Definition

Hemiplegia, a paralysis of one side of the body, is the classic sign of neurovascular disease of the brain. It is one of many manifestations of neurovascular disease, and it occurs with strokes involving the cerebral hemisphere or brain stem. A stroke, or cerebrovascular accident (CVA), results in a sudden, specific neurological deficit and occurs when a brain blood vessel is either occluded by a clot or bursts. It is the suddenness of this neurological deficit—occurring over seconds, minutes, hours, or a few days—that characterizes the disorder as vascular. Although the motor deficits of hemiplegia may be the most obvious sign of a CVA and a major concern of therapists, other symptoms are equally disabling, including sensory dysfunction, aphasia or dysarthria, visual field defects, and mental and intellectual impairment. The specific combination of these neurovascular deficits enables a physician to detect both the location and the size of the defect. CVAs can be classified according to pathological type—thrombosis, embolism, or hemorrhage—or according to temporal factors, such as completed stroke, stroke-in-evolution, or transient ischemic attacks (TIAs).

Epidemiology

In the United States, stroke is the third ranking cause of death—more than 137,000 people die each year—and is the leading cause of adult disability.¹ The National Stroke Association estimates that 795,000 new or recurrent strokes occur each year. The incidence of stroke rises rapidly with increasing age: two thirds of all strokes occur in people older than the age of 65 years; and after the age of 55 years, the risk of stroke doubles every 10 years. With the over-50-years age group growing rapidly, more people than ever are at risk. In the United States, the incidence of stroke is greater in men than in women, and it is twice as high in blacks as in whites. Cerebral infarction (thrombosis or embolism) is the most common form of stroke, accounting for 70% of all strokes. Hemorrhages account for another 20%, and 10% remain unspecified. Stroke is the largest single cause of neurological disability. Approximately 4 million Americans are dealing with impairments and disabilities from a stroke. Of these, 31% require assistance, 20% need help walking, 16% are in long-term care facilities, and 71% are vocationally impaired after 7 years.¹ One study reported that 12% of subjects have complete functional arm recovery and 38% have some dexterity 6 months after stroke. In addition, loss of leg movement in the first week after stroke and no arm movement at 4 weeks are associated with poor outcomes at 6 months.²

The three most commonly recognized risk factors for cerebrovascular disease are hypertension, diabetes mellitus, and heart disease. The most important of these factors is hypertension.³ Because high blood pressure is the greatest risk factor for stroke, human characteristics and behaviors that increase blood pressure, including increased high serum cholesterol levels, obesity, diabetes mellitus, heavy alcohol consumption, cocaine use, and cigarette smoking, increase the risk of stroke.

Ostfeld⁴ noted that mortality rates for stroke declined, slowly at first (from 1900 to 1950) and then more quickly (from 1950 to 1970), with a sharp drop noted around 1974. Experts have speculated that the greater use of hypertensive drugs in the 1960s and 1970s started this decline, and the creation of screening and treatment referral centers for high blood pressure may account for the marked decline in the late 1970s.

Outcome

The long-term follow-up on the Framingham Heart Study revealed that long-term stroke survivors, especially those with only one episode, have a good chance for full functional recovery.⁵ For people left with severe neurological and functional deficits, studies have demonstrated that rehabilitation is effective and that it can improve functional ability.^6,7 It has been demonstrated that age is not a factor in determining the outcome of the rehabilitation process.⁸ Currently it is thought that clients should be given an opportunity to participate in the rehabilitation process, regardless of age, unless it is medically contraindicated.

The prediction of ultimate functional outcome has been hampered by the inaccuracy of commonly used predictors (medical items, income level, intelligence, functional level). Computed tomography (CT), functional magnetic resonance imaging, and regional cerebral blood flow studies are used in diagnosis and increasingly as predictors of functional recovery after stroke. Positron emission tomography and single-photon emission CT are newer techniques that are used in research centers to define areas of dysfunctional but perhaps “salvageable” tissue.^2,9

Pathoneurological and pathophysiological aspectsclassification

The pathological processes that result from a CVA can be divided into three groups—thrombotic changes, embolic changes, and hemorrhagic changes.

Thrombotic infarction.

Atherosclerotic plaques and hypertension interact to produce cerebrovascular infarcts. These plaques form at branchings and curves of the arteries. Plaques usually form in front of the first major branching of the cerebral arteries. These lesions can be present for 30 years or more and may never become symptomatic. Intermittent blockage may proceed to permanent damage. The process by which a thrombus occludes an artery requires several hours and explains the division between stroke-in-evolution and completed stroke.¹⁰

TIAs are an indication of the presence of thrombotic disease and are the result of transient ischemia. Although the cause of TIAs has not been definitively established, cerebral vasospasm and transient systemic arterial hypotension are thought to be responsible factors.

Embolic infarction.

The embolus that causes the stroke may come from the heart, from an internal carotid artery thrombosis, or from an atheromatous plaque of the carotid sinus. It is usually a sign of cardiac disease. The infarction may be of pale, hemorrhagic, or mixed type. The branches of the middle cerebral artery are infarcted most commonly as a result of its direct continuation from the internal carotid artery. Collateral blood supply is not established with embolic infarctions because of the speed of obstruction formation, so there is less survival of tissue distal to the area of embolic infarct than with thrombotic infarct.²

Hemorrhage.

The most common intracranial hemorrhages causing stroke are those resulting from hypertension, ruptured saccular aneurysm, and arteriovenous (AV) malformation. Massive hemorrhage frequently results from hypertensive cardiac-renal disease; bleeding into the brain tissue produces an oval or round mass that displaces midline structures. The exact mechanism of hemorrhage is not known. This mass of extravasated blood decreases in size over 6 to 8 months.

Saccular, or berry, aneurysms are thought to be the result of defects in the media and elastica that develop over years. This muscular defect plus overstretching of the internal elastic membrane from blood pressure causes the aneurysm to develop. Saccular aneurysms are found at branchings of major cerebral arteries, especially the anterior portion of the circle of Willis. Averaging 8 to 10 mm in diameter and variable in form, these aneurysms rupture at their dome. Saccular aneurysms are rare in childhood.

AV malformations are developmental abnormalities that result in a spaghetti-like mass of dilated AV fistulas varying in size from a few millimeters in diameter to huge masses located within the brain tissue. Some of these blood vessels have extremely thin, abnormally structured walls. Although the abnormality is present from birth, symptoms usually develop at ages 10 to 35 years. The hemorrhage of an AV malformation presents a pathological picture similar to that for the saccular aneurysm. The larger AV malformations frequently occur in the posterior half of the cerebral hemisphere.¹⁰

Clinical findings

The focal neurological deficit resulting from a stroke, whether embolic, thrombotic, or hemorrhagic, is a reflection of the size and location of the lesion and the amount of collateral blood flow. Unilateral neurological deficits result from interruption of the carotid vascular system, and bilateral neurological deficits result from interruption of the vascular supply to the basilar system. Clinical syndromes resulting from occlusion or hemorrhage in the cerebral circulation vary from partial to complete. Signs of hemorrhage may be more variable as a result of the effect of extension to surrounding brain tissue and the possible rise in intracranial pressure. Table 23-1 summarizes the clinical symptoms and the anatomical structures involved according to specific arterial involvement.

TABLE 23-1 

Clinical Symptoms of Vascular Lesions

AFFECTED VESSEL	CLINICAL SYMPTOMS	STRUCTURES INVOLVED
Middle cerebral artery	Contralateral paralysis and sensory deficit	Somatic motor area
	Motor speech impairment	Broca area (dominant hemisphere)
	“Central” aphasia, anomia, jargon speech	Parieto-occipital cortex (dominant hemisphere)
	Unilateral neglect, apraxia, impaired ability to judge distance	Parietal lobe (nondominant hemisphere)
	Homonymous hemianopia
	Loss of conjugate gaze to opposite side	Optic radiation deep to second temporal convolution
	Avoidance reaction of opposite limbs	Frontal controversive field
	Pure motor hemiplegia	Parietal lobe
	Limb—kinetic apraxia	Upper portion of posterior limb of internal capsule Premotor or parietal cortex

Anterior cerebral artery Paralysis—lower extremity Motor area—leg   Paresis in opposite arm Arm area of cortex   Cortical sensory loss     Urinary incontinence

Posteromedial aspect of superior frontal gyrus

Medial surface of posterior frontal lobe

  Contralateral grasp reflex, sucking reflex Uncertain   Lack of spontaneity, motor inaction, echolalia Uncertain   Perseveration and amnesia   Posterior cerebral artery     Peripheral area Homonymous hemianopia Calcarine cortex or optic radiation   Bilateral homonymous hemianopia, cortical blindness, inability to perceive objects not centrally located, ocular apraxia Bilateral occipital lobe   Memory defect Inferomedial portions of temporal lobe   Topographical disorientation Nondominant calcarine and lingual gyri Central area Thalamic syndrome Posteroventral nucleus of thalamus   Weber syndrome Cranial nerve III and cerebral peduncle   Contralateral hemiplegia Cerebral peduncle   Paresis of vertical eye movements, sluggish pupillary response to light Supranuclear fibers to cranial nerve III   Contralateral ataxia or postural tremor   Internal carotid artery Variable signs according to degree and site of occlusion—middle cerebral, anterior cerebral, posterior cerebral territory Uncertain Basilar artery Ataxia Middle and superior cerebellar peduncle Superior cerebellar artery Dizziness, nausea, vomiting, horizontal nystagmus Vestibular nucleus   Horner syndrome on opposite side, decreased pain and thermal sensation Descending sympathetic fibersSpinal thalamic tract   Decreased touch, vibration, position sense of lower extremity greater than that of upper extremity Medial lemniscus   Nystagmus, vertigo, nausea, vomiting Vestibular nerve Anterior inferior cerebellar artery Facial paralysis on same side Cranial nerve VII Tinnitus Auditory nerve, lower cochlear nucleus   Ataxia Middle cerebral peduncle   Impaired facial sensation on same side Fifth cranial nerve nucleus   Decreased pain and thermal sensation on opposite side Spinal thalamic tract Complete basilar syndrome Bilateral long tract signs with cerebellar and cranial nerve abnormalities     Coma     Quadriplegia     Pseudobulbar palsy     Cranial nerve abnormalities   Vertebral artery Decreased pain and temperature on opposite side Spinal thalamic tract   Sensory loss from a tactile and proprioceptive Medial lemniscus   Hemiparesis of arm and leg Pyramidal tract   Facial pain and numbness on same side Descending tract and fifth cranial nucleus   Horner syndrome, ptosis, decreased sweating Descending sympathetic tract   Ataxia Spinal cerebellar tract   Paralysis of tongue Cranial nerve XII   Weakness of vocal cord, decreased gag Cranial nerves IX and X   Hiccups Uncertain

Thrombosis and transient ischemic attacks.

Although infarcted tissue cannot at present be restored, medical management of the acute stroke from thrombosis or TIA is geared toward improving the cerebral circulation as quickly as possible to prevent ischemic tissue from becoming infarcted tissue. Cells that have 80% to 100% ischemia will die in a few minutes because they cannot produce energy, specifically adenosine triphosphate. This energy failure results in an activation of calcium, which causes a chain reaction resulting in cell death.¹ Around this area of infarction is a transitional area where the blood flow is decreased 50% to 80%. Cells in the transitional area are not irreversibly damaged.^12,13

One of the newer drugs available for immediate stroke treatment is tissue plasminogen activator (t-PA) (see Chapter 36). It is approved for use within 3 hours of symptom onset but is most effective if used within the first 90 to 180 minutes. Recent studies indicate that 42% of patients who have sustained a stroke wait 24 hours before getting care, with the average being 13 hours.¹³ The importance of community-wide programs to increase awareness of symptoms and effectiveness of emergency medical responses is immense for this drug’s usage. The American Heart Association and the National Stroke Association are creating community campaigns to increase awareness of the medical emergency nature of stroke symptoms. These campaigns encourage people to call 911 immediately when any of the following warning signs occur:

Anticoagulant drugs are used to prevent TIAs and may stop a stroke-in-evolution. Before anticoagulant drugs are used, an accurate differential diagnosis is necessary because of the danger of excessive bleeding if hemorrhage is present. Heparin is often used in the early stage of the stroke, and warfarin (Coumadin) or dabigatran (Pradaxa) is commonly used in the months after the stroke. Cerebral edema, if present, is managed pharmacologically during the first few days. Antiplatelet drugs such as aspirin, dipyridamole (Persantine), and sulfinpyrazone (Anturane) are used to prevent clotting by decreasing platelet “stickiness.”¹⁰

Surgical treatment (thromboendarterectomy or grafting) is used when TIAs are the result of arterial plaques. Areas accessible to and suitable for surgery include the carotid sinus and the common carotid, innominate, and subclavian arteries. Although both surgery and anticoagulant therapy are used for TIAs, Adams and Victor¹⁰ extensively reviewed the wide divergence of opinions. For clients who have had a stroke yet recovered quickly and well, medical care focuses on prevention. Prevention usually includes maintaining blood pressure and blood flow, monitoring hypotensive agents (if given), and avoiding oversedation, especially for sleep, to prevent cerebral ischemia.

Embolic infarction.

Management of embolic infarction is similar to that of thrombotic infarction. The primary emphasis is on prevention. Long-term anticoagulant therapy is effective in preventing embolic infarction in clients with cardiac problems such as atrial fibrillation, myocardial infarction, and valve prostheses. The diagnostic use of CT is important in anticoagulant therapy to rule out hemorrhage after the infarct.

Hypertensive hemorrhage.

Medical procedures for hypertensive hemorrhage parallel those for thrombosis and embolism. Surgical removal of the clot and lowering of the systemic blood pressure to decrease hemorrhage have generally not been helpful. Again, the preventive use of antihypertensive drugs in clients with essential hypertension is the soundest medical management available.¹⁰

Ruptured aneurysm.

Comatose clients are not good candidates for surgery. However, if the client survives the first few days and if the state of consciousness improves, surgical intervention, whether extracranial or intracranial, is the treatment of choice. Medical treatment consists of lowering arterial blood pressures. Bed rest for 4 to 6 weeks with all forms of exertion avoided is prescribed. Antiseizure medication may be used. Often a systemic antifibrinolysin is given to impede lysis of the clot at the site of rupture. Vasospasm, resulting in severe motor dysfunction, occurs with the use of drugs such as reserpine (Serpasil) and kanamycin (Kantrex) (see Chapter 36).

Regardless of the cause of the stroke, comatose clients are managed by (1) treatment of shock; (2) maintenance of clear airway and oxygen flow; (3) measurement of arterial blood gases, blood analysis, CT, and spinal tap; (4) control of seizures; and (5) gastric tube feeding (if coma is prolonged). Hypertensive hemorrhage is one of the most common vascular causes of coma.¹⁴

Medical management of associated problems

Spasticity.

Spasticity and its treatment constitute a major medical problem after stroke because clients complain about it, it may fluctuate, and it does not respond to one fixed treatment. The relationship between spasticity and movement after stroke is an area of continued interest for researchers. Recent studies have refuted the earlier belief that spasticity was inversely related to voluntary movement.^15,16 Although therapists are more hesitant to treat spasticity now, physicians continue to treat it aggressively. Various pharmacological, surgical, and physical means are used to decrease spasticity. The pharmacological and surgical means are examined here, and therapy management is discussed later.

Two types of drugs are used to counter the effects of spasticity: centrally acting and peripherally acting agents. Centrally acting drugs, such as diazepam, have been used to depress the lateral reticular formation and thus its facilitatory action on the gamma motor neurons. This form of drug is used widely to treat spasticity, although the greatest disadvantage of centrally acting drugs is that they depress the entire CNS. Drowsiness and anxiety are common side effects.

Peripherally acting drugs are used to block a specific link in the gamma group. Procaine blocks selectively inhibit the small gamma motor fibers, resulting in a relaxation of intrafusal fibers. The effect of procaine blocks is transient. Intramuscular neurolysis with the injection of 5% to 7% phenol has been used to destroy the small intramuscular mixed nerve branches.¹⁷ Phenol blocks relieve hypertonicity and improve function, especially when followed by an intensive course of therapy.¹⁸ It can provide relief for 2 to 12 months, and the effects have been documented to last as long as 3 years.^17,18 Disadvantages of phenol use include its toxicity to tissue and the complications of pain that occasionally result.

Botulinum toxin type A (Botox) is also used to decrease the effects of hypertonicity on functional movement in hemiplegia.19–21 Local injection of the toxin into spastic muscles produces selective weakness by interfering with the uptake of acetylcholine by the motor end plate. The effect of the toxin is temporary, depends on the amount injected, and is associated with minimal side effects. Repeat injections are recommended no sooner than 12 to 14 weeks to avoid antibody formation to the toxin. Researchers report positive functional results when botulinum toxin A injections are followed by intensive muscle reeducation and appropriate splinting.²²

Dantrolene sodium is used to interrupt the excitation-contraction mechanism of skeletal muscles. Trials have shown that it has reduced spasticity in 60% to 80% of clients while improving function in 40% of these clients. The side effects—drowsiness, weakness, and fatigue—can be decreased through titration of dosage. Serious side effects, including hepatotoxicity, precipitation of seizures, and lymphocytic lymphoma, have been reported when the drug has been used in high doses over a long time.¹⁷

Baclofen, in pill form, is used as a skeletal muscle relaxant to decrease spasticity. It can now be delivered intrathecally into the spinal cord with a pump that is surgically inserted into the body. It relieves spasticity with a small amount of medication (10 mg/20 mL, 10 mg/5 mL). Intrathecal baclofen has had dramatic results in cases of severe spasticity because it acts directly on the affected muscles instead of circulating in the blood. It is used for extremity spasticity that interferes with the ability to assume functional positions in patients with severe stroke, multiple sclerosis, head injury, and cerebral palsy.²³

The surgical treatment of spasticity through tenotomy or neurectomy is considered when all other treatments fail, and it is used to correct deformity, especially of a hand or foot. A peripheral nerve block is often used as a diagnostic tool to evaluate the effect of surgical treatment. If anatomical or functional gains are made through a temporary nerve block, consideration is given to surgical release. The surgical treatment of spasticity does not necessarily result in increased movement control and, with the increased understanding of the causes of spasticity, does not seem appropriate in stroke.

Seizures.

The highest risk for seizure after a stroke is immediately afterward; 57% of seizures occur in the first week and 88% occur within the first year.²⁴ Seizures after thrombotic and embolic stroke are usually of early onset, whereas seizures after hemorrhagic stroke are of late onset. The management of seizures after stroke is usually with antiseizure medication. Commonly used drugs include phenytoin (Dilantin), carbamazepine (Tegretol), gabapentin (Neurontin), and divalproex (Depakote).²⁵ Side effects that interfere with movement therapy include drowsiness, ataxia, distractibility, and poor memory.

Respiratory involvement.

Fatigue is a major problem for the person with hemiplegia. This fatigability, which interferes with everyday life processes and active rehabilitation, is attributed to respiratory insufficiency resulting from paralysis of one side of the thorax. Haas and colleagues²⁶ studied respiratory function in hemiplegia and found decreased lung volume and mechanical performance of the thorax to be significant factors, in addition to abnormal pulmonary diffusing capacity. Clients with hemiplegia consume 50% more oxygen while walking slowly (regardless of the presence or absence of orthotic devices) than that used by subjects without hemiplegia.²⁶ The decreased respiratory output and the increased oxygen demand that result from atypical movement patterns are responsible for early fatigue in persons with hemiplegia. Treatment objectives and techniques must reflect the understanding of this respiratory problem. For clients who walk at velocities greater than 0.48 m/s, a gain in walking capacity is associated with an increased peak Vo₂

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