MULTIPLE SLEROSIS

Presented by HARSHA.J
Jane is a 24-year-old store clerk. Bob is a 32-year-old stockbroker.
 The Discovery of MS
 August 4, 1421, when Jan Van Bieren, count of holland, described the
“strange disease of the virgin lidwina
 The first descriptions of the physical changes that MS Jean Cruveilhier,
professor of pathologic anatomy
 The first scientific description of the signs and symptoms of MS came
from Jean-martin Charcot (1825–1893). Charcot outlined a condition
called la sclérose en plaques
Multiple sclerosis
Multiple sclerosis (MS) is an autoimmune disease
characterized by inflammation, selective demyelination, and gliosis.
It causes both acute and chronic symptoms and can result in
significant disability and impaired quality of life.
Charcot’s triad Paralysis
and
Dr. Jean Charcot in 1868 intention
defined its clinical and pathological tremor
characteristics: paralysis and the
cardinal symptoms of intention
tremor, scanning speech, and
nystagmus. Using autopsy studies he Charcot’s
identified areas of hardened plaques triad
and termed the disease sclerosis in
plaques. Scanning
Nystagmus
speech
 Incidence and prevalence
 MS affects approximately 400,000 persons in the united states; worldwide
MS affects approximately 2.1 million people.
 Between ages 20 and 40 years. MS is rare in children, as is the onset of
symptoms in adults older than age 50 years.
 More common in woman than in men by a ratio of 2:1 to 3:1.
 The incidence and prevalence of MS overall have increased over the last 5
decades.
Aetiology
 The risk of MS is increased in persons with an affected family member.
 Genetic studies have revealed many interacting alleles that may contribute to
MS susceptibility with mutations in the human leukocyte antigen major
histocompatibility complex (MHC) gene most strongly correlated.
 molecular mimicry
 Implicated viruses in this process under investigation include the Epstein-Barr
virus, measles, canine distemper, human herpesvirus-6, and Chlamydia
pneumoniae, though none have been definitely proven to trigger MS.
 Risk of MS may also be increased with vitamin D deficiency and smoking.
 Pathophysiology
The immune response triggers activation of immune cells

Activate autoantigens, producing autoimmune cytotoxic

effects within the CNS

Phagocytic activity of macrophages may also contribute to

demyelination

Disruption of the myelin sheath and active demyelination

slows neural transmission and causes nerves to fatigue
rapidly
 An acute inflammatory event emerges

Edema and infiltrates surround the acute lesion and can cause a mass effect
further interfering with the conductivity of the nerve fiber

This inflammation (which gradually subsides) may, in part, account for the
pattern of fluctuations in function that characterize this disease

With repeat attacks, the anti-inflammatory processes become less effective

and are unable to keep up
 One form of MS, primary-progressive
MS, appears to be associated
exclusively with disease of the
oligodendrocytes.
 Gliosis refers to the proliferation of
neuroglial tissue within the CNS and
results in glial scars (plaques).
 DISEASE COURSE
 Highly variable and unpredictable
 Benign MS malignant MS (Marburg
Disease)

Four major disease courses (clinical subtypes) of MS

 Relapsing-remitting MS (RRMS)
 Secondary-progressive MS (SPMS)
 Primary-progressive MS (PPMS)
 Progressive-relapsing MS (PRMS)
 Exacerbating Factors
 MS relapses (exacerbations) are defined by new and recurrent MS symptoms
lasting more than 24 hours but generally of longer duration that are unrelated
to another etiology.
 Avoiding these factors is important in ensuring the patient’s optimal function.
1. Viral or bacterial infections (e.g., cold, flu, urinary tract infection, sinus
infection) and diseases of major organ systems (e.g., hepatitis, pancreatitis,
asthma attacks)
2. Stress (Both major life stress events and minor stresses)
 Pseudoexacerbation
 The overwhelming majority of individuals with MS demonstrate an adverse
reaction to heat, known as Uthoff’s symptom.
SYMPTOMS
 Symptoms of MS vary considerably, depending on the location of
specific lesions.
 Early symptoms typically include minor visual disturbances (e.g.,
episodes of double vision) and paresthesias progressing to
numbness, weakness, and fatigability.
Symptoms contd.,
Sensory:
 Focal deficits can produce limited areas of diminished sensation.
 Paraesthesia (pins-and-needles sensation) or numbness of the face, body, or
extremities.
 Disturbances in position sense are also common, as are lower extremity (le)
impairments of vibratory sense.
Pain :
 80% of patients with MS experience pain
 The pains are described as intense, sharp, shooting, electric shock–like, and burning.
 The most common types are trigeminal neuralgia, paroxysmal limb pain, and
headache.
 Musculoskeletal pain
Lhermitte’s sign
A common sign of posterior column damage in the spinal cord is
Lhermitte’s sign in which flexion of the neck produces an
electric shock–like sensation running down the spine and into
the LEs.
Visual:
 Found in approximately 80% of patients.
 Optic neuritis
 Scotoma
 Vision generallyimproves within 4 to 12 weeks.
 Marcus Gunn Pupil
 Nystagmus
 Internuclear ophthalmoplegia - lateral gaze palsy on the affected side and
nystagmus of the opposite abducting eye with gaze to one side.
 Diplopia
Contd.,

Motor :
 Weakness
 Spasticity
 Fatigue

Comes on abruptly without warning and typically worsens throughout the day.

Interferes with physical functioning (79% of patients), overall role performance (67%
of patients), social participation, and perceived health status.

Severity of disease does not seem to be related to fatigue severity;

Aggravating factors contributing to fatigue include physical exertion, exposure to heat
and humidity, disturbed or reduced sleep, depression, low self-esteem and mood disorders,
and medical conditions
Contd.,

Coordination and balance:

 Demyelinating lesions in the cerebellum and cerebellar tracts are
common in MS
 Clinical manifestations - Ataxia, postural and intention tremors,
hypotonia, and truncal weakness.
Gait and Mobility:
 Ataxic gait
 Scissoring gait pattern

Speech and Swallowing:

 Dysarthria
 Dysphonia
 Dysphagia (Aspiration pneumonia)
Contd.,
Cognitive:
 50% of patients
 Most likely affects - short-term memory, attention and concentration,
information processing, executive functions
Depression:
 Common in patients with MS
 Due to focal lesion or as side effects or due to stress of the unpredictive
nature of the disease.
Emotional:
 Pseudobulbar effect ( emotional incontinence or involuntary emotional
expression disorder)
Contd.,
Bladder
 Demyelinating lesions affecting the lateral and posterior spinal tracts
unmask the sacral reflex arc producing loss in volitional and synergistic
control of the micturition reflex.
 Types of bladder dysfunction in MS can include a small, spastic bladder (a
failure to store problem), a flaccid or big bladder (a failure to empty
problem), or a dyssynergic bladder.
Bowel
 Constipation is the most common bowel complaint in MS and results from
lesions affecting control of the gastrocolic reflex.
Sexual
 Sexual dysfunction has tremendous functional and psychosocial implications
for both patient and partner.

DIAGNOSIS
The diagnosis of MS is made by the neurologist based on a careful medical history, a
complete neurological examination, and supportive laboratory tests.
 Evidence of damage must be present in at least two separate areas of the CNS
(dissemination of lesions in space) and damage must have occurred at two separate
points in time at lease 1 month apart.
 McDonald Criteria of the International Panel on Diagnosis of MS
 Laboratory tests used to help confirm the diagnosis include magnetic resonance
imaging (MRI), evoked potentials (EP), and lumbar puncture (LP) with cerebrospinal
fluid (CSF) analysis.
MRI
 MRI is highly sensitive for detecting MS plaques
in the white matter of the brain and spinal cord.
 New lesions with active inflammation that occur
during the preceding 6 weeks or so are seen as
areas of increased signal intensity, “bright
spots.”
 Contrast-enhanced T1- weighted images
(gadolinium-enhanced) are used to detect more
long-term disease activity. These lesions are
seen as “black holes” on the MRI
Evoked potentials:
 Up to 90% of individuals with MS demonstrate abnormal EP. The
presence of demyelinating lesions on visual, auditory, and somatosensory
pathways produces slowed conduction.
Lumbar puncture with CSF analysis:
 Patients with MS show elevated total immunoglobulin (IgG) in CSF and
the presence of oligoclonal IgG bands (seen in 90% to 95% of patients) in
response to inflammatory demyelinating lesions.
ICD-10-CM Diagnosis Code
 G35 is a billable/specific ICD-10-CM code that can be used to indicate a
diagnosis for reimbursement purposes.
Applicable To
 Disseminated multiple sclerosis
 Generalized multiple sclerosis
 Multiple sclerosis NOS
 Multiple sclerosis of brain stem
 Multiple sclerosis of cord
 MEDICAL MANAGEMENT
Management of Acute Relapses
Corticosteroid therapy (methylprednisolone) is used to treat acute disease relapses
(exacerbations), shortening the duration of the episode.
Disease-Modifying Therapeutic Agents
Synthetic interferon drugs (interferon beta-1b [Betaseron, Extavia], interferon beta 1-
a [Avonex and Rebif])
Management of Symptoms – spasticity:
Oral baclofen (Lioresal) is commonly used and is highly effective in reducing muscle
tone and decreasing the frequency of spasms and clonus.
Botulinum toxin (BT) injections are used to provide localized relief of muscle tone and
spasms.
Contd.,
 Surgical intervention:

severing tendons (tendonotomy), nerves (neurectomy), or nerve roots

(rhizotomy).
Fatigue :
Amantadine (Symmetrel) and modafinil (Provigil)
Tremor:
Medications used to decrease tremor include hydroxyzine (Atarax, Vistaril),
clonazepam (Klonopin), propranolol (Inderal), buspirone (Buspar),
ondansetron (Zofran), and primidone (Mysoline).
Tools to measure clinical impairment
 Expanded disability status scale (EDSS)
 Completed by a physician
 An assessment of neurologic function and a scale to measure a client’s ambulatory and
functional mobility status.
 The OT practitioner should be familiar with the EDSS because it is often mentioned in
the literature as a baseline for evaluating disability and has been adopted by the
international federation of MS societies
 Limitations - does not allow specific assessment of all adls and is not sensitive to
potential cognitive and sexual deficits in MS
 The MS functional composite (leg function and ambulation, arm and hand function, and
cognition.) – More sensitive
FRAMEWORK FOR REHABILITATION
 In a Cochrane Database Systematic Review of multidisciplinary
rehabilitation for adults with MS, researchers identified 10 trials (9
randomized controlled trials [RCTs] and 1 controlled clinical trial
[CCT] with 954 participants and 73 caregivers) that met the
inclusion criteria. Support was strong for producing both short- and
long-term gains (up to 12 months) following rehabilitation in activity
and participation for both inpatient and outpatient programs.
 Low-intensity programs conducted over longer time periods
produced stronger evidence in improving quality of life.
 Restorative intervention
 Preventative intervention
 Secondary prevention
 Tertiary prevention
 Compensatory intervention
 Maintenance therapy

Defined as a series of occasional clinical, educational, and administrative

services designed to maintain the patient’s current level of function.
Individuals with MS who benefit from maintenance therapy typically are in
the late stages of the disease (expanded disability status scale [EDSS] stages
7.0 to 9.5
Occupational therapy evaluation

Occupational Occupational Performance

profile performance skills
Goal setting
 For a client with a progressive disease such as MS, goal setting focuses on
the client’s need to adapt as the disability progresses.
 Families often need to negotiate role changes to accommodate the
person with MS, who may not be able to participate consistently in a
previously established family role.
 The client’s ability to adapt depends on the family and client’s
acknowledgment of deficits and willingness to consider alternatives.
OT Intervention
OT intervention may include

(1) Problem-solving compensatory strategies;

(2) Time and energy management;

(3) Role delegation; and

(4) The use of adaptive equipment to compensate for motor, sensory,

endurance, cognitive, and visual deficits.

Journal
Effects of an Energy Conservation Course on
Fatigue Impact for Persons With Progressive
Multiple Sclerosis
 OBJECTIVE. Fatigue is a common, troublesome symptom for persons with
multiple sclerosis. This study evaluated the effects of an energy conservation
course on fatigue impact for persons with multiple sclerosis whose
symptoms cause moderate to severe disability.
 METHODS. Thirty-seven persons with progressive multiple sclerosis
participated in an 8-week experimental energy conservation course
treatment and an 8-week control period of traditional treatment using a
crossover design. The Fatigue Impact Scale (FIS) was used to assess fatigue
impact before and after the experimental and control periods, and 8 weeks
post-energy conservation course.
 RESULTS. After participation in the energy conservation course, the
average FIS total score and physical, cognitive, and psychosocial subscale
scores decreased significantly, whereas the total and subscale scores did
not change significantly during the control period. Additionally,
decreased fatigue impact was maintained 8 weeks after course
completion for evaluated participants.
 CONCLUSION. This study provides evidence that this energy
conservation course can be a beneficial intervention for persons with
progressive multiple sclerosis.
Energy Conservation Education
 The principles presented throughout the course include:
 (a) the value of rest;
 (b) budgeting and banking energy;
 (c) incorporating rest periods throughout the day;
 (d) learning to communicate personal needs to others;
 (e) using good body mechanics and posture;
 (f ) using energy-efficient appliances and organizing stations of activity;
 (g) separating fatiguing tasks into components;
 (h) prioritizing and setting standards for activities;
 (i) planning rest periods with self-care, productivity, and leisure activities so
that a balance can be maintained; and
 (j) reviewing course principles and setting short-term and long-term goals.
PROGNOSIS
 Multiple sclerosis is seldom fatal and life expectancy is shortened by
only a few months. Concerns about prognosis center primarily on the
quality of life and prospects for disability. Most patients and
physicians harbor an unfounded view of MS as a relentlessly
progressive, inevitably disabling disease. The truth is that 15 years
after the onset of MS, only about 20% of patients are bedridden or
institutionalized.
PROGNOSIS
 Another 20% may require a wheelchair, or use crutches, or a cane to
ambulate, but fully 60% will be ambulatory without assistance and
some will have little deficit at all. Perhaps as many as 1/3 of all
patients with MS go through life without any persistent disability,
and suffer only intermittent, transient episodes of symptoms.
References
 PHYSICAL REHABILITATION 6th edition Susan B. O’Sullivan, PT, EdD, Thomas J. Schmitz, PT,

PhD, George D. Fulk, PT, PhD Chapter 16: Multiple Sclerosis 721 (Susan B. O’Sullivan, PT,
EdD • Robert J. Schreyer, PT, DPT, NCS, MSCS, CSCS)
 PEDRETTI’S OCCUPATIONAL THERAPY: PRACTICE SKILLS FOR PHYSICAL DYSFUNCTION 7th

edition Chapter 35. Degenerative Diseases of the Central Nervous System - Section

4: Multiple Sclerosis, 936, Winifred Schultz-Krohn, Diane Foti, Carolyn Glogoski

 WILLARD & SPACKMAN’S Occupational Therapy 11th EDITION UNIT 15: Common
Conditions: Related Resources and Evidence page no.-1033
 Multiple Sclerosis, The Facts You Need Paul O’Connor, 5th edition Key Porter Books,
2014.