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.

Early in the course of the disease, focal inflammatory WM lesions are composed of immune system components that produce demyelination, axonal injury, and loss of oligodendrocytes. Astrogliosis activated by the damaged neurons produces gliotic scarring (visualized as sclerosis in postmortem brain tissue) called plaques. Active disease is followed by periods of remission in which acute inflammation is reduced. Axonal remyelination occurs but is highly variable and is related to recovery of function during periods of remission. The degree of axonal loss is associated with the severity of the inflammation; however, axons are spared in the majority of WM lesions. Treatment in the initial stages of the disease is aimed at reducing inflammation and immune system infiltration with disease-modifying agents (DMAs).

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.

Incidence and prevalence

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.

Figure 19-1 World distribution of multiple sclerosis. (From Multiple Sclerosis Resource Center, www.msrc.co.uk.)

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

Types of multiple sclerosis and clinical characteristics

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.

Figure 19-2 Types of multiple sclerosis.

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

Relapsing remitting MS (RRMS) represents about 85% of people with MS, characterized by exacerbations (attacks, flairs, relapses) that can last days to months and are typically followed by periods of improved function. During remissions, function can return to prerelapse levels, but most frequently it does not recover fully. Attacks normally occur with a frequency of one or two per year. Approximately 90% of people with RRMS transition to SPMS after 20 years or around 40 years of age.

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

Figure 19-3 Natural history of relapsing remitting multiple sclerosis (RRMS)—conversion to secondary progressive multiple sclerosis (SPMS). Figure shows the typical clinical course of RRMS with conversion to SPMS. Magnetic resonance imaging (MRI) activity *(gray line and boxes)* indicates the inflammatory lesions; they occur more frequently early in the disease and occur with greater frequency than in clinical disability *(solid black line).* Brain volume indicated by the stippled line shows brain atrophy increasing as the inflammatory component of the disease slows and is replaced by neurodegeneration.

Primary progressive MS (PPMS) is less common, affecting only 10% to 15% of people with MS. From disease onset, progression results in a gradual worsening of symptoms without relapses. People tend to be older when diagnosed (late 30s or early 40s), have fewer abnormalities on brain MRI, and respond less favorably to standard MS therapies. Progressive myelopathy is commonly associated with PPMS.

Progressive relapsing MS (PRMS) is the least common form (5%). This form of MS typically begins with a progressive course with clear relapses or exacerbations.

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

Clinical manifestations

MS can affect the optic nerve and any tissue within the brain or spinal cord, so almost any neurological symptom can result. Individual assessments are required to identify the problems present. Even so, the following list constitutes the most common problems encountered by people with MS.

Fatigue

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

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.

People with MS can have pain associated with the damage to neural tissue (neuropathic pain). This may manifest as neuralgias with burning, itching, or electric shocklike sensations. Lhermitte sign is an electric shock–like shooting sensation that can run into the upper extremities or down the back in response to flexion of the neck.

Motor systems impairments

Deficits in the motor system include weakness, spasticity, ataxia, and tremor. Paresis or muscular weakness is frequently seen in people with MS and is associated with several causes. Like fatigue, weakness can be caused by damage to the myelination and axons of motor and premotor neurons in the CNS that can manifest in many different patterns including monoparesis, paraparesis, hemiparesis, or quadriparesis. However, additional causes of muscle weakness can also be associated with disuse deconditioning and may also result in muscle atrophy. When muscle weakness or loss of motor control is seen in the muscles of speech, it results in dysarthria. Paralysis or total loss of muscle strength occurs with less frequency but can be devastating for patients. Several patterns of paralysis (or “-plegia”) occur in people with MS including paraplegia, hemiplegia, and quadriplegia.

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

Bowel and bladder dysfunction

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

Sexual dysfunction

Sexual dysfunction affects 40% to 85% of women with MS and 50% to 90% of men. It can manifest as erectile dysfunction, impotence, inability to achieve orgasm, and, in men, retrograde ejaculation.²⁸^,³⁰^,³¹

Cognitive impairments

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

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

Heat intolerance

Uhthoff phenomenon is a temporary worsening of MS-related problems associated with an increase in core body temperature. Such increases can occur with physical exertion such as exercise or with a change in the environment such as hot baths or showers, hot weather, and hot air temperature.

Medical management

Diagnosis

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).

Figure 19-4 T2-weighted magnetic resonance imaging (MRI) scan of plaques associated with multiple sclerosis. Plaques are indicated by arrows. (From Frey H, Lahtinen A, Heinonen T, Dastidar P: Clinical application of MRI image processing in neurology. *Int J Bioelectromagnet* 1(1), 1999.)

Two additional medical tests can be used to aid in the diagnosis of MS and differentiate it from other diseases and conditions. The first is the analysis of CSF. This requires a lumbar puncture in which CSF is gathered and analyzed to identify oligoclonal bands representing the presence of immune system proteins indicating that the body is attacking itself. The majority of people with MS have oligoclonal bands; however, because people with other diseases or conditions also have oligoclonal bands, the test is not specific for MS. The lack of oligoclonal bands at diagnosis has been related to a slower progression of the disease and increased time to reach markers of disability such as walking with an assistive device or confinement to a wheelchair.

Evoked potentials record the nervous system’s response to stimulation of a specific sensory pathway (visual, auditory, vestibular, or general somatosensory). Demyelination and axonal degeneration cause a slowing of signal transmission along neurons and therefore will increase the response time to an externally applied sensory stimulus. Damage to the optic system is a common first symptom in MS, and therefore visual evoked potentials are often most helpful in diagnosis.

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

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

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. Fox 2 suggests that early treatment is needed to compensate for the later stages of the disease when inflammation is less prevalent.

Medications

Disease-modifying agents

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

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

CIS, Clinical isolated syndrome; FDA, U.S. Food and Drug Administration; IFN, interferon; RRMS, relapsing remitting multiple sclerosis; SPMS, secondary progressive multiple sclerosis.

Antiinflammatory medications

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.

Symptom management

Tremor

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

Bowel and bladder management

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 and cognitive impairments

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

Rehabilitation management

Overview

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.

Figure 19-5 Interaction among impairments, inactivity, and deconditioning. People with multiple sclerosis often experience physical and/or cognitive impairments that can lead to or be increased by inactivity. Deconditioning and disuse can reduce activity levels or be caused by inactivity. This can become a cycle that is self-perpetuating. (Modified from Multiple sclerosis treatment: impact on quality of life (Clinical monograph, p. 10): Proceedings from Clinical Medical Education/Clinical Education Symposium at the Consortium of Multiple Sclerosis Centers Annual Meeting. Washington, DC, June 2007.)

Rehabilitation for people with MS occurs in every setting: inpatient hospitals, outpatient clinics, skilled nursing facilities, home care settings, and the community. With the current climate of decreasing access to and reducing coverage for rehabilitation, therapists must be able to make evidence-based arguments to primary care providers and insurers, as well as patients, to support effective therapeutic interventions that will achieve the goals of optimal physical and cognitive functioning, safety, and QOL.

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

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Multiple sclerosis

Overview of multiple sclerosis

Pathophysiology

Incidence and prevalence

Types of multiple sclerosis and clinical characteristics

Clinical manifestations

Fatigue

Sensory impairments

Motor systems impairments

Bowel and bladder dysfunction

Sexual dysfunction

Cognitive impairments

Depression

Heat intolerance

Medical management

Diagnosis

Medications

Disease-modifying agents

Antiinflammatory medications

Symptom management

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