebellum. Usually these hemorrhages develop from small penetrating arteries in the deep brain that have had damage from hypertension. The pathological features of hypertension include lipohyalinosis (fat infiltration of pathologically degenerated tissue) and Charcot-Bouchard aneurysms.⁵⁰ The usual hypertensive ICH develops over the span of a few minutes but occasionally can take as long as 60 minutes. Unlike ischemic infarcts, hemorrhagic bleeds do not follow the anatomical distribution of blood vessels but dissect through tissue planes spherically. This commonly leads to severe damage and complications, such as hydrocephalus and mass shift (movement of brain tissues to one side to accommodate the volume of the hemorrhage).^83,128 Within 48 hours of the hemorrhage, macrophages begin to phagocytize the hemorrhage at its outer margins. Patients with a cerebral hemorrhage often experience a rapid recovery within the first two to three months after the hemorrhage. ICHs usually occur while patients are awake and often while they are under emotional stress. Vomiting and headache are associated commonly with ICH and are unique features that differentiate ICHs from ischemic strokes. Table 1-4 outlines the four major hypertensive ICH syndromes.

Table 1-4 The Four Major Hypertension Intracerebral Hemorrhage Syndromes

Lobar intracerebral bleed.

Lobar hemorrhages are ICHs that occur outside the basal ganglia and thalamus in the white matter of the cerebral cortex. These types of hemorrhages and hypertension are not correlated clearly; the most common underlying condition in patients with this type of ICH is the presence of AVMs.⁸³ Other associated conditions include bleeding diatheses, tumors (e.g., melanoma or glioma), aneurysms in the circle of Willis, and a large number of idiopathic cases.⁴⁹ Patients with lobar ICH initially have acute onset of symptoms, and most lobar ICHs are small enough to cause discrete clinical syndromes that may resemble focal ischemic events. Because lobar bleeds occur far from the thalamus and the brainstem, coma and stupor are much less common than they are in patients with hypertensive ICHs. Headaches are also common and can help differentiate lobar bleeds from ischemic strokes, which they can resemble so closely.¹²⁶ Detection of a hemorrhage on a CT scan or MRI is the best way to distinguish these two entities.

Saccular aneurysm and subarachnoid bleed.

A saccular aneurysm rupture is the most common cause of a subarachnoid hemorrhage (SAH).¹⁵⁰ Saccular aneurysms occur at the bifurcation (branching) points of the large arteries in the brain and are most commonly found in the anterior portion of the circle of Willis.⁸³ An estimated 0.5% to 1% of normal individuals harbor saccular aneurysms.¹⁵⁸ Despite the high number, bleeding from them is rare (6 to 16 per 100,000). Unlike other stroke syndromes, however, the incidence of SAH has not declined since 1970.¹⁰² The rupture risk correlates best with the size of the aneurysm. Aneurysms smaller than 3 mm have little chance of hemorrhage, whereas aneurysms 10 mm or larger have the greatest chance of rupture.⁹⁵ SAH usually is characterized by acute, abrupt onset of a severe headache of atypical quality.¹⁰² These headaches are often the most severe that patients have ever experienced. A brief loss of consciousness, nausea and vomiting, focal neurological deficits, and a stiff neck at the onset of symptoms also may occur. The diagnosis is based on clinical suspicion, subarachnoid blood found on the CT scan, or blood found in the cerebrospinal fluid from a spinal tap. One determines the definitive location of the aneurysm by cerebral angiography.

The development of further delayed neurological deficits results from three major events: rerupture, hydrocephalus, and cerebral vasospasm. Rerupture occurs in 20% to 30% of cases within one month if treatment is not aggressive, and rebleeding has an associated mortality rate of up to 70%.¹⁰² Hydrocephalus occurs in up to 20% of cases, and aggressive management often is required. Chronic hydrocephalus is also common and often requires permanent cerebrospinal fluid drainage (shunting). Vasospasm also is a common problem after SAHs, occurring in approximately 30% of cases.¹⁰² The normal time course for vasospasm is an onset in three to five days, peak narrowing in five to 14 days, and resolution in two to four weeks. In half of cases, the vasospasm is severe enough to cause a cerebral infarction with resulting stroke or death. Even with modern management, 15% to 20% of patients who develop vasospasms still suffer strokes or die.⁹⁶ A permanent ischemic deficit develops in approximately 50% of patients with symptomatic vasospasms after SAHs.⁶⁹ Vasospasm therefore must be treated rapidly and as aggressively as possible to prevent permanent ischemic damage.

Arteriovenous malformation.

AVMs are found throughout the body and can occur in any part of the brain. They are usually congenital and consist of an abnormal tangle of blood vessels between the arterial and venous systems. They range from a few millimeters in size to large masses that can increase cardiac output because of the amount of their blood flow. The larger AVMs in the brain tend to be found in the posterior portions of the cerebral hemispheres.⁵⁰ AVMs occur more frequently in men, and if found in one family member, they have a tendency to be found in other members. AVMs are present from birth, but bleeding most often occurs in the second and third decades of life. Headaches and seizures are common symptoms, as is hemiplegia. Half of AVMs initially occur as ICHs. Although rebleeding in the first month is rare, rebleeding is common in larger lesions as more time passes. Contrast CT, MRA, and MRI are useful noninvasive tests, whereas cerebral angiography is the best test for delineating the nature of the lesion. The management of these lesions is accomplished best by a team approach, a combination of surgical treatment and interventional angiography for definitive management. Treatment of hydrocephalus and increased intracranial pressure is the same as treatment for SAH and ICH.

Posttraumatic hemorrhagic stroke.

A traumatic brain injury commonly results in hemorrhagic damage to the brain in addition to ischemic and other injuries. The four major types of injury caused by traumatic brain injury include SAH and ICH, diffuse axonal injury, contusions, and anoxic injury from hypoperfusion (decreased flow in the vessels) and hypoxemia (decreased oxygen level). This combination of injuries leads to a constellation of findings that mixes the features of a number of individual ischemic and hemorrhagic injuries.

Arterial and medical disease.

Numerous medical conditions can result in arterial system diseases and lead to thrombosis and thromboembolism. Some conditions may cause disease in the cerebral vasculature (Table 1-5).

Table 1-5 Medical Conditions That Cause Arterial System Disease

* CNS, Central nervous system; TIA, transient ischemic attack.

Strokelike syndromes.

A number of conditions in addition to TIAs and cerebral infarctions can cause transient paralysis. These conditions generally resolve spontaneously with no long-term sequelae. The most common cause of transient hemiparesis is Todd paralysis, which develops postictally (after a seizure). Todd paralysis results from neurotransmitter depletion and neuronal fatigue in focal areas of the brain caused by the extremely high neuronal firing rate during a seizure.³⁷ Patients usually regain function within 24 hours. Another common cause of focal neurological deficits is migraine headaches. These headaches are actually thought to result from cerebral vasospasms, but an actual ischemic infarct rarely if ever occurs. The deficits resolve with the resolution of the migraine and are not permanent.

Cerebral neoplasm.

Obviously, cerebral neoplasms (whether primary or metastatic) can lead to focal neurological deficits that resemble a stroke. The treatment of the sequelae and the long-term management of the deficits are the same as they are in stroke patients. Treating the primary lesions is the focus of the acute care. Often the initial symptoms are seizures and ICHs.

Pharmacological therapies

The use of naloxone, a narcotic antagonist, is based on the in vitro observation that naloxone has neuroprotective effects. Unfortunately, the clinical trials to date have not demonstrated any benefit.³³ The therapeutic rationale of using calcium channel blockers is that they prevent injury to ischemic neurons by preventing calcium influx, which decreases metabolic activity in the neuron.⁹⁰ Initial hope was that the treatment results for SAH, in which nimodipine decreases secondary ischemia, would be similar for stroke. Unfortunately, the results of several studies have not shown any clear benefits from treatment with these agents,¹⁰⁸ and none of them currently are used routinely for stroke treatment.

In animal experiments, glutamate antagonists decrease the size of infarction area in stroke.⁹⁰ However, the few studies done in human beings have been inconclusive and have shown serious neuropsychiatric side effects.³³

Gangliosides may reduce ischemic damage by counteracting toxic amino acids in ischemic tissue. Despite the many studies that have been performed, no clearly demonstrated benefits have resulted from use of these agents.³³

The free-radical scavengers include 21-amino steroids (lazaroids), ascorbic acid (vitamin C), and tocopherol (vitamin E). They have not been well-evaluated, and some studies to establish their clinical use are being undertaken.⁹⁰ However, vitamin E has been demonstrated clinically to reduce the risk of heart disease, so secondarily its use may decrease the risk of stroke.

Cooling therapy.

An exciting new development in the treatment of acute stroke has been the initiation of cooling therapy on presentation with the induction of a medical coma to limit the extent of brain injury after stroke. In most patients who present with stroke, there is a natural tendency for the body temperature to be elevated between 4% and 25%, which is associated with increased injury and poorer outcomes.^18,35 Studies have shown that injury could be slowed with supercooling, and the technique has been used in surgery to help limit injury and to prolong safe surgical time in both neurosurgical and cardiothoracic procedures.^28,131,139 The pooled analysis of existing studies does not yet provide convincing evidence that death or long-term disability are significantly changed from the application of mechanical or pharmacological cooling, but the therapy is just starting to be used on a larger scale, and new research findings published in the next several years may show a benefit to routine cooling of acute stroke victims.

Surgical therapies

Prevention of rebleeding.

Before 1980, six weeks of bed rest were prescribed routinely for the care of patients with acute SAH to prevent rebleeding. In 1981 a study demonstrated that bed rest was inferior to surgical treatment, lowering of blood pressure, and carotid ligation.¹⁵⁸ Antihypertensive medications for the prevention of rebleeding are still controversial, and no consensus exists as to their use. Carotid ligation used to be popular, but more recent reevaluations of the benefits of the technique have not been as conclusive, and because of its surgical risks, direct repair of the aneurysm is a better choice. Antifibrinolytic agents have been studied and have been beneficial for low-risk patients in whom surgery must be delayed, but they seem to increase the risk of ischemic events. The placement of intraluminal coils, balloons, and polymers has shown some benefit in the short-term prevention of rebleeding, but the long-term efficacy is still unclear, and the techniques remain experimental.¹⁰² Because the risk of rebleeding is also very high in post-SAH seizures, even though the incidence of seizure is low, the recommendation is that patients receive antiseizure medications for prophylaxis.

Control of vasospasm.

The treatment of vasospasm is important for the reasons previously outlined. The current treatments include the use of orally administered nimodipine, a calcium channel blocker shown to improve outcomes of patients who have had an SAH with vasospasm. The results of using other calcium channel antagonists are unclear. The use of hypertension/hypervolemia/hemodilution has been recommended by some studies. Creating more volume than normal results in hypertension. The stretch caused by the volume stimulates the smooth muscle pressure receptors that line the vessels. These receptors inhibit muscle action by a protective response, and the blood vessel dilates to accommodate the increased volume. Hypertension/hypervolemia/hemodilution is most effective in preventing vasospasm after surgically clipping the aneurysm. Significant cardiac and hemodynamic risks are associated with this therapy, so intensive care unit (ICU) monitoring is required.¹⁰²

Hypertension.

Although the treatment of hypertension is an important primary preventive measure in the management of stroke, whether blood pressure reduction after stroke is beneficial has not been proved definitively. The transient rise in blood pressure after stroke usually settles without intervention.¹⁶⁴ Because of the uncertainty about whether overaggressive treatment of acute elevated blood pressure is harmful, definitive antihypertensive therapy probably should be delayed for two weeks.⁹⁰ At that time, one should follow the usual recommendations regarding adequate control of hypertension because some evidence indicates that it is beneficial. This seems especially appropriate in patients who have had a lacunar stroke because the development of multiple lacunae is related to uncontrolled blood pressure.

Antiplatelet medications.

In patients who have had a TIA or stroke, long-term use of aspirin has been shown to decrease the incidence of death, myocardial infarction, and recurrent events by up to 23%.⁷ The doses of aspirin in numerous studies have ranged from 30 mg to 600 mg; all doses resulted in a 14% to 18% reduction in recurrent cerebral events, but gastrointestinal complications increased with the higher doses.^1,48,153 In general, a standard dosage of one regular adult aspirin (325 mg a day) is the usual treatment for recurrent ischemic stroke. Studies are underway that compare the efficacy of warfarin versus aspirin in treating ischemic stroke; the results of these studies are not yet available. Ticlopidine is another antiplatelet medication effective in reducing the incidence of recurrent stroke.⁸¹ Ticlopidine is most efficacious in women, patients who are not helped by aspirin therapy, and patients with vertebrobasilar symptoms, hypertension, diabetes, and no severe carotid disease.⁶²

Anticoagulation.

The incidence of recurrent stroke and TIA in patients with atrial fibrillation is approximately 7% per year. For patients who have atrial fibrillation with cardiac sources of emboli, warfarin is the clear treatment of choice; this is true for primary and secondary prevention. Although aspirin has some preventive effects, it is not as efficacious. In the presence of structural cardiac disease or atrial fibrillation, aspirin should be used only to treat patients in whom warfarin anticoagulation is contraindicated.⁹⁰

The odds ratio for recurrence is approximately 0.36 in those treated with warfarin versus control and 0.84 for those treated with aspirin versus control.⁴⁵ However, problems exist with warfarin anticoagulation in the elderly. Cognitive and compliance difficulties can lead to an increase in complications. Unclear issues in anticoagulation use include when to start anticoagulants after stroke, the safety of anticoagulants in clinical practice, and the optimum anticoagulant blood level. Several studies are currently examining these questions.

Treatment of dysrhythmias or underlying disease.

Obviously, primary and secondary prevention should treat the underlying cause of the ischemic stroke. Prevention can include cardioversion to normal sinus rhythm and treatment with antidysrhythmic medications, and treatment of underlying medical conditions if they can be found. Unfortunately, only a small proportion of patients who have had TIAs and strokes can benefit from these specific treatments.

Carotid endarterectomy.

The surgical treatment of carotid artery stenosis has been shown to be beneficial in recent studies of stroke recurrence in patients with severely (greater than 70%) stenosed carotid arteries.^12,46 The data on the intermediate group of patients (stenosis from 30% to 70%) are being collected. For patients with high-grade stenosis, carotid endarterectomy reduces the range of stroke risk from 22% to 26% down to 8% to 12%.

Contractures.

Contractures are periarticular motion impairments that result from loss of elasticity in the periarticular tissues, which include muscles, tendons, and ligaments. Contractures can occur in any immobilized joint but are particularly prevalent in the paretic limbs after a stroke. In fact, only 10% of stroke patients recover limb strength and mobility rapidly enough to avoid developing contractures.⁶³ Shoulder pain, contractures, and muscle pain occur in 70% to 80% of patients who have had a hemiplegic stroke.¹²⁸ Chapter 10 addresses the management and related issues of the hemiplegic shoulder. Contractures also occur in other areas and begin to be problematic within a few days of onset or several days after the stroke when symptoms of immobility and spasticity may begin to develop. Usually contractures occur in a pattern of flexion, adduction, and internal rotation; muscles that span two joints are more susceptible to contracture formation.⁶⁶ To prevent shortening of the connective tissue in muscles and joints, an active range of motion (ROM) program must be initiated. Because certain muscles span two joints, joints must be positioned to allow full physiological stretch of the muscles involved. Once a contracture is present, the mainstay of treatment is gradual, prolonged stretch. The minimal treatment is a sustained stretch greater than 30 minutes.⁸⁴ Other treatments include splinting, deep-heating modalities,²³ and possible surgical release for long-standing, tight contractures⁶⁶ (see Chapter 13).

Osteoporosis.

Bone is a metabolically active tissue normally in a state of equilibrium between active bone resorption and deposition. The ratio of bone formation to bone resorption is influenced by the stressors to which the bone is subjected, a relationship known as Wolff law.²³ The lack of weight-bearing and normal stress on long bones on the hemiplegic side of a stroke patient leads to a predominance of bone resorption. This loss of bone mass can start as early as 30 hours after the beginning of immobility¹⁵⁵ and with bed rest can be as high as 25% to 45% in 30 to 36 weeks.³⁹ In patients who have had a stroke, osteoporosis is often worse, and the rate of hip fracture is far higher on the side of the hemiplegia.⁶⁷

Osteoporosis prevention is accomplished best with measures that include active weight-bearing exercise and active muscle contraction. Medical therapies for individuals at risk for osteoporosis should be initiated. Therapies include bone-forming agents, calcium and vitamin D supplementation, hormone replacement, and other measures as needed. Box 1-1 shows some of the medical treatments available for osteoporosis.

Heterotopical ossification.

Heterotopical ossification is the deposition of calcium in the form of mature bone in the soft tissues. The condition is not particularly common after stroke but occurs with increased incidence after traumatic brain injury. The incidence ranges from 11% to 76% in various studies.¹⁷ Spasticity is associated with the development of heterotopical ossification as are long-bone fractures and a prolonged coma. Symptoms of heterotopical ossification usually develop one to three months after injury with pain and limited ROM.²⁴ The diagnosis is based on clinical examination, elevated alkaline phosphatase levels in the serum, and a positive bone scan.

Treatment for heterotopical ossification includes active ROM; no studies indicate that the condition is caused or worsened by active ROM exercises.¹⁷ Pharmacological treatment options include the use of etidronate disodium and nonsteroidal antiinflammatory drugs.²⁴ Other treatments include radiation therapy and, for refractory cases after the lesion has matured, surgical excision of the heterotopical ossification. Performance of ROM exercises after surgery is particularly important. Low-dose radiation or etidronate disodium can also be used to prevent recurrence.³⁴

Falls.

Falls are of particular concern in survivors of stroke. These patients are at increased risk of hip fracture because of developed osteoporosis, and the acuity of their balance, visual perceptions, and spatial perceptions is decreased. The increased risk of falls has been documented in several studies and is greater in patients who have had a right hemispheric stroke.^36,106,118 Fall prevention should emphasize balance and cognitive training, removing environmental hazards, and using adaptive devices. (These measures are reviewed in Chapters 8, 14, 15, 19, 27, and 28.)

Seizures.

Seizures after strokes have been documented since the nineteenth century. The incidence of late-onset seizures (epilepsy) in the individuals who have had strokes ranges from 6% to 18%,^59,162 whereas the incidence of early seizures is approximately 10%, with reports ranging from 3% to 38%.^14,168 The risk for seizures is highest right after stroke; 57% of seizures occur in the first week, and 88% of all seizures after strokes occur in the first year.¹⁴ Seizures are more common in patients who have had an SAH; 85% of these seizures are early seizures.¹⁴⁸ The timing of seizures that occur after stroke varies according to the mechanism of injury. The timing of seizures after thrombotic and embolic strokes appears about equal. Patients with SAH have more seizures soon after the stroke, whereas patients with ICH are more similar to patients with ischemic stroke and may have more late-onset seizures.¹⁶⁸

The treatment and management of seizures associated with stroke are usually straightforward, and monotherapy often produces adequate results. If the patient only has acute-onset seizures in the setting of his or her stroke, the patient often does not require long-term antiseizure medication. A single, brief seizure or a nongeneralizing local seizure also can often be managed conservatively. If seizures do require treatment, a single agent usually suffices and is beneficial, because the drug interactions are fewer, and the compliance is better with monotherapy. Carbamazepine and phenytoin are the preferred agents for treating epilepsy after stroke. Management of the medication requires close follow-up to ensure that the desired outcome is achieved: an asymptomatic, seizure-free patient. Excessive medication can lead to a number of symptoms (Box 1-2). Inadequate control of the condition leads to additional seizures. For situations in which seizures become refractory to treatment, one must remember several factors.¹⁶⁸ Intercurrent illness or metabolic disarray that lowers the seizure threshold may make the seizures more frequent and difficult to treat. Patient compliance may be a problem, especially if the stroke created cognitive and behavioral deficits. Progressive lesions or new infarcts are also causes of increasing seizure frequency. Finally, a stroke that occurs in highly epileptogenic areas—such as the hippocampus, the parietooccipital cortex surrounding the rolandic fissure, and calcarine cortex—may engender refractory epilepsy and require combination therapy. Table 1-7 lists the common seizure medications and their side effects.

Table 1-7 Medical Management of Seizures: Drug Therapy

Hydrocephalus.

Hydrocephalus can occur acutely, especially in patients with SAH and ICH as discussed previously, or it can develop symptoms insidiously later. Hydrocephalus is usually heralded by the gradual onset of a triad of symptoms, including lethargy with decreased mental function, ataxia, and urinary incontinence. Once hydrocephalus is suspected, one should perform a CT scan promptly because the increasing size of the ventricles is readily visible. Once diagnosed, one should surgically place a ventricular shunt. The procedure is well-tolerated and can lead to resolution of all the symptoms of hydrocephalus if performed promptly. Patients with an occluded shunt have symptoms that mimic the initial symptoms of hydrocephalus.

Spasticity.

Spasticity is defined as a motor disorder characterized by a velocity-dependent increase in tonic stretch reflexes with exaggerated tendon jerks. Spasticity results from hyperexcitability of the stretch reflex (which is one component of the upper motor neuron syndrome).⁸⁹ In a normal recovery after a flaccid stroke, an initial period occurs with little resistance to passive motion of the muscles and joints. Approximately 48 hours after the stroke, tendon reflexes and muscle resistance to passive motion begin to return.⁶⁶ Spasticity is most pronounced in the flexor muscles and occurs throughout the hemiplegic side. The lower extremity later develops a component of extensor spasticity that can assist with function, whereas the upper extremity spasticity is usually in a flexor pattern.¹⁰

The management of spasticity includes encouraging voluntary movement, ROM exercises, and a functional rehabilitative approach.⁶⁶ The research data on the different neurorehabilitative treatment approaches do not define clearly which approach is most effective, so an individualized approach to treating each patient is the best course. Pharmacological treatments for spasticity are numerous, and they need to be tailored to each patient to find the best balance of side effects and efficacy. The most commonly used agents are baclofen, dantrolene sodium, and diazepam. These medications and a representative sample of the other medications used to treat patients who have had a stroke are presented in the table of medications and their side effects on the inside cover of the book. Other treatments for severe spasticity that are more invasive include phenol blocks and neurolysis, botulinum toxin (Botox) injections, and implantable baclofen pumps. Botox injections and baclofen pumps are still experimental approaches, and ongoing studies will elucidate their future roles (see Chapter 10).

Deconditioning.

Physiological deconditioning in patients after a stroke results from the acute medical illness and the associated bed rest and immobility that may result. Table 1-8 lists some of the effects of deconditioning. All of these factors can alter the ability of the patient to recover. Therefore, to get the patient out of bed and to increase activity as early and aggressively as possible is important.

Table 1-8 Deconditioning Effects of Stroke

Psychological complications.

Stroke is a major life event and is associated with significant alterations in the individual’s well-being and independence. Negative emotional reactions are common in patients following a stroke¹⁵² and can have a significant effect on the patient’s eventual outcome. After a stroke, patients may go through the four stages of bereavement described by Worden.¹⁷² These include accepting the loss, experiencing the pain of the loss, adjusting to a new environment in which previous abilities are missing, and investing in new activities. Not all patients become depressed, and this lack of depression does not necessarily mean the patient is in denial.¹⁷³ Denial is a normal defense mechanism, and as long as it does not interfere with the rehabilitative process, it is not a concern.¹⁵² The indifference reaction, a persistent denial reaction, is more common in patients who have had a right-sided stroke than a left-sided stroke.⁵³

Another common consequence of stroke is emotional lability, which is rapidly shifting from one extreme emotion to another. Approximately 20% of patients have emotional lability six months after a stroke, and up to 10% have lability for one year. Emotional lability is more common in patients with pseudobulbar palsy and right hemispheric strokes, particularly if the patient is depressed.⁷⁴

Anxiety is also common after stroke and is more frequent in patients with left hemispheric strokes⁹⁴ and cortical lesions.¹⁴⁴ Many sources of anxiety exist, including financial affairs, family issues, and a fear of dying or recurrent stroke. Reassurance and constant positive feedback during rehabilitation can help, and in severe cases, treatment with anxiolytics and psychological support may be needed.

Fortunately, outbursts and aggressive behavior are rare after a stroke, but when they occur, they are more common in patients with left-sided infarcts who are more aware of their deficits. The approach to management of these outbursts should not include restraints and threats but should be based on avoiding excessive frustration in the patient by removing emotional triggers and alternating easy and difficult tasks.¹⁵²

Depression is common after stroke, developing in 20% to 50% of stroke survivors, with 30% being the most commonly accepted figure.¹⁵² The depression can be a reaction to the stroke or a neuropsychological sequela of the stroke. The consequences of depression after stroke are numerous: hospital stays are longer,⁴² cognitive impairment is greater,¹²⁵ and motivation decreases.¹⁴⁰ Depression is more common in patients with left cortical lesions¹⁴⁵ and lesions close to the frontal poles and is shorter in patients with subcortical and brainstem lesions. Depression after stroke often is treated best with antidepressant medications.¹⁵² In patients who are unable to tolerate antidepressants, are unresponsive to therapy, or have active suicidal ideation, electroconvulsive therapy can be a last resort.¹¹⁰ (See Chapter 2 for more information about the psychological effects of stroke.)

Urinary tract dysfunction.

Urinary incontinence is common after stroke, affecting 51% to 60% of patients,²⁰ and can cause difficulties with rehabilitation, influence eventual discharge location, and place stress on caregivers.⁴³ One month and six months after stroke, 29% and 14% of patients, respectively, still have urinary incontinence.¹¹ The usual pathophysiology of incontinence is detrusor hyperreflexia, which is common in patients with cortical lesions. The incontinence assessment includes a thorough history of the urinary symptoms and can include urodynamic studies to help define the problem. Incontinence treatment includes timed voiding and use of pharmacological agents and intermittent catheterization. If these treatments do not work, incontinence may need to be treated by indwelling catheterization. This is performed on patients who cannot independently self-catheterize and do not have caretakers who can provide this care or on patients who have physical barriers such as urethral strictures that prevent regular catheterizations. Unfortunately, indwelling catheters have a high incidence of associated urinary tract infections. Male patients also may use external condom catheters, which can provide socially acceptable continence when the individual is traveling or physically active. Patients with continuous dribbling also benefit from condom catheters. The goal of all of these therapies is to maintain continence and prevent urinary tract infections and other complications such as skin breakdown from skin maceration.

Skin breakdown and decubitus ulcers.

Pressure ulcer formation is a serious health problem in debilitated and immobilized patients. After a stroke, patients are at particular risk for pressure ulcers because they have numerous factors contributing to skin breakdown. Abnormal sensation, contracture, malnutrition, immobility, and muscle and soft-tissue atrophy often develop and may be complicated by advanced age. Prevention of pressure ulcers, rather than treatment of developing ulcers, should be the focus of care. Preventive measures include frequent repositioning, keeping skin clean and dry, maintaining an adequate level of nutrition, and, especially in high-risk patients, using pressure-relief mattresses.¹³² Once pressure ulcers have formed, in addition to strictly observing the preventive and pressure relieving measures previously noted, treatments include meticulous wound care with a variety of agents and possibly surgical reconstruction.

Dysphagia.

Swallowing disorders are common after a stroke. Dysphagia is more common in the elderly, with an incidence of 25% to 45%.^59,61 Aspiration can lead to pneumonia, and a decreased eating ability can lead to dehydration and malnutrition. Chapter 24 covers the details of the pathology of aspiration and the methods of its treatment.

Aspiration.

Aspiration causes chemical pneumonitis that can lead to a secondary bacterial infection. Because numerous anaerobic organisms are in the mouth, aspiration pneumonia can develop into an anaerobic abscess.⁹² Such abscesses occur less frequently in edentulous individuals because they have less oral flora and can occur in up to a third of cases in hospitalized patients.⁹⁷ The treatment of choice is to reduce the risk of aspiration and to administer antibiotics. Examining a radiographic film for evidence of abscess cavities and the sputum for organisms can help one develop a specific medical treatment. Sputum culture growth often requires up to three or four days, so initial treatment is often empirical and should be the administration of a wide-spectrum antibiotic that is effective against hospital-acquired organisms (which are often resistant to certain antibiotics) and anaerobic bacteria.⁹² The usual course of antibiotics is seven to 10 days, but cavitary pneumonia may require far longer treatment for eradication of the organism.⁹³ Determination of which specific antibacterial agents to use depends on the resistance patterns in the institution in which the aspiration takes place; the infectious disease team at that institution should make the decision about which antibiotics to use.

Deep venous thrombosis.

DVT is a common problem after stroke and has an incidence of 23% to 75% depending on the severity of the stroke. Most of the morbidity and mortality associated with DVT results from venous thromboembolism (VTE). Pulmonary embolism after stroke has an incidence of 10% to 29% and a mortality rate of 10%.¹⁹ The formation of DVT is caused by the triad of risk factors outlined by Virchow postulates: altered blood flow, damage to the blood vessel wall, and altered blood coagulability. Box 1-3 lists the common risk factors for DVT. Of the risk factors for DVT, stasis is one of the most important. After a stroke, DVT is 10 times more common in the paretic leg.¹⁶⁵ DVT usually begins in the calf, and although the emboli from calf thrombi are not dangerous, these thrombi propagate in about 20% of cases, and about 50% of the proximal deep venous thrombi embolize. About 20% of symptomatic pulmonary emboli are fatal.¹³⁴ After a stroke, ambulation in itself is not preventive in the subacute setting: pulmonary embolism occurred in 57% of ambulatory patients in the rehabilitation setting.¹⁴⁷ Lower extremity and pelvic DVT are the most common, but proximal upper extremity DVT also can occur, although it is rare. All of the diagnostic and management issues discussed in the section on VTE that follows applies to this condition as well.

The diagnosis of DVT in the clinical setting is unreliable,¹⁹ and many patients with life-threatening embolism and thrombosis have no clinical symptoms of DVT. Other patients with swelling and tenderness may not have DVT at all and may have any of a number of other diagnoses. The differential diagnosis of lower extremity pain and swelling includes trauma, fracture, gout, cellulitis, and superficial phlebitis. The usual clinical signs of DVT include pain and tenderness, swelling, the presence of Homans sign (elicited by dorsiflexion of the ankle while the knee is flexed resulting in pain in the calf), superficial venous distention, a palpable cord, and fever. Some of these signs, such as Homans, are unreliable indicators. Homans sign is present in less than one third of patients with DVT and is present in half of patients without DVT.⁷³ Objective testing for DVT has venography as the gold standard, but this procedure is associated with significant risks, including anaphylaxis and causing DVT. More commonly used risk-free procedures are impedance plethysmography, which is a noninvasive test that measures volume changes in the leg with circumferential calf electrodes,⁷⁵ and Doppler ultrasound, which is also a noninvasive test that uses a handheld probe to detect blood flow in deep leg veins.¹⁶⁶ Doppler ultrasound and impedance plethysmography have similar sensitivities and specificities for DVT detection, but Doppler ultrasound is not as portable and has a higher cost than impedance plethysmography.¹⁹

The clinical diagnosis of pulmonary embolism is also unreliable, and only 30% of patients with pulmonary embolism have clinical DVT, even though 70% have venographic evidence of DVT.¹⁹ The symptoms of submassive pulmonary embolism overlap with the symptoms of many other pulmonary conditions, including tachypnea, tachycardia, rales, hemoptysis, pleuritic chest pain, pleural effusion, general malaise, bronchospasm, and fever. In patients with massive pulmonary embolism with greater than 60% of the pulmonary circulation obstructed, patients are critically ill and develop heart failure, circulatory collapse, hypotension, and coma and can die suddenly.¹⁴⁷ The gold standard for testing for pulmonary embolism is the pulmonary angiogram, but its use is associated with significant morbidity and mortality. The preferred noninvasive test is the ventilation/perfusion scan.¹⁰⁵

The best approach to VTE is to prevent DVT. The National Institutes of Health Consensus Conference on the Prevention of Venous Thrombosis and Pulmonary Embolism recommends using low doses of subcutaneously administered heparin in all stroke patients with no hemorrhagic components.¹²¹ In all other patients, external pneumatic calf compression is recommended. More recently, low-molecular-weight heparin has been introduced and actually may be more effective than standard heparin for DVT prophylaxis.⁷² Low doses of warfarin for DVT prophylaxis in stroke patients has not been well-studied, but its use in other conditions has proved its effectiveness in DVT reduction. Dextran, aspirin, and static compression stockings are not effective for preventing DVT.¹⁹ Physical treatments alone, such as ROM exercises, have not been studied. Ambulatory patients must be able to walk at least 50 feet to have a reduction in risk of DVT,²¹ but as previously stated, the risk of pulmonary embolism in ambulatory patients is still significant.¹⁴⁷ The length of time prophylaxis should continue is still not definite, but evidence shows that continuing prophylaxis well into the subacute phase is warranted.¹⁹

The treatment of VTE (DVT and pulmonary embolism) is based on preventing pulmonary embolism, which can be fatal. A patient who is identified with acute VTE is started on intravenous (IV) heparin as long as no contraindications to anticoagulation exist.⁷⁰ The effectiveness of the heparin is determined by monitoring the partial thromboplastin time, and the heparin is adjusted to a dose between 1.5 and 2.5 times control. In a patient with only DVT, warfarin can be started on the first day, and the heparin can be discontinued when the warfarin dose is therapeutic as measured by the increase in the prothrombin time or international normalized ratio. Targets are a prothrombin time of 1.25 to 1.5 times control or an international normalized ratio of 2 to 3.¹⁹ In patients with pulmonary embolism, warfarin may be started a few days later, and after management of the acute stage, the patient keeps receiving it longer; patients with DVT receive warfarin for approximately three months, and patients with pulmonary embolism, for six months.⁷² All patients who recently have been diagnosed with VTE are placed on bed rest initially and usually are allowed to become mobile two days after the partial thromboplastin time has become therapeutic.⁷⁶ The rehabilitation of patients with VTE who are beginning treatment should continue at the bed side, and, in the case of patients with lower extremity DVT, the rehabilitation program should include activity of daily living (ADL) training, upper extremity programs, communication work, and dysphagia treatments.

Foley catheter.

A Foley catheter is indwelling and is used to drain urine from the bladder. The therapist should avoid clamping the catheter; doing so could result in a backup of urine in the bladder. The bag, which collects the urine, needs to be at a lower level than the patient’s bladder for the urine to flow in the correct direction.

Nasogastric tube.

A nasogastric tube (NGT) is placed through the nostril down the esophagus to the stomach for liquid feeds to pass. It is generally used as a short-term alternative for nutritional intake.

Percutaneous endoscopic gastrostomy.

A percutaneous endoscopic gastrostomy is a tube inserted surgically with an endoscope through the mouth and into the stomach, exiting out through the stomach wall and dermis (Fig. 1-13).

Figure 1-13 Percutaneous endoscopic gastrostomy in abdomen.

(Photo courtesy of Millie Hepburn Smith.)

Precautions for both feeding tubes include elevating the head of bed to 30 degrees or greater while administering the tubes to prevent aspiration. Depending upon the hospital guidelines, the therapist may be allowed to turn off the feeding prior to the therapy session, but it is recommended that the primary care nurse be consulted prior to doing so, for patient safety (see Chapter 24).

Functional activity suggestions during the acute phase

Bed mobility

Rolling to the affected side.

Rolling to the affected side promotes early active trunk control and may increase awareness of the weaker side.

Rolling to the unaffected side.

Rolling to the unaffected side promotes awareness and initial management of the weak upper extremity by teaching the patient to passively guide the arm across the trunk (Fig. 1-18).

Figure 1-18 Bed level activities. Rolling to the unaffected side and engaging the affected arm in early reaching task and at the same time engaging affected trunk and lower extremity muscles.

Maintaining side lying.

A rolled pillow placed at the midthoracic spine to the lumbar area may assist the patient in maintaining the side-lying position. A towel roll can be placed under the patient’s waist to provide a stretch to the shortened trunk. A primary goal is to assure proper spine alignment, to avoid pressure build up over the bony prominences in the lower extremities (knees and ankles), and to position the scapula in protraction if the patient is positioned on the weakened side.

Bridging.

Bridging strengthens the back and hip extensors. From a functional perspective, this movement aids in getting on and off the bed pan, can be used during lower body dressing, and also assists moving the lower body toward the side of the bed in anticipation of assuming a sitting position.

Side lying to sitting toward the affected side.

Side lying to sitting toward the affected side promotes early stage weight-bearing on the weak upper extremity. The therapist needs to ensure that the shoulder is properly aligned, and the patient will usually require assistance with initiation of the movement.

Side lying to sitting toward the unaffected side.

Therapists need to be mindful that the involved shoulder remains in a forward position during the motion of side lying to sitting toward the unaffected side.

Weight-bearing for function

Upper extremity weight-bearing activities may be done while the patient is side lying as mentioned previously, during bed mobility, or for stabilizing items. It can also be accomplished using the bed side table during meals or grooming tasks. The arm or back rest of a chair can be incorporated in the treatment plan for positioning and setup for weight-bearing (Figs. 1-19 and 1-20). The patient should be taught to push off with both upper extremities when moving from sit to stand. Weight-bearing as a postural support can reverse or prevent tissue shortening of the elbow, wrist, and finger flexors. It can also be used to strengthen the scapula musculature and the triceps. Arm extended weight-bearing can be done in front of the sink during grooming or be done in front of the bed side table while reaching for items nearby (Fig. 1-21).

Figure 1-19 While the patient sits on the edge of the bed, a bed side chair is used to facilitate upper extremity weight-bearing activities.

Figure 1-20 Forearm weight-bearing on bed side table while patient dangles off edge of bed.

Figure 1-21 Supported standing with bed side table to facilitate upper extremity involvement in activity. Early upright ADL training can be initiated, and weight shifting through the lower extremities is encouraged.

For the lower extremity, bed level activities include: bridging, sitting at the edge of the bed with both feet on the floor, and early transfer training once patients are medically stable.