Approaches to Stroke Rehabilitation

Prevention and Treatment of Secondary Complications in Stroke Rehabilitation

It is estimated that up to 75% of stroke patients admitted to an inpatient rehabilitation unit will suffer some medical complication(s). Approximately 20% of stroke patients in general re-enter acute care due to medical complications of stroke, mostly of a cardiopulmonary nature. It is thought that the hospitalization rates for other complications remain low because the nature of rehabilitation programs is to teach the patient to improve function and compensate for deficits all of which related to prevention or early identification of medical complications.

Cardiovascular Complications

Cardiovascular complications occur in 40-75% of stroke survivors. They include:

  • Hypertension
  • Angina
  • Heart attack
  • Heart arrhythmia
  • Congestive heart failure

Some of these complications may be related to prolonged bed rest and minimal mobility, and some may be related to the general older age of the stroke population. In addition, the presence of hemiparesis can increase the demands on the cardiovascular system during physical activities. Evaluation of cardiovascular disease may be difficult due to cognitive impairment of the patient which interferes with recognition and reporting of symptoms and previous medical history. It is important that all medications prescribed for the treatment of complications be coordinated by a health professional since some drugs may interact with those being used to control other comorbid conditions.

Cardiac and Neuromuscular Deconditioning

Deconditioning refers to the general physiologic effects of prolonged immobility experienced by many stroke patients which is an increased burden on the cardiovascular and neuromuscular systems of the stroke survivor. Deconditioning plays an important role in the overall functional status of a stroke patient as it impacts the intensity of physical training and effort he/she will be able to tolerate during rehabilitation. Preventing or reversing deconditioning has a strong impact on the physical status of stroke survivors.

There are many ramifications for the stroke patient associated with deconditioning including:

  • Increased heart rate at rest
  • Increased heart rate with minimal exercise
  • Reduced aerobic fitness
  • Reduced levels of maximal oxygen uptake (VO2max) during exercise
  • Angina in patients with previous coronary disease
  • Changes to the reflexes that prevent the ability to maintain an upright posture (orthostasis)

Deconditioning can occur within 3 days of immobilization and is more severe in elderly patients. The key to reversing deconditioning is to avoid prolonged bed rest and immobility by progressive steps starting with helping patients sit up on the bed or in a chair, exercise (regular or isometric) while laying down, and helping patients stand upright as soon as it is safe to do so. If the patient shows signs of mild deconditioning, treatment may consist of progressively increasing the sitting time in a chair; for more severe deconditioning or orthostatic hypotension, treatment may consist of using a tilt-table where the patient is secured to a table that can then be progressively tilted in varying degrees towards the standing position.

Some studies have shown that aerobic exercise is beneficial for reversing chronic cardiac deconditioning. Poor physical fitness is a risk factor for stroke so it is not surprising that many stroke patients have reduced peak oxygen consumption (aerobic capacity) and poor endurance for physical activity. Low aerobic fitness is also associated with cardiopulmonary disease in general and osteoporosis. The physical limitations of the stroke patient exacerbate the already low levels of aerobic capacity and therefore need to be addressed in rehabilitation. A literature review of aerobic exercise among stroke patients showed that aerobic exercise training 3-5 days a week for 20-40 minutes is beneficial for the improvement of aerobic capacity at the end of the training period (12-14 weeks). This applies to patients with mild or moderate impairment who have low-risk of cardiovascular complications from exercise training. Equipment used in the study included exercise on a cycle ergometer, treadmill; functional activities such as brisk stepping; and water based activities. Any improvement in aerobic capacity also positively impacts tolerance for other physical training and activities of daily living.

For more information regarding aerobic exercise training in stroke survivors, please click on the following link:

http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed&cmd=Retrieve&dopt=AbstractPlus&listuids=15735998&queryhl=6&itool=pubmed_DocSum

Confusion

Confusion after stroke occurs in up to 25% of patients older than 40 years of age. It is also more common in patients with cognitive impairment prior to the stroke, patients with metabolic diseases (such as diabetes), and patients with infectious diseases. Confusion in stroke patients may also be related to medications such as benzodiazepines, anticonvulsants, or antidepressants. It is generally associated with poorer functional outcome at 6 months post- stroke.

Pressure Sores

Pressure sores, also called decubitus ulcers result from both extrinsic (pressure, shear forces, friction, moisture) and intrinsic (anemia, contraction of muscles, spasticity, diabetes, malnutrition, edema, obesity) etiologies. General measures to prevent pressure sores include adequate nutrition and hydration, as well as proper incontinence care. While in bed, stroke survivors should be turned regularly. Generally, the affected upper extremity should be elevated on a pillow to decrease distal edema and promote awareness. In a side lying position, the affected upper extremity should be positioned with flexion at the shoulder, extension at the elbow, and the wrist in a neutral position. A pillow should be placed between the knees with the affected hip in extension, knee in slight flexion and the ankle in dorsiflexion (ankle bent with foot pointed upward). Assessment of the skin should be performed frequently by caregivers if the stroke survivor has sensory deficits, neglect or a loss in any part of their visual field (visual field cut). In a wheelchair, the stroke survivor should have an appropriate seating system and cushion for maximal skin protection. They or their caregivers should learn pressure relief techniques.

Bladder Dysfunction

Approximately 45-75% of stroke survivors experience urinary incontinence immediately after stroke and most cases resolve within 8 weeks without any treatment. It may persist in up to 10% of patients at 2 years after the stroke. Incontinence appears to increase with the severity of the stroke, age of patient, patients who suffer from aphasia, dysphagia, visual field deficits, and motor weakness. It has a significant impact on the quality of life of the patient since it affects their self image and can interfere with their involvement in social activities. Urinary incontinence may be attributable to physiological changes caused by the stroke that effect many dimensions of daily life (such as communication, mobility, loss of function); or to neurophysiological changes that take place in the centers of the brain that regulate urinary function namely urine retention and urgency/frequency of urination. In addition, the majority of the stroke population is elderly and many may have preexisting urinary or bladder conditions such as urinary incontinence and bladder outlet obstruction (e.g., enlarged prostate).

Reversible causes of incontinence, such as urinary tract infection, fecal impaction, and reduced mobility, should be evaluated and treated. Post-void residuals should be measured to assess for urinary retention. Symptoms of urinary incontinence, frequency, and urgency should be noted. Patients with voiding dysfunction should be referred for urodynamic studies to characterize the voiding disorders and to determine appropriate intervention.

The overall goal of treatment is to help the patient manage with a socially acceptable level of bladder function while minimizing the risk of urinary tract infections. Toileting every 2 to 4 hours during the day and fluid restriction after dinner may prevent incontinence in a majority of patients. External catheters may decrease the incidence of enuresis (involuntary discharge of urine, usually at night while sleeping). Intermittent or indwelling catheterization may be indicated in patients with areflexic bladders (bladders with poor sensation and reflex activity; also bladders which cannot initiate urination normally). Some patients may require medication (such as Tolterodine) or surgery.

Additional steps for management of urinary incontinence include:

  • Mobility - caregivers should help the patient walk if possible to a commode or toilet to void as movement helps bladder function. Being able to use proper toilet facilities also helps the morale and self image of the patient.
  • Communication - if the patient has a communication deficit such as aphasia, the caregiver should create a method for the patient to signal that they need help getting to the bathroom.
  • Maintaining adequate fluid intake - this is a challenge for some stroke patients who may either be physically unable to drink efficiently, to pour drinks for themselves, may not feel thirsty, or may lack motivation to drink. Fluid intake is very important for proper bladder function and also prevents urinary tract infections.
  • Eating a proper diet - this is important in order to avoid fecal impaction or constipation which can cause or exacerbate urinary incontinence.
  • Checking all medications prescribed to the patient to make sure they do not have side effects affecting the urinary system.

Bowel Dysfunction

Approximately 30% of stroke patients experience bowel dysfunction right after the stroke which typically resolves on its own within the first few weeks. Strokes may interfere with the reflex mechanisms for emptying the bowels, and reduced sensation or cognitive impairments may prevent control of defecation. Diet should include adequate fluids and fiber. Patients should be toileted after meals to take advantage of the gastrocolic reflex (an increase of peristaltic activity in the intestines and colon after food is introduced into an empty stomach). Stool softeners and bowel stimulants may be prescribed as necessary. Patients who remain incontinent may require suppositories every 1 to 2 days to prevent incontinence at socially inappropriate times. Persistent bowel incontinence greater than 4 weeks usually is a poor functional predictor.

Shoulder Pain

Estimates are that up to 84% of stroke survivors will experience at least one episode of shoulder pain during the first year of recovery. Common causes of painful hemiplegic shoulder include:

  • Adhesive capsulitis
  • Traction (compression) neuropathy
  • Complex regional pain syndrome type I (CRPS-I, formerly known as reflex sympathetic dystrophy) which develops in up to 12% of patients with shoulder pain
  • Shoulder trauma
  • Bursitis
  • Tendonitis
  • Rotator-cuff tear
  • Spastic muscles
  • Peripheral nerve injury
  • Infection

The most common cause of shoulder pain is spastic muscles which impair passive range of motion, especially external rotation. Diagnosis often may be determined from a physical examination alone, but radiographs, electromyography, bone scans, or magnetic resonance imaging may support clinical findings. Education in an effective self-range of motion exercise program is responsible for a decrease in the prevalence of significant shoulder pain and its complications. In addition, patients may be advised to take analgesic medication such as non-steroidal anti-inflammatory drugs (NSAIDs).

The most serious cause (or result) of shoulder pain is CRPS-I. Diagnosis is usually clinical, with metacarpophalangeal (MCP) joint (finger joint) tenderness highly predictive. However, delayed increased uptake in the wrist or proximal finger joints on bone scan may support the diagnosis. Treatment may include aggressive range of motion of the involved joint accompanied by the use of non-steroidal agents, corticosteroids, antidepressants, treating the source of the pain, TENS, sympathetic nerve blockade, local injections, spinal electrical stimulation, injectable drugs into the spine (such as intrathecal morphine or clonidine), or surgical sympathectomy. Shoulder-hand syndrome is considered to be a variant of reflex sympathetic dystrophy and is characterized by reddening of the skin over the knuckles, trophic changes in the skin (e.g., thinning or wasting away) and hair (e.g. thickening or thinning); and nonlocalized pain.

Treatment is difficult and typically consists of:

  • Treating the source of pain
  • Medication such as nonsteroidal anti-inflammatory (NSAIDs), tricyclic antidepressants or lidocaine
  • Sympathetic nerve blockade
  • Spinal stimulation
  • Injectable drugs into the spine (intrathecal) such as morphine or clonidine

Shoulder Subluxation

Shoulder subluxation, a temporary partial dislocation of the should joint, is a common complication after stroke. The pathogenesis of subluxation is not well understood, but weakness of the supraspinatus muscle has been implicated as a causative factor. The treatment for ambulatory patients usually includes shoulder supports although the effectiveness of shoulder supports has not been definitively established in clinical trials. If they will be used in rehabilitation, a number of different shoulder supports should be evaluated for best fit. In addition, shoulder supports must be easy to don and doff to discourage synergistic patterns and incipient contractures, must permit the affected extremity to function as a postural support, and must not compromise circulation or hamper function.

Other treatments for shoulder subluxation include functional electrical stimulation (FES). Primary wheelchair users may require armboards, arm troughs, or lapboards to support the extremity with poor recovery. Overhead slings may prevent hand edema, but are usually substituted with foam wedges on the armboard.

Spasticity

Spasticity of the affected upper extremity is a common problem in stroke survivors and is thought to occur in up to 65% of stroke survivors. Symptoms of spasticity include:

  • Increased muscle tone as velocity of movement increases
  • Spasm of flexor muscles (muscles which flex the fingers and toes)
  • Hyperreflexia (exaggeration of the reflexes)
  • Painful muscle spasms
  • Clonus (repeated involuntary jerking or shaking of a limb due to rhythmic muscle contractions)
  • Slowness of movement
  • Lack of coordination in movement
  • Cocontraction - the simultaneous activation of opposing muscles when trying to execute a movement

Treatment of spasticity is usually more successful for symptoms such as flexor spasms and clonus and not as successful for relief of slow or uncoordinated movement.

Treatment typically includes:

  • Prevention of potential sources of spasm such as pain, infection, fatigue, or abdominal complications (such as bowel, or bladder problems) by treating sources such as bedsores, in-grown toenails, pressure points from remaining in one position, pain syndromes such as reflex sympathetic dystrophy, or poorly fitting braces
  • Stretching orthoses for the inhibition of tone, maintenance of muscle fiber length, elongation of shortened tissues by prolonged positioning, and reduction of pain
  • Inhibitory orthoses, such as anti-spasticity splints, decrease tone by placing a low-intensity, prolonged duration stretch on appropriate joints to achieve full range of motion.
  • Conventional wrist-hand orthoses may be fabricated to preserve the balance between extrinsic and intrinsic musculature, provide joint support, and prevent deformities.
  • Daily prolonged stretching exercises
  • Weight-bearing exercises

More aggressive interventions may be used to decrease more diffuse spasticity. Appropriate medications for cerebral spasticity include dantrolene (Dantrium), clonidine (Catapres), or tizanidine (Zanaflex). Neurolytic agents, such as phenol or denatured alcohol, may decrease spasticity immediately upon injection, but may cause dysesthesias (distortion of the sense of touch such that an ordinary stimulus can be perceived as painful, or vise versa where a painful stimulus can go unnoticed) or edema in the injected extremity. Botulinum toxin prevents the release of acetylcholine from the nerve terminal and is better tolerated by most patients. Intrathecal baclofen, normally used in patients with traumatic brain or spinal cord injury, may be used in selected stroke survivors without loss of strength in the unaffected limbs. Muscle release or tendon lengthening procedures may be indicated to reverse contractures in conjunction with other interventions.

Falling

Falling is one of the most common complications of stroke. The number of falls while still in the hospital is quite high (up to 22% of patients) and is considered to be a strong predictor of falling after discharge. Second falls tend to occur twice as often as the first fall. Falling is generally associated with the presence of other complications including:

  • Increased age
  • Right hemisphere strokes
  • Male gender
  • Visuospatial neglect
  • Urinary incontinence
  • Medications such as diuretics, antidepressants, or sedatives
  • Impaired levels of functioning for activities of daily living
  • Postural instability
  • Impulsivity

One of the most serious complications of a falling is hip fracture. An important part of any rehabilitation program must include fall prevention strategies such as balance training, exercise, call bells, bed or chair alarms, and other precautionary steps that can be effective in the patient's environment. Patients should be screened to determine who may be at high risk for falling and intensive preventive measures should be taught to both the patient and caregiver. In addition, medications prescribed for the patient should be examined to evaluate side effects of fatigue, imbalance, or lack of coordination. Caregivers should also be trained in fall-prevention and should be guided regarding modifying the home environment for the safety of the patient.

Dysphagia

Swallowing dysfunction, or dysphagia, may occur in up to one-third of patients with cortical or brainstem lesions. It is characterized by impairment of the voluntary control of chewing and moving food around in the mouth, or by difficulty with the actual process of swallowing. Dysphagic patients with hemispheric lesions are usually characterized by weakness of the tongue or lips on the affected side, range of motion, and sensation; delayed pharyngeal swallow; contralateral pharyngeal dysfunction; oral apraxia (inability to make a voluntary muscle movement); auditory comprehension deficits; reduced orientation; perceptual and attention deficits; impulsivity; errors in judgment; and loss of intellectual control over swallowing. Patients with brainstem lesions may exhibit decreases in muscle strength and range of motion; decreased sensation; pharyngeal swallow absence or delay; pharyngeal dysfunction; or unilateral vocal cord paresis.

Signs of dysphagia include:

  • Drooling
  • Poor control of the tongue, tongue thrust, unintentionally spitting food from the mouth
  • Pocketing food in the cheek or under the tongue
  • Coughing or choking while eating
  • Complaints by patients that food is stuck in their throats
  • Excessive chewing time
  • Facial weakness
  • Slurred speech

Following evaluation by a speech-language pathologist, a videofluorographic swallowing study of liquids, purees, and solids may be undertaken to identify the swallowing disorder and organize a treatment plan. Fiberoptic laryngoscopy may be a useful means to rule out tracheal aspiration if tracheal aspiration and pharyngeal pooling are not observed during laryngoscopy and the gag reflex is normal. Other diagnostic procedures may include ultrasound of the oral musculature, scintigraphy to assess gastroesophageal reflux, and manometry of the pharynx and esophagus.

Suspicion of dysphagia should be high in stroke survivors since only 40% of patients who aspirate food or fluid may be identified during a bedside evaluation. Presence of aspiration or other types of swallowing disorders are not associated with the stroke lesion site. However, patients with combined bilateral hemispheric and brainstem lesions are more likely to aspirate than patients with cortical or brainstem lesions alone. Symptoms associated with aspiration include dysphonia (altered voice) and an impaired gag reflex associated with impaired cough. Rehabilitation programs which include identification and treatment of dysphagia also report reductions in rates of pneumonia.

Consequences of dysphagia include:

  • Malnutrition - This is estimated to occur in up to 64% of patients immediately following stroke onset, 35% of stroke patients 2 weeks after the stroke, and in up to 50% of stroke patients with severe stroke or prolonged hospitalizations. At two to four months poststroke, the incidence is thought to drop to approximately 20%. Malnutrition in stroke survivors is correlated with:
    • impaired function
    • longer stay in rehabilitation/nursing facility
    • frequency of infection
    • decubiti (bed sores)
    • death
  • Weight loss
  • Dehydration
  • Aspiration of food - Some studies have identified aspiration in 30-50% of stroke patients. It is a common cause of pneumonia.
  • Pneumonia - Up to 11% of stroke survivors develop pneumonia in the first three months after stroke and it is the most common cause of death in stroke survivors in the second and third month following stroke.

Other complications of stroke that could result in dysphagia include depression, factors preventing patients from feeding themselves such as paralysis or visual-spatial deficits, cognitive changes affecting concentration during eating, sensory deficits, or agnosia (denial of existence of a deficit).

Treatment of dysphagia includes modification in diet, head positioning, or other compensatory strategies to prevent aspiration. Many stroke survivors will regain normal swallowing function within 2 to 3 weeks. Most patients tolerate a full oral diet by the conclusion of rehabilitation, although some cannot drink thin liquids safely. When enteral feedings are necessary, the use of gastrostomies (a hole, or stoma, in the abdomen where a feeding tube is inserted) significantly lowers mortality when compared to that of nasogastric tubes. Even when stroke survivors are fed exclusively by gastrostomy, every attempt should be made to begin some oral feeding. The ability to take even small amounts of food by mouth allows the stroke survivor to practice swallowing and also provides some social element when friends and family gather together for a meal. In addition, patients who undergo therapy for dysphagia have lower rates of pneumonia than those who do not.

Depression

Depression may affect as many as 60% of stroke survivors, although the exact incidence is unclear. Yet it is estimated that less than 5% of these patients are properly diagnosed and treated. Depression may be related to mourning the loss of function or to actual alteration of function of catecholamine-containing neurons (specialized cells in the brain). There appears to be no association between the presence of depression and neuroanatomical location of the stroke. Though depression may occur in the period immediately following a stroke, it appears to be more prevalent in stroke survivors 6 months to 2 years poststroke.

Major depression generally abates 1-2 years after stroke with medications and is not typically chronic. However, minor depression may persist for many years. Studies have shown that depression at different stages of recovery relates to different aspects of handicap being experienced by the patient. For example, depression in early stages right after stroke may relate to presence of aphasia and not being able to live alone; after a few months depression may be association with dependence on other people for activities of daily living; after 1 year, depression may be association with lack of social contacts and feelings of isolation.

Poststroke depression has a strong impact on recovery and is associated with poor functional outcome. Additional affects of depression include:

  • Increased mortality
  • Severe physical disability
  • Reduced social activities
  • Reduced response to rehabilitation program
  • Poor language and communication
  • Longer hospitalizations

Management of poststroke depression includes traditional approaches, such as exercise, proper diet, counseling, and good sleeping habits. However, because patients typically need faster relief for their depression than these treatments provide, most clinicians will also begin treatment with antidepressant medications as soon as the patient is diagnosed. Some of the medications used to treat poststroke depression include sertaline (Zoloft), trazodone (Desyrel), fluoxetine (Prozac), citalopram (Celexa), nortriptyline (Aventyl), and methylphenidate (Ritalin).

Poststroke depression may be difficult to distinguish from symptoms resulting from the stroke itself, such as fatigue, loss of appetite, or difficulty focusing. In some cases, these common symptoms are mistakenly attributed to depression while in other cases, they may be attributed to the stroke when they are indicative of depression. One of the major factors in the difficulty of diagnosing true poststroke depression is the presence of cognitive deficits or communication difficulties such as aphasia which prevent the patient from accurately responding to questions or limit their reporting of symptoms. In addition, some stroke patients experience anosognosia (denial of a handicap) where they deny their depressive state even though it can be observed clinically. Also, the most common Depression Scales used for diagnosing poststroke depression (Beck Depression Inventory, Hamilton Depression Rating Scale, and the Zung Self-Rating Scale) are not specific to poststroke depression and, therefore, do not account for the special communication difficulties that relate to this specific population of patients.

In order to address the issue of stroke patients whose deficits may prevent them from being properly diagnosed with depression, researchers are designing new instruments to use more of a non-verbal assessment, including:

  • Biochemical markers of depression in the blood
  • Depression scales such as the Stroke Aphasic Depression Scale and the Poststroke Depression rating scale. They have not yet undergone rigorous testing for reliability and sensitivity, however, they are helping clinicians use different modalities to assess the needs of this particular population.

Fatigue

Approximately 40% of stroke patients experience fatigue in the first six months. It is important to evaluate if the fatigue is related to sources other than stroke, such as depression, medications (such as antidepressants, beta-blockers, or anticonvulsants), thyroid function or other comorbid conditions such as diabetes, infections, or renal disease. The patient should also be evaluated for sleep-disordered breathing which may manifest itself in snoring, sleep apnea, or oxygen desaturation, and causes excessive daytime sleepiness. Daytime sleepiness often resolves during the recovery period in the months after stroke. If fatigue interferes with rehabilitation, a daytime stimulant such as modafinil (Provigil) may be suggested. A large study of poststroke fatigue in Sweden indicated that fatigue may predict dependency on others for primary daily living activities and also may signify a higher long-term mortality rate.

Sleep Apnea

Sleep apnea is an important complication of stroke since it is associated with several issues that interfere with rehabilitation, including:

  • Fatigue resulting in difficulty cooperating during therapy
  • Exacerbation of cognitive deficits
  • Nocturnal incontinence
  • Changes in personality
  • Changes in memory
  • Cardiovascular changes such as hypercapnia (higher than normal carbon dioxide level in the blood); hypoxia (a deficiency of oxygen in the tissues which can result in pulmonary hypertension); hypertension; oxygen desaturation (less than normal amount of oxygen carried by hemoglobin in the blood)

Management of sleep apnea is difficult. Continuous Positive Airway Pressure (CPAP) is the fist-line treatment in non-stroke patients but this may be difficult for stroke patients since placement of the mask on the face may disorient the patient or weakness of facial muscles may prevent a good fit. It is important to check medications being taken by the patient to assess if they have any have side-effects related to sleep. In some cases, these medications cannot be discontinued. Daytime sleepiness due to sleep apnea often resolves during the recovery period in the months after stroke. If it interferes with rehabilitation, a daytime stimulant such as modafinil (Provigil) may be suggested.

Emotional Disturbances

Survivors of stroke may exhibit a wide range of emotions including fear, frustration, anxiety, sadness, or anger. Some of these emotions are caused by the stroke itself, and some may be caused as they begin to comprehend what has happened to them. Stroke survivors may also experience emotional lability - in which they may cry or laugh for no specific reason and at random or inappropriate times. Patients may need to be treated with medications to control severe emotional swings. As the brain heals from the stroke, the emotional outbursts may lessen over time.