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.

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 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.

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.

Evaluation.

Assessment for severity of symptoms, time of onset, and differentiation of type of stroke as ischemic or hemorrhagic is critical in medical decision making. Speech difficulty and hemiparesis are the most common symptoms of an ischemic stroke. Facial weakness, arm or leg numbness, confusion, headache, and nonorthostatic dizziness may also occur. Severe and sudden headache is the most common symptom of a hemorrhagic stroke. Hemorrhagic strokes may also present with gradual development of reduced consciousness, vomiting, and hemiparesis. A neurological exam will help quantify the severity of symptoms by assessing mental status, focal weakness of the arm, leg and/or face, speech impairments, gait impairments, impaired eye movements, and visuospatial perceptual impairments. The National Institutes of Health Stroke Scale (NIHSS) is highly recommended due to its diagnostic and prognostic power of stroke severity. Additionally, imaging should be performed for differential diagnosis of other conditions as well as to differentiate the type of stroke as ischemic or hemorrhagic. Noncontrast head CT will help rule out hemorrhagic origin while an MRI is more sensitive for identifying ischemic stroke. Other tests that may be performed include blood glucose, renal function, electrocardiogram (ECG), complete blood count, oxygen saturation, toxicology screen, blood alcohol level, and electroencephalography (EEG). Additionally, continuous cardiac monitoring is strongly recommended for a minimum of 24 hours.

Ischemic stroke.

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. Around this area of infarction is a transitional area, the penumbra, where the blood flow is decreased 50% to 80%. Cells in the transitional area are not irreversibly damaged. ^,

An established pharmaceutical approach to acute ischemic stroke management is tissue plasminogen activator (t-PA) (see Chapter 36 ). t-PA must be given within 3 hours of symptom onset but is most effective if used within the first 90 to 180 minutes. It is absolutely contraindicated for hemorrhagic stroke. Permissive hypertension is often prescribed to assist with improving perfusion beyond the clot to limit the area of penumbra. Cerebral edema, if present, is managed pharmacologically during the first few days. Antiplatelet drugs such as aspirin are used to prevent clotting by decreasing platelet “stickiness” following TIA and/or within 24 to 48 hours following ischemic stroke.

Endovascular surgical intervention may be indicated for ischemic stroke to remove/reduce the blood clot. 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, recently Ropper extensively reviewed the wide divergence of opinions.

For individuals who have had a stroke yet recovered quickly and well, medical care focuses on prevention of recurrent stroke. Prevention usually includes maintaining blood pressure and blood flow, monitoring hypotensive agents (if given), and avoiding oversedation, especially for sleep, to prevent cerebral ischemia. Long-term anticoagulant therapy is effective in preventing embolic infarction in persons with cardiac problems such as atrial fibrillation, myocardial infarction, and valve prostheses.

Hemorrhagic stroke.

Medical management to reduce ICP includes sedation, hyperosmolar agents, and hyperventilation. Surgical interventions including decompressive craniotomy and craniectomy are recommended only under extreme circumstances of rapid deterioration or if the ICP is not responding to other efforts. Following surgical intervention, medical management consists of lowering arterial blood pressures. Pharmaceutical management of hypertension for hemorrhagic stroke differs from that of ischemic stroke with an emphasis on reducing blood pressure as quickly as possible to reduce bleeding. Antiseizure medication may be used. Often a systemic anti-fibrinolysin is given to impede lysis of the clot at the site of rupture. Vasospasms are a common secondary condition following subarachnoid hemorrhage (SAH). Vasospasms result in secondary cerebral ischemia following the initial hemorrhage and result in increased morbidity and mortality. Nimodipine is considered a first-line drug to reduce the risk of vasospasm.

Regardless of the type of the stroke, individuals who are comatose 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; and (4) control of seizures. Hypertensive hemorrhage is one of the most common vascular causes of coma.

Recent studies indicate that 42% of patients who have sustained a stroke wait 24 hours before getting care, with the average being 13 hours. The importance of community-wide programs to increase awareness of symptoms and effectiveness of emergency medical responses is immense in order to administer t-PA for best possible outcomes. 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, entitled BEFAST, occur:

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  B alance – trouble walking, dizziness, loss of balance or coordination

  
  
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  E yes – trouble seeing with one or both eyes

  
  
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  F ace – numbness or weakness of the face

  
  
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  A rm – numbness or weakness of the arm (or leg) especially on one side of the body.

  
  
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  S peech – confusion or trouble speaking and/or understanding

  
  
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  T ime – call 911 immediately

Spasticity.

Research findings have refuted the earlier belief that spasticity is the cause of the atypical movement patterns in people with CNS dysfunction. ^, Spasticity, a reflex measured by velocity dependent stretch in the passive state, is an indication of damage to the CNS. The term “spasticity” is often used synonymously with hypertonicity, a resistance to passive stretch that is not velocity-dependent. Its treatment constitutes a major medical problem after stroke because patients complain about it and physicians continue to treat it aggressively. 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. Phenol blocks relieve hypertonicity and improve function, especially when followed by an intensive course of therapy. It can provide relief for 2 to 12 months, and the effects have been documented to last as long as 3 years. ^, 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 spasticity on functional movement in hemiplegia. 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.

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 individuals while improving function in 40% of these patients. 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.

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.

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 after the event; 57% of seizures occur in the first week and 88% occur within the first year. 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). 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 colleagues 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. Individuals with hemiplegia consume 50% more oxygen while walking slowly (regardless of the presence or absence of orthotic devices) than subjects without hemiplegia. 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 patients who walk at velocities greater than 0.48 m/s, a gain in walking capacity is associated with an increased peak Vo ₂ . Research exploring the role of exercise after stroke indicate that gains in respiratory fitness were associated with increased walking capacity. In clinical practice, therapists should remember to include standard respiratory measures and functions to evaluate the efficacy of treatment techniques.

Stroke fatigue syndrome.

Another potential cause of fatigue following stroke is Stroke Fatigue Syndrome or post-stroke fatigue. Although its etiology is not well understood, post-stroke fatigue is reported in 23% to 75% of Individuals following a stroke. It is known to reduce the quality of life and increase the risk of death in those who experience it. Research related to etiology and intervention for prevention and treatment is relatively new. Suspected mechanisms under current research include biological, psychosocial, and behavioral causes. Suggested interventions under recent and current investigation include pharmacological agents such as antidepressants and stimulants; psychological approaches including cognitive behavioral therapy and educational programming; and physical training including graded aerobic training. A recent systematic review indicated continued, high-quality research is needed to identify the most effective treatment intervention strategy.

Cardiovascular health.

In the chronic stage of recovery, Patients may have significant cardiovascular deconditioning with half the fitness levels of age-matched controls. This decrease in fitness affects the performance of daily activities and adds to these patients’ morbidity and mortality risk. This decreased fitness results in part from decreased mobility of the leg, muscular atrophy, altered muscle physiology, increased muscular fat, and altered peripheral blood flow. ^,

Fractures.

If the patient with hemiplegia has severe extremity or trunk weakness and relies heavily on the nonparetic extremities for function, poor balance and falls are possible. After a stroke the risk of hip fracture is greatest in the first year of recovery. Eighty percent of hip fractures occur on the paretic side and are the result of bone loss or falls. In addition, other common fracture sites are the humerus and wrist.

Therapy intervention for a hip fracture with a hemiplegia is complicated by increased difficulty sustaining a symmetrical trunk posture over the fractured hip, decreased strength in the leg, pain, and spasticity. In addition to the loss of balance and protective mechanisms, the development of osteoporosis from disuse is a limiting factor for functional recovery after a fracture.

Thrombophlebitis.

Thrombophlebitis may occur in the acute and subacute stages of recovery and rehabilitation. Deep vein thrombosis is caused by altered blood flow, damage to the vessel wall, and changes in blood coagulation times. The vascular changes are aggravated by the inactivity and dependent postures of the weak extremities. Deep vein thrombosis is many times more common in the weaker leg.

Complex regional pain syndrome.

Formerly known as reflex sympathetic dystrophy, complex regional pain syndrome is a chronic pain condition affecting the paretic arm or leg. The extremity pain is reported as intense and burning and may be accompanied by swelling and redness. It leads to changes in bone and skin and, if left untreated, becomes debilitating . Medical treatment includes the use of chemical sympathetic blocks and oral or intramuscular corticosteroids. The use of blocks and corticosteroids often stops the burning pain. The length of time of the relief varies from patient to patient. Adverse reactions from blocks and corticosteroids occur about 20% of the time. ^,

Pain.

The pharmacological management of joint pain after stroke (usually shoulder pain) includes the local injection of corticosteroids.

Primary and secondary impairments.

Primary impairments are a direct result of the brain damage and are present immediately. Secondary impairments develop over time and in body systems not originally affected by the brain lesion.

Composite impairments.

Composite impairments are the combined effects of the primary and secondary impairments, stage of motor recovery, previous treatment, and behavioral factors.

The composite impairment category used in this chapter has three generalized movement patterns that create one model of classification: (1) movement deficits, (2) atypical movements, and (3) undesirable compensatory patterns.

Movement deficits result from severe neurological weakness with either gradual, balanced return or no significant return. Functional movement patterns and levels of independence are based on the distribution and amount of return: trunk control greater than extremity control, extremity control greater than trunk control, distal extremity return greater than proximal extremity return or vice versa, and arm control greater than leg control or vice versa. These individuals do not have problems with hypertonicity but, when neurological weakness is severe, have long-term problems with the secondary impairments of muscle shortening and loss of joint range.

In the acute stage, the arm hangs by the side, the humerus is internally rotated, the elbow is extended, and the forearm is pronated. Inferior shoulder subluxation is common. The trunk is weak, the ribs flare, and spinal alignment is impaired: a convex lateral curve is seen on the affected side. In standing, the patient has problems recruiting sufficient force production in the affected leg to counteract the downward pull of gravity. The pelvis lists downward, the hip and knee flex, and the ankle moves into plantarflexion. As the patient relearns to walk, the hip and knee may remain in flexion from weakness or the patient may compensate and push/lock the knee into extension.

A reliance on a cane for balance and the accompanying compensatory weight shift of the upper body onto a cane results in the use of pelvic elevation for swing initiation ( Figs. 24.1 and 24.2 ).

(A) Patient with right hemiplegia. Movement deficit: neurological weakness (lack of initiation); patient was unable to move arm or leg in standing or sitting. (B) Patient uses cane and tries to shift to the right as he gets ready to step forward with the left leg. Note how the heavy weight of the right arm pulls the upper body into forward flexion and rotation left. (C) Patient prepares to step forward with the right leg. Note that his attendant has corrected his upper-body position. (D) Patient leans heavily onto cane (his upper body translates laterally to the left) to lessen weight on the right leg. He will accomplish the “step” by rotating his upper body to the left, a compensation for the loss of leg control in standing.

Atypical movement patterns are found in patients with unbalanced muscle return and deficits of muscle activation not only in initiation/cessation, but also sequencing and timing. Atypical movements are movements that deviate from normal patterns of muscle coordination. They use patterns of muscle activation and sequences of joint movement that deviate from normal muscle synergies or biomechanical rules. Atypical movement patterns develop as a consequence of primary and secondary impairments. When motor recovery is incomplete, patients use the muscles that are available to produce movement. During attempts at functional activities, patients’ movement patterns may occur with excessive effort and cocontraction ( Fig. 24.3 ).

(A) Individual with right hemiplegia. Movement deficit: Difficulty sequencing; patient is able to walk with a brace and does not need a cane. (B) During stance, his upper body moves laterally to the right and his right femur internally rotates as his knee hyperextends. (C) He has enough trunk control to stand and balance and sufficient leg control to lift the leg with knee flexion.

(A) Individual with right hemiplegia. Movement deficit: atypical movement patterns—loss of initiation/cessation, timing, and sequencing. ( B and C ) Patient walking.

Undesirable compensatory patterns are patterns of function that may arise from either of the two previously described movement categories. Compensations are alternative movements or movement substitutions used to circumvent the challenge to the impaired side during daily activities. Although compensatory movements may be necessary and desirable to achieve the highest level of activity performance when there is no ability for recovery to occur, some may be more desirable than others. Undesirable compensatory patterns are noticeably one-sided; they rely on movements of the uninvolved arm and leg and are accompanied by asymmetrical postural trunk movements. They lead to unsafe patterns, or to secondary impairments, or contribute to strategies that may have the potential to block or hinder future motor recovery. These undesirable compensatory patterns create “learned nonuse” of the affected arm and leg and foster asymmetrical postural patterns. Recent research findings indicate that limiting compensatory trunk movements may actually increase the performance of arm-reaching activities.

Patients in the subacute to chronic phase of recovery who come into therapy with strongly established undesirable compensatory patterns do not respond quickly to any type of intervention. Although therapists may be tempted to train a one-sided pattern in early rehabilitation to quickly meet a stated goal, the long-term effects of learned nonuse of one side of the body include increased severity of secondary impairments and poor balance with an increased chance of falls ( Fig. 24.4 ).

Patient With Right Hemiplegia.

Severe compensatory patterns. She walks with a quad cane and standby assistance. Pelvis rotates to the right, upper body rotates to the left, hip flexes, and knee hyperextends. There is strong lateral translation of upper body to the left (to the stable cane).