After reading this chapter the student or therapist will be able to: 1. Describe the pathological processes, prevalence, and clinical presentation of people with multiple sclerosis. 2. Compare and contrast the types of multiple sclerosis and the common disease progression in each. 3. Discuss the medical management of the disease and the disease symptoms. 4. Describe how the International Classification of Functioning, Disability and Health provides a common language for describing the impact of disease on people with multiple sclerosis and how it provides a framework for rehabilitation management. 5. Describe the outcome measures that can be used to examine people with multiple sclerosis that cover body system problems (impairments), functional skill and activity limitations, and participation restrictions. 6. Develop a rehabilitation plan of care using evidence-based interventions to maximize patient function and quality of life. Multiple sclerosis (MS) is a chronic, inflammatory disease of the brain, optic nerve, and spinal cord mediated by the immune system.1 It is characterized by lesions of disseminated focal demyelination accompanied by variable axon damage and destruction and reactive gliosis. Initially, MS was thought to be a disease of the white matter (WM); however, recent investigations have shown that the gray matter (GM) is significantly involved. Lesions found in the GM typically contain demyelination and loss of neurons without the immune system infiltrates and inflammation characteristic of lesions in the WM. Tissue damage has been found outside the focal lesions throughout the GM that is associated with brain and spinal cord atrophy. These areas of demyelination and axonal damage interfere with normal conduction of neural signals, leading to a disruption of function. Later in the course of the disease, inflammation becomes uncommon while demyelination and axonal loss continue, suggesting replacement by a neurodegenerative disease process. Disease progression becomes more constant with a lack of exacerbation. The motor, sensory, and cognitive disability that accumulates in the advanced stages of the disease appears to be associated with the cortical GM pathology.2 Owing to the lack of inflammation, DMAs have not been shown to be beneficial in the later stages of the disease. MS is the primary cause of nontraumatic disability in young and middle-aged adults and the most common inflammatory condition of the central nervous system (CNS). It is reported that approximately 350,000 to 400,000 people in the United States and over 2.5 million people worldwide have the disease.3,4 People are most commonly diagnosed at age 20 to 50 years, with an average age of 32. However, MS can be diagnosed in people of any age. Approximately 5% of all patients with MS are diagnosed before their sixteenth birthday.5 MS is found in people who reside above the northern or below the southern 40° latitude with greater frequency than those who live closer to the equator (Figure 19-1). Given the increased sun exposure of people living closer to the equator, lack of vitamin D is being investigated as a potential factor contributing to disease development.6 Many researchers believe that exposure to an infectious agent may trigger the disease process: Epstein-Barr virus is currently considered a likely candidate. Women are affected two to four times more frequently than men. Even so, men are more likely to have a more aggressive disease progression and a worse prognosis.4,7 Caucasians with Northern European ancestry have the greatest incidence of MS, whereas people of Asian, African, or Hispanic ethnicity are at lower risk. African Americans have a lower incidence, but become disabled earlier than Caucasians, suggesting that tissue destruction occurs earlier and more rapidly.8 Inuits, Yakutes, Hutterites, Hungarian Romani, Norwegian Lapps, Australian Aborigines, and New Zealand Maoris do not appear to develop MS.9 Being diagnosed with MS may be related to age, gender, genetics, geography, or ethnic background. An identical twin with MS means that the other twin will have a 25% chance of diagnosis, suggesting something beyond genetics. Having a first-degree relative with MS will increase the risk of disease from 1/750 to 1/40.3 At least four types of MS have been identified (Figure 19-2). Although the course of the disease is highly variable even within a subtype of MS, there are characteristics common to each. The initial neurological episode or attack is typically identified as clinical isolated syndrome (CIS). Symptoms must last for at least 24 hours and can be monofocal or multifocal. If there are lesions present on magnetic resonance imaging (MRI), there is a high risk of developing MS. In one group of people with CIS followed for 20 years, 63% were diagnosed with definite MS.10 In secondary progressive MS (SPMS), relapses decrease in frequency over time and convert to a slow steady progression of increasing disability or disease severity. Relapses may occur early in SPMS but gradually lessen over time. People with RRMS eventually convert to SPMS 10 to 20 years after diagnosis.11 It is thought that the clinical disability associated with SPMS results from the neurodegeneration that occurs as a result of tissue injury that accumulates from early in the disease process. In addition to less inflammation, there is a greater amount of brain atrophy in people with SPMS compared with RRMS. Figure 19-3 shows the natural history of RRMS and SPMS, comparing the change in brain volume with increasing clinical disability and disease burden.2 Benign MS is identified when symptoms occur once and never recur. This happens in roughly 25% of cases.12 Recently, Sayao and colleagues13 reported that 52% of people with benign MS had not developed MS 20 years later. However, the remainder of people went on to develop MS, with at least 21% requiring the use of a cane. The authors could not identify any criteria associated with either developing MS or continuing to have the benign form. The risk of a more rapid disease progression is correlated with older age at diagnosis; male sex; initial symptoms involving the motor, sphincter, or cerebellar systems; multifocal disease at onset; shorter time between first and second attacks; and frequent attacks in the first 5 years postdiagnosis.7,14 Of people with MS, 65% to 97% report fatigue during the course of the disease; as many as 40% of people with MS state that fatigue is their most disabling symptom.15 There are two types of fatigue in people with MS: primary and secondary. Primary fatigue, often called lassitude, is caused by the effects of the demyelination and axonal destruction and its effect on nerve conduction. Restorative rehabilitation has little effect on primary fatigue from neurodegeneration. Secondary fatigue results from problems such as deconditioning, infections, sleep disturbances, poor nutrition, medication side effects, other medical conditions (such as thyroid disease), and heat intolerance. Clinicians should be extremely careful to separate the types of the fatigue in order to determine the most appropriate interventions. Sensory impairments are among the most common symptoms associated with MS and can affect the visual, somatosensory, and vestibular systems.16 The most common problem of the visual system is optic neuritis, which can produce blurry or double vision and/or painful eye movements and nystagmus. Somatosensory or proprioception disturbances can include dysesthesias (tingling, buzzing, or vibrations) or anesthesias (complete loss of sensation in part of the body). People may experience paresthesia or anesthesia in half of the body—upper or lower or side to side—or below a certain spinal cord level. Dysesthesias may be limited to small body areas such as a patch of skin on the head or a single upper or lower extremity. Vestibular system involvement occurs in 20% of people with MS at some time during their disease course17 and may manifest as dizziness and/or vertigo. A broad clinical definition of spasticity is a velocity-sensitive resistance to muscle stretch or a muscle spasm during movement.18 Some people report heaviness in the limbs, difficulty moving a joint, jumping of the extremities, or involuntary painful movements. Muscle spasms or cramping are frequently experienced by people with MS. Eighty four percent of people with MS report spasticity, with 34% indicating that their spasticity is moderate to severe.19 Female sex or longer disease duration are both associated with higher prevalence of spasticity. Spasticity has been highly correlated with patient-reported disability and poorer quality of life (QOL).19 Spasticity may change according to position and may result from increased effort during activity or from the presence of a noxious stimulus such as an infection, skin lesions, fractures, renal stones, distention of bladder or colon, or other physiological stressors such as certain medications (DMAs or serotonin reuptake inhibitors) or psychological distress. Environmental factors such as tight clothing, hunger, or elevated body or air temperature may also lead to increased spasticity. Spasticity can cause muscle contractures, skin breakdown, pain, and sleep disturbances, which often lead to secondary activity limitations and participation restrictions that limit performance of activities of daily living (ADLs) and mobility. Ataxia occurs in up to 80% of people with MS at some point in their disease progression.20 This motor deficit can occur from disturbances in the vestibular system or cerebellum or a loss of proprioception. Ataxia or a lack of coordination can manifest as difficulty with walking to difficulty with movements of the extremities such as overshooting or undershooting targets (dysmetria) or an inability to produce rapid alternating movements (dysdiadochokinesia). Occasionally, patients experience sustained body positioning (dystonia) of the extremities or head and neck. In different research studies, tremor is reported by 25% to 58% of people with MS, with the majority of people experiencing mild to moderate dysfunction.21,22 Action tremor, both postural and intention, are found in people with MS, pointing to the cerebellum as a likely source (see Chapter 21). Tremors affect the head, neck, vocal cords, limbs, and torso, with the upper extremities having the greatest occurrence.21,22 MS affects many of the systems required for postural control and balance, including sensory input (visual, somatosensory, and vestibular), central processing, and motor output. Therefore it is not surprising that over 50% of people with MS report falling one or more times in the previous 6 months.23–26 The incidence of bowel problems (35% to 68%) and bladder problems (52% to 97%) make them common in people with MS, as reported by two research studies.27,28 Symptoms include urinary urgency, nocturia, or retention of urine or feces.29 Incontinence of either system can also occur. Neurogenic detrusor muscle overactivity is the most common urological impairment in people with MS; 20% have detrusor muscle underactivity, and only 10% report no symptoms.28 Cognitive dysfunction occurs in roughly 40% to 70% of people with MS, with 70% demonstrating mild to moderate impairment.32,33 Although cognitive problems can occur at anytime, abilities affected early in the course of the disease are verbal fluency and verbal memory.34 Other cognitive dysfunctions common in people with MS include impairments in memory, processing speed, executive functioning, attention, and visuospatial learning. There is a fair correlation between cognitive decline and ability to work and unemployment because of the impairments in short- and long-term memory, problems with concentration, forgetfulness, and slowed word recall.35,36 This is a likely source of frustration for both patients and caregivers alike. Depression is two to three times more common in people with chronic health conditions than in the general population and has a greater incidence than other neurological conditions.37 From 26% to 50% of people with MS have been reported to experience depression during the course of the disease.32,38 Several factors contribute to the high incidence of depression in people with MS. The fact that MS is a chronic, progressive, and unpredictable disease that affects people in their early to middle adult years, is often invisible, and limits participation in many life roles often leads to a perceived reduction in QOL.39 Suicide is of great concern for people with depression, and rates are significantly higher in people with MS than in the general population.40 Depression is associated with a lower QOL and other symptoms of MS including fatigue, disability, pain, and cognitive impairment.41 Historically, people with MS would wait for a diagnosis for a year or more. Although there are no definitive tests that diagnose MS, the addition of MRI has accelerated diagnosis. In 2001 the International Panel on the Diagnosis of Multiple Sclerosis updated criteria to include MRI, visual evoked potentials, and cerebrospinal fluid (CSF) analysis. The 2005 Revised McDonald Criteria for MS diagnosis were designed to make the diagnostic process even more efficient and easier.42 The Poser criteria require the presence of two separate episodes over time, plus evidence of two or more lesions in separate brain or spinal cord regions identified by radiological imaging studies. Even with the improved technological measures used to facilitate diagnosis, an accurate clinical history is critical. Often patients will recall episodes of transient symptoms that did not last long enough to require attention by a primary care provider. In addition to the clinical history, MRI studies have improved diagnosis of MS. Although T2-weighted MRI images show MS lesions as hyperintense and identify new or active lesions, MRI has been shown (Figure 19-4) to overestimate clinical relapses. Conventional MRI with T1 weighting identifies lesions as hypointense (black holes) and is able to identify brain atrophy. T1 imaging demonstrates a stronger correlation with clinical status and disease severity than the lesion load found with T2 weighting. Gadolinium-enhanced T1-weighted MRI images show active MS lesions as hyperintense (white). Disease severity and progression are monitored by ongoing medical checkups, MRI imaging, and the use of several outcome measures. The Kurtzke disease severity scale was developed to allow primary care providers a way to measure clinical disability and chart disease progression. It has been replaced by the Expanded Disability Status Scale (EDSS) (Table 19-1).43 The EDSS is a 10-point ordinal scale completed by a physician or physician extender, with 0 indicating no disability and 10 indicating death caused by MS. Using a cane relates to an EDSS score of 6.0. The National MS Society (NMSS) Task Force on Clinical Outcomes Assessment also recommends the Multiple Sclerosis Functional Composite (MSFC)44 as a measure of disease severity and progression. This set of outcome measures is used to chart change in physical and cognitive function and will be discussed later in this chapter. It includes three tests that measure upper-extremity function (Nine-Hole Peg Test [NHPT]), lower-extremity function and mobility (25-Foot Timed Walk [25FTW]), and cognitive function (Paced Auditory Serial Addition Test [PASAT]). TABLE 19-1 ABBREVIATED EXPANDED DISABILITY STATUS SCALE Medical management of MS has two major goals: long-term management of the disease and exacerbations and symptomatic management. Early after diagnosis with CIS, it is recommended that people take DMAs. Recent evidence suggests that as the disease progresses it becomes less inflammatory and more neurodegenerative. Therefore medications aimed at reducing inflammation will be less effective as the disease progresses. Fox2 suggests that early treatment is needed to compensate for the later stages of the disease when inflammation is less prevalent. DMAs are aimed at reducing immune system dysfunction, thereby reducing damage to neural tissue and long-term disability for people with RRMS. There are several different medications that act on various components of the immune system with the intention of modifying the course of the disease (Table 19-2). In general, these drugs are approved for use with RRMS and are used off-label for other forms of MS and have been shown to reduce the number of attacks experienced. The majority of the drugs require injections; however, in 2010 the U.S. Food and Drug Administration (FDA) approved the first oral DMA, fingolimod. Measurement of therapeutic effectiveness includes relapse rate, progression of disability (EDSS), and quantitative evidence of lesions on MRI. All DMAs have side effects (see Table 19-2), but rarely are they serious. These medications are costly, and some people do not respond well or tolerate the side effects. It is common that people will try more than one type before finding the DMA they tolerate the best. TABLE 19-2 DISEASE-MODIFYING AGENTS: INDICATIONS AND SIDE EFFECTS High-dose corticosteroids (such as prednisone or methylprednisolone) are used to reduce inflammatory response during exacerbations for people with RRMS. Although no medications have demonstrated effectiveness in people with PPMS, anecdotal evidence suggests that intermittent pulses of intravenous methylprednisolone can help slow progression of clinical disability in some patients.2 A host of additional medications are used to manage the symptoms associated with MS. Each will be discussed as part of symptom management. Also refer to Chapter 36 for additional information. Spasticity can interfere with physical function and hygiene. However, spasticity can also add support to weakened limbs, allowing more effective mobility. The goal of medical management of spasticity is to maintain full range of motion (ROM) of muscle and soft tissue structures to allow maximal physical function and proper hygiene. Haselkorn and colleagues18 describe the clinical practice guidelines for managing spasticity in people with MS written by the Multiple Sclerosis Council. A complete assessment of the spasticity and how it affects the individual’s life is required. Typically, successful management includes both pharmaceuticals and rehabilitation. Management of focal spasticity may include local anesthetics such as lidocaine, bupivacaine, etidocaine, all of which are short acting with side effects of CNS and cardiovascular toxicity and hypersensitivity. Neurolysis treatment with phenol or alcohol is longer acting; however, these agents can have the side effects of pain, swelling, fibrosis, and dysesthesias. Focal spasticity affecting functional muscle groups can also be effectively treated with neuromuscular blocking agents including alcohol, phenol, or botulinum toxin. Botulinum toxin type A (Botox) has been shown to improve spasticity as measured by the Ashworth Scale and the hygiene score, but no changes were noted in spasm frequency score.45 Blocks last 1 to 3 months with relatively few side effects. Similarly, botulinum toxin type B was shown to reduce hip adductor spasticity.46 Clinical practice guidelines18 recommend that neuromuscular blocks be performed by appropriate specialists in conjunction with a rehabilitation program. Refractory spasticity is defined as unsuccessful treatment with oral medications and/or rehabilitation. In this situation two other options exist: surgery or placement of an intrathecal baclofen pump (ITB). Surgical procedures include tendon lengthening or tendon transfer and are performed to maintain adequate hygiene or prevent or correct contractures and therefore preserve function. Intrathecal pumps, inserted into the spinal cord, allow adjustable drug delivery. Baclofen, the drug of choice for the intrathecal pump, can be given in higher doses; use of the pump avoids the side effects often encountered when the drug is taken orally. Relapses are more commonly reported in people on oral medications than those using ITB. People using ITB also report higher levels of satisfaction, less spasticity, and fewer painful spasms compared with those on oral medications.19 Both nociceptive and neuropathic pain can be present in people with MS. Therefore it is important to discern the type of pain in order for the most appropriate treatment to be rendered. Nociceptive pain can often be treated with analgesics (acetaminophen, nonsteroidal antiinflammatory drugs [NSAIDs], or opioids) and is more amenable to physical therapy (discussed later under rehabilitation management). Neuropathic pain generally requires pharmacological intervention, although an interdisciplinary team approach may be valuable. First-line medications for neuropathic pain that occurs in the spinal cord are calcium channel blockers (gabapentinoids) or N-methyl-d-aspartate (NMDA) antagonists (ketamine). When pain is present in the head, the primary treatment is opioid drugs such as antidepressants (tricyclics) or anticonvulsants (gabapentin or pregabalin).47 In the case of trigeminal neuralgia, the first choice is often carbamazepine. Refer to Chapter 32 on pain management for additional information. Physical rehabilitation is the primary intervention used to manage mobility dysfunctions. However, one medication has recently been FDA approved to improve gait. In clinical studies dalfampridine (Ampyra) demonstrated the ability to improve walking speed in people with MS.48 However, changes in the quality of gait or movement were not measured. Tremor management using medications such as isoniazid, carbamazepine, ondansetron, or cannabis extract has been minimally effective.49 Surgical interventions including stereotaxic thalamotomy and deep brain stimulation have been studied, but the evidence to support the effects on functional status and disability is lacking. The effectiveness of other options including physical therapy, tremor-reducing orthoses, and extremity cooling have yet to be proven beneficial in clinical trials.49 Behavioral modification and rehabilitation are used to help alleviate the symptoms of bladder incontinence or detrusor muscle overactivity. A few medications have been shown to be helpful: anticholinergic agents are used to manage detrusor overactivity or dyssynergia, and underactivity is treated with cholinomimetic agents.2 People with constipation are encouraged to combine adequate fluid intake with dietary fiber or bulk-forming medications.2 Depression is very common in people with MS, yet it is infrequently identified or treated.50 Therapy can include supportive psychotherapy and medication given individually or in combination. To date two pharmacological therapies have shown the most promise in reducing cognitive deficits (l-amphetamine sulfate and donepezil), and neither has serious adverse effects.51,52 Chronic neurodegenerative conditions, such as MS, result in a loss of physical and cognitive function from the destruction of neurons and from a lack of activation of the affected systems. People with MS experience physical and cognitive impairments potentially leading to inactivity and resultant deconditioning (Figure 19-5). This often becomes a cycle that is difficult to break. One question that frames the rehabilitation strategy chosen is whether the focus should be compensation for or restoration of lost function. Compensation includes interventions such as wheelchairs or walkers to assist with mobility or braces for absent or inadequate muscle power. Restoration is aimed at increasing the capacity of the system—for example, maximizing cardiovascular endurance by increasing maximal oxygen uptake or restoring full ROM. Therefore, prescribing programs, activities, and exercises that provide an adequate stimulus to produce adaptation is critical to restore function or improve motor and cognitive performance. Although each patient case is unique, the most likely answer is that both strategies will be employed. The challenge for rehabilitation professionals is to sort out how much of a patient’s dysfunction arises from neurodegeneration, which necessitates compensation, and how much occurs from inactivity and system deconditioning, in which case system capacity can be restored to some extent. Rehabilitation professionals must choose therapeutic interventions based on whether compensation or restoration is the goal. For rehabilitation professionals managing people with MS, the International Classification of Functioning, Disability and Health (ICF) model (refer to Chapter 1) provides an excellent framework for assessment and management regardless of the setting in which the patient or client is encountered.53 Although guided by the opening interview and chart review, the initial assessment must include how the individual with MS is functioning in home, at work, and in recreation environments and which impairments of bodily structure or function might be contributing to the identified activity limitations and participation restrictions. Rehabilitation professionals must consider how personal and environmental factors may impede or facilitate achievement of rehabilitation goals. Personal factors in people with MS may include whether the patient is heat intolerant, experiences MS-related fatigue, or has the confidence or motivation to perform certain tasks. Environmental factors that may be of particular importance for the patient with MS may be living in a hot climate or having access to cooling equipment such as air conditioning or cooling garments. It is critical to understand how the disease affects the lives of both individual patients and their caregivers. Outcome measures designed to test impairments, activity, and participation, along with assessments of environmental and personal factors, will help health care professionals understand the deficits of their patients and determine the best place to focus rehabilitation efforts and monitor the patient’s response to intervention.54 Because of the myriad CNS lesions and variable clinical presentations in people with MS, there is no one approach that is the gold standard for rehabilitation management. Whatever the approach, evidence is growing that rehabilitation is beneficial. Intensive inpatient therapy programs provide long-term improvement in a number of functional skills, participation, and QOL but may not change underlying impairments. Prospective studies have shown that intensive inpatient rehabilitation improves disability and QOL and that these benefits can be long lasting.55–58 High-intensity programs in the outpatient clinic or home environment offer evidence of short-term symptomatic changes that have translated into improved participation and QOL.56,59 The initial interview must include a quick screen or questioning about the body systems and areas that are commonly impaired in people with MS and the problems commonly encountered: motor strength, coordination, spasticity, sensory disruption (vestibular, visual, and somatosensory), bladder control, depression, and cognition. If impairments are present, there is a strong likelihood of negative impact on the patient’s ability to perform ADLs or participate in activities related to work, home, and leisure. All patients with MS must be asked if they have fallen in the last 6 months because of the high rate of falling in people with MS.23–25,26 Results of the interview and chart review will help develop hypotheses about which potential impairments might be contributing to the patient’s or client’s physical or cognitive dysfunctions. Therefore the examination needs to be designed to observe the problematic tasks and test the hypotheses developed. During the assessment, examiners must determine if the problems identified by the patient (or those found by the assessor) fit within their scope of practice or whether the patient requires a referral to an appropriate health care professional. A good example is identifying people with depression using a quick two-question screen. According to Mohr and colleagues,60 these questions are 98.5% sensitive for identifying major depressive disorder. The two questions are (1) “During the past 2 weeks, have you often been bothered by feeling down, depressed, or hopeless?” and (2) “During the past two weeks, have you often been bothered by having little interest or pleasure in doing things?”61 An answer of yes to either question should trigger a referral to the patient’s primary care provider for follow-up. Comprehensive lists of standardized tests and measures for impairment, activity limitations, and participation restrictions or QOL are provided in Chapter 8. The next section of this chapter will primarily focus on the tests and measures found to be valid and reliable in the examination of individuals with MS. Spasticity can be measured using resistance to passive ROM and Ashworth62 and Modified Ashworth Scales.63 However, because these scales measure spasticity at rest, they may not reflect the degree to which spasticity may be interfering with function. Careful observation of the patient’s movements may also inform the clinician about how spasticity is affecting the patient’s ability to move.
Multiple sclerosis
Overview of multiple sclerosis
Pathophysiology
Incidence and prevalence
World distribution of multiple sclerosis. (From Multiple Sclerosis Resource Center, www.msrc.co.uk.)
Types of multiple sclerosis and clinical characteristics
Types of multiple sclerosis.
Clinical manifestations
Fatigue
Sensory impairments
Motor systems impairments
Bowel and bladder dysfunction
Cognitive impairments
Depression
Medical management
Diagnosis
SCORE
FUNCTION
1.0
Normal neurological examination findings
2.0
Minimal disability
3.0
Moderate disability
4.0
Ambulates 12 hours without aid
5.0
Disability impairs activity (walks 1500 feet without assistance)
6.0
Intermittent or unilateral constant assistance
6.5
Bilateral support required (walker, crutches, two canes)
7.0
Unable to walk 15 feet without assistance
8.0
Basically constrained to bed
9. 0
Bedridden
10.0
Death from multiple sclerosis
Medications
Disease-modifying agents
FDA-APPROVED DISEASE-MODIFYING AGENTS
INDICATION
COMMON SIDE EFFECTS
IFN beta-1a (Avonex)
CIS
RRMS
SPMS
Flulike symptoms
Injection-site reactions
Depression
Elevated liver enzymes
IFN beta-1a (Rebif)
IFN beta-1b (Betaseron)
IFN beta-1b (Extavia)
Glatiramer (Copaxone)
CIS
RRMS
Injection-site reactions
Systemic reactions, immediately postinjection
Elevated liver enzymes
Natalizumab (Tysabri)
RRMS
Progressive multifocal leukoencephalopathy
Infusion reactions
Hepatotoxicity
Mitoxantrone (Novantrone)
Intravenous infusion
RRMS
SPMS
PRMS
Cardiotoxicity
Treatment-related leukemia
Infection risk
Alopecia
Amenorrhea
Fingolimod (Gilenya)
RRMS
Flulike symptoms
Increased liver enzymes
Headache
Diarrhea
Back pain
Cough
Antiinflammatory medications
Symptom management
Fatigue
Spasticity
Pain
Mobility
Tremor
Bowel and bladder management
Depression and cognitive impairments
Rehabilitation management
Overview
Assessment
Assessing body system problems contributing to activity limitations
Spasticity.
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